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recombinant human gas6  (R&D Systems)


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    Structured Review

    R&D Systems recombinant human gas6
    A qPCR analysis of <t>GAS6</t> expression in Calu-3 and MKN7 parent cells treated with nonspecific (control) or GAS6-specific siRNAs for 48 h. * P < 0.05 (unpaired t-tests). B MTT assays evaluating cell viability of Calu-3 and MKN7 cells treated with nonspecific or GAS6-specific siRNAs were incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 72 h. These cell lines were incubated in an RPMI 1640 medium with 0.1% fetal bovine serum, penicillin (100 U/mL), and streptomycin (100 μg/mL) in a humidified 5% CO2 incubator at 37 °C for 72 h (* P < 0.05, one-way ANOVA). C Western blotting analysis of Calu-3 and MKN7 cells transfected with nonspecific or GAS6-specific siRNAs for 48 h, followed by treatment with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h. D Calu-3 and MKN7 cells with nonspecific siRNA or AXL-specific siRNAs were treated for 72 h with or without mobocertinib (0.01 or 0.1 μmol/L) and/or GAS6 (50 ng/mL). Cell growth was determined using MTT assays. * P < 0.05 (two-way ANOVA). E Western blotting of Calu-3 and MKN7 cells transfected with nonspecific or AXL-specific siRNAs and treated with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h and GAS6 (50 ng/mL) for 15 min. F MKN7 cells treated with or without mobocertinib (Mobo, 0.1 μmol/L) for 24 h were detected by western blotting with immunoprecipitation of the indicated proteins.
    Recombinant Human Gas6, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 95 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "AXL–SHC1 signaling axis mediates adaptive resistance to HER2-targeted tyrosine kinase inhibitors in HER2-aberrant lung and gastric cancers"

    Article Title: AXL–SHC1 signaling axis mediates adaptive resistance to HER2-targeted tyrosine kinase inhibitors in HER2-aberrant lung and gastric cancers

    Journal: NPJ Precision Oncology

    doi: 10.1038/s41698-026-01385-2

    A qPCR analysis of GAS6 expression in Calu-3 and MKN7 parent cells treated with nonspecific (control) or GAS6-specific siRNAs for 48 h. * P < 0.05 (unpaired t-tests). B MTT assays evaluating cell viability of Calu-3 and MKN7 cells treated with nonspecific or GAS6-specific siRNAs were incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 72 h. These cell lines were incubated in an RPMI 1640 medium with 0.1% fetal bovine serum, penicillin (100 U/mL), and streptomycin (100 μg/mL) in a humidified 5% CO2 incubator at 37 °C for 72 h (* P < 0.05, one-way ANOVA). C Western blotting analysis of Calu-3 and MKN7 cells transfected with nonspecific or GAS6-specific siRNAs for 48 h, followed by treatment with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h. D Calu-3 and MKN7 cells with nonspecific siRNA or AXL-specific siRNAs were treated for 72 h with or without mobocertinib (0.01 or 0.1 μmol/L) and/or GAS6 (50 ng/mL). Cell growth was determined using MTT assays. * P < 0.05 (two-way ANOVA). E Western blotting of Calu-3 and MKN7 cells transfected with nonspecific or AXL-specific siRNAs and treated with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h and GAS6 (50 ng/mL) for 15 min. F MKN7 cells treated with or without mobocertinib (Mobo, 0.1 μmol/L) for 24 h were detected by western blotting with immunoprecipitation of the indicated proteins.
    Figure Legend Snippet: A qPCR analysis of GAS6 expression in Calu-3 and MKN7 parent cells treated with nonspecific (control) or GAS6-specific siRNAs for 48 h. * P < 0.05 (unpaired t-tests). B MTT assays evaluating cell viability of Calu-3 and MKN7 cells treated with nonspecific or GAS6-specific siRNAs were incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 72 h. These cell lines were incubated in an RPMI 1640 medium with 0.1% fetal bovine serum, penicillin (100 U/mL), and streptomycin (100 μg/mL) in a humidified 5% CO2 incubator at 37 °C for 72 h (* P < 0.05, one-way ANOVA). C Western blotting analysis of Calu-3 and MKN7 cells transfected with nonspecific or GAS6-specific siRNAs for 48 h, followed by treatment with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h. D Calu-3 and MKN7 cells with nonspecific siRNA or AXL-specific siRNAs were treated for 72 h with or without mobocertinib (0.01 or 0.1 μmol/L) and/or GAS6 (50 ng/mL). Cell growth was determined using MTT assays. * P < 0.05 (two-way ANOVA). E Western blotting of Calu-3 and MKN7 cells transfected with nonspecific or AXL-specific siRNAs and treated with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h and GAS6 (50 ng/mL) for 15 min. F MKN7 cells treated with or without mobocertinib (Mobo, 0.1 μmol/L) for 24 h were detected by western blotting with immunoprecipitation of the indicated proteins.

    Techniques Used: Expressing, Control, Incubation, Western Blot, Transfection, Immunoprecipitation

    A Combination of mobocertinib and knockdown of several adapter proteins in Calu-3. and MKN7 cells. Calu-3 and MKN7 cells treated with nonspecific control, FYN, GRB2, PTPN11, Shc1, or SRC-specific siRNAs were incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 72 h, and cell viability was detected using MTT assays. * P < 0.05 compared with nonspecific control siRNA (two-way ANOVA). Data are represented as the mean ± S.D. B Western blotting of Calu-3 and MKN7 cells treated with nonspecific control siRNA or Shc1-specific siRNA and incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 24 h. C Calu-3 and MKN7 cells treated with or without mobocertinib (Mobo; 0.01 or 0.1 μmol/L) for 24 h were detected by western blotting with immunoprecipitation of the indicated proteins. D Western blotting showing nuclear localization of ShcBP1 in Calu-3 and MKN7 cells treated with mobocertinib (0.01 or 0.1 μmol/L) for 72 h. E Immunofluorescence showing nuclear localization of ShcBP1 in Calu-3 and MKN7 cells treated with mobocertinib (0.01 or 0.1 μmol/L) for 72 h. F MTT assays assessing cell viability of Calu-3 and MKN7 treated with nonspecific siRNA or ShcBP1-specific siRNAs, and incubated with or without mobocertinib * P < 0.05 (one-way ANOVA). G Schematic diagram illustrating the drug tolerance mechanisms, including GAS6–AXL activation through the SHC1BP–SHC1 complex, in HER2-aberrant cancer cells.
    Figure Legend Snippet: A Combination of mobocertinib and knockdown of several adapter proteins in Calu-3. and MKN7 cells. Calu-3 and MKN7 cells treated with nonspecific control, FYN, GRB2, PTPN11, Shc1, or SRC-specific siRNAs were incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 72 h, and cell viability was detected using MTT assays. * P < 0.05 compared with nonspecific control siRNA (two-way ANOVA). Data are represented as the mean ± S.D. B Western blotting of Calu-3 and MKN7 cells treated with nonspecific control siRNA or Shc1-specific siRNA and incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 24 h. C Calu-3 and MKN7 cells treated with or without mobocertinib (Mobo; 0.01 or 0.1 μmol/L) for 24 h were detected by western blotting with immunoprecipitation of the indicated proteins. D Western blotting showing nuclear localization of ShcBP1 in Calu-3 and MKN7 cells treated with mobocertinib (0.01 or 0.1 μmol/L) for 72 h. E Immunofluorescence showing nuclear localization of ShcBP1 in Calu-3 and MKN7 cells treated with mobocertinib (0.01 or 0.1 μmol/L) for 72 h. F MTT assays assessing cell viability of Calu-3 and MKN7 treated with nonspecific siRNA or ShcBP1-specific siRNAs, and incubated with or without mobocertinib * P < 0.05 (one-way ANOVA). G Schematic diagram illustrating the drug tolerance mechanisms, including GAS6–AXL activation through the SHC1BP–SHC1 complex, in HER2-aberrant cancer cells.

    Techniques Used: Knockdown, Control, Incubation, Western Blot, Immunoprecipitation, Immunofluorescence, Activation Assay



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    TAM receptor (TYRO3, AXL, MERTK) and ligand (PROS1, <t>GAS6)</t> expression in: a keloid-prone ( n = 8, K) versus healthy ( n = 6, N) individual wounds ( GSE113619 ; 1st and 2nd: initial and 42-day biopsies); b normal human skin ( n = 24, NS), early (≤7 days, n = 22, EW), late (8 days–1 month, n = 29, LW), and chronic (>1 month, n = 3, CW) wounds ( GSE178411 ); c normal ( n = 5, NS), acute ( n = 5, AW), type I ( n = 5, DW Ⅰ), and type II diabetic ( n = 3, DW Ⅱ) mouse wounds ( GSE283228 ); d IFN-γ/LPS-stimulated macrophages ( n = 4; GSE53986 ). Conserved GAS6 downregulation in datasets e GSE113619 , f GSE178411 , g GSE283228 , and h GSE53986 (mean ± SD; n values as in a – d ). i – l Single-cell RNA-seq analysis of human wounds ( GSE241132 ; n = 3). i UMAP plot colored by cell type. j GAS6 expression over time. k FeaturePlot visualization of GAS6 expression at representative times. l GAS6 expression across cell types. m – o In vivo analysis of RU-301-treated mice. m Representative wound images (POD0, 3, 7, 10, 14) and H&E-stained scar (POD30); scale bars, 1 mm, 500 µm. n Relative wound area over time (Ctrl, n = 6; RU-301, n = 7). o Scar length on POD30 (Ctrl, n = 3; RU-301, n = 3). p , r Apoptosis in POD3 wounds. p Quantification of Cleaved caspase 3 MFI (Control, n = 6; RU-301, n = 5). r Representative immunofluorescence images; scale bars, 500 µm, 100 µm. q , s Macrophage migration towards POD3 dermal samples. q Quantification of migrated macrophages ( n = 3). s Representative Transwell images; scale bars, 100 µm. All quantitative data are presented as mean ± SD. Statistical significance was determined using two-tailed unpaired t-tests for comparisons between two groups or one-way ANOVA with Tukey’s post-hoc test for multi-group comparisons. n represents independent biological experiments. Ctrl control group, POD postoperative day, MFI mean fluorescence intensity. Control groups received vehicle. Source data are provided as a file.
    V Recombinant Gas6 Protein, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems recombinant human gas6
    A qPCR analysis of <t>GAS6</t> expression in Calu-3 and MKN7 parent cells treated with nonspecific (control) or GAS6-specific siRNAs for 48 h. * P < 0.05 (unpaired t-tests). B MTT assays evaluating cell viability of Calu-3 and MKN7 cells treated with nonspecific or GAS6-specific siRNAs were incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 72 h. These cell lines were incubated in an RPMI 1640 medium with 0.1% fetal bovine serum, penicillin (100 U/mL), and streptomycin (100 μg/mL) in a humidified 5% CO2 incubator at 37 °C for 72 h (* P < 0.05, one-way ANOVA). C Western blotting analysis of Calu-3 and MKN7 cells transfected with nonspecific or GAS6-specific siRNAs for 48 h, followed by treatment with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h. D Calu-3 and MKN7 cells with nonspecific siRNA or AXL-specific siRNAs were treated for 72 h with or without mobocertinib (0.01 or 0.1 μmol/L) and/or GAS6 (50 ng/mL). Cell growth was determined using MTT assays. * P < 0.05 (two-way ANOVA). E Western blotting of Calu-3 and MKN7 cells transfected with nonspecific or AXL-specific siRNAs and treated with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h and GAS6 (50 ng/mL) for 15 min. F MKN7 cells treated with or without mobocertinib (Mobo, 0.1 μmol/L) for 24 h were detected by western blotting with immunoprecipitation of the indicated proteins.
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    R&D Systems reconbinant human gas6 protein 885 gsb
    A qPCR analysis of <t>GAS6</t> expression in Calu-3 and MKN7 parent cells treated with nonspecific (control) or GAS6-specific siRNAs for 48 h. * P < 0.05 (unpaired t-tests). B MTT assays evaluating cell viability of Calu-3 and MKN7 cells treated with nonspecific or GAS6-specific siRNAs were incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 72 h. These cell lines were incubated in an RPMI 1640 medium with 0.1% fetal bovine serum, penicillin (100 U/mL), and streptomycin (100 μg/mL) in a humidified 5% CO2 incubator at 37 °C for 72 h (* P < 0.05, one-way ANOVA). C Western blotting analysis of Calu-3 and MKN7 cells transfected with nonspecific or GAS6-specific siRNAs for 48 h, followed by treatment with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h. D Calu-3 and MKN7 cells with nonspecific siRNA or AXL-specific siRNAs were treated for 72 h with or without mobocertinib (0.01 or 0.1 μmol/L) and/or GAS6 (50 ng/mL). Cell growth was determined using MTT assays. * P < 0.05 (two-way ANOVA). E Western blotting of Calu-3 and MKN7 cells transfected with nonspecific or AXL-specific siRNAs and treated with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h and GAS6 (50 ng/mL) for 15 min. F MKN7 cells treated with or without mobocertinib (Mobo, 0.1 μmol/L) for 24 h were detected by western blotting with immunoprecipitation of the indicated proteins.
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    R&D Systems recombinant human gas6 protein
    A qPCR analysis of <t>GAS6</t> expression in Calu-3 and MKN7 parent cells treated with nonspecific (control) or GAS6-specific siRNAs for 48 h. * P < 0.05 (unpaired t-tests). B MTT assays evaluating cell viability of Calu-3 and MKN7 cells treated with nonspecific or GAS6-specific siRNAs were incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 72 h. These cell lines were incubated in an RPMI 1640 medium with 0.1% fetal bovine serum, penicillin (100 U/mL), and streptomycin (100 μg/mL) in a humidified 5% CO2 incubator at 37 °C for 72 h (* P < 0.05, one-way ANOVA). C Western blotting analysis of Calu-3 and MKN7 cells transfected with nonspecific or GAS6-specific siRNAs for 48 h, followed by treatment with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h. D Calu-3 and MKN7 cells with nonspecific siRNA or AXL-specific siRNAs were treated for 72 h with or without mobocertinib (0.01 or 0.1 μmol/L) and/or GAS6 (50 ng/mL). Cell growth was determined using MTT assays. * P < 0.05 (two-way ANOVA). E Western blotting of Calu-3 and MKN7 cells transfected with nonspecific or AXL-specific siRNAs and treated with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h and GAS6 (50 ng/mL) for 15 min. F MKN7 cells treated with or without mobocertinib (Mobo, 0.1 μmol/L) for 24 h were detected by western blotting with immunoprecipitation of the indicated proteins.
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    PCB126 elevated levels of <t>GAS6/ESR2</t> axis to enhance ESR2 activity. (A, B) GAS6 mRNA levels in IHEECs (A) and IHESCs (B) following treatment with various doses of PCB126 or vehicle. (C, D) ESR2 mRNA levels in IHEECs (C) and IHESCs (D) after treatment with increasing doses of PCB126 or vehicle. (E) Assessment of the intrinsic transcriptional activity of ESR2 induced by GAS6. HeLa cells were transiently transfected with an ESR2 expression vector and an ERE-luciferase reporter, followed by treatment with varying concentrations of GAS6 or vehicle for 48 hours. Relative luciferase activity was calculated as the fold change in GAS6-treated vs vehicle-treated cells. * P < .05; ** P < .01; *** P < .001. Abbreviations: ERE, estrogen response element; ESR2, estrogen receptor β; GAS6, growth arrest–specific 6; IHEEC, immortalized human endometrial epithelial cell; IHESC, immortalized human endometrial stromal cell; NS, nonspecific.
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    Image Search Results


    TAM receptor (TYRO3, AXL, MERTK) and ligand (PROS1, GAS6) expression in: a keloid-prone ( n = 8, K) versus healthy ( n = 6, N) individual wounds ( GSE113619 ; 1st and 2nd: initial and 42-day biopsies); b normal human skin ( n = 24, NS), early (≤7 days, n = 22, EW), late (8 days–1 month, n = 29, LW), and chronic (>1 month, n = 3, CW) wounds ( GSE178411 ); c normal ( n = 5, NS), acute ( n = 5, AW), type I ( n = 5, DW Ⅰ), and type II diabetic ( n = 3, DW Ⅱ) mouse wounds ( GSE283228 ); d IFN-γ/LPS-stimulated macrophages ( n = 4; GSE53986 ). Conserved GAS6 downregulation in datasets e GSE113619 , f GSE178411 , g GSE283228 , and h GSE53986 (mean ± SD; n values as in a – d ). i – l Single-cell RNA-seq analysis of human wounds ( GSE241132 ; n = 3). i UMAP plot colored by cell type. j GAS6 expression over time. k FeaturePlot visualization of GAS6 expression at representative times. l GAS6 expression across cell types. m – o In vivo analysis of RU-301-treated mice. m Representative wound images (POD0, 3, 7, 10, 14) and H&E-stained scar (POD30); scale bars, 1 mm, 500 µm. n Relative wound area over time (Ctrl, n = 6; RU-301, n = 7). o Scar length on POD30 (Ctrl, n = 3; RU-301, n = 3). p , r Apoptosis in POD3 wounds. p Quantification of Cleaved caspase 3 MFI (Control, n = 6; RU-301, n = 5). r Representative immunofluorescence images; scale bars, 500 µm, 100 µm. q , s Macrophage migration towards POD3 dermal samples. q Quantification of migrated macrophages ( n = 3). s Representative Transwell images; scale bars, 100 µm. All quantitative data are presented as mean ± SD. Statistical significance was determined using two-tailed unpaired t-tests for comparisons between two groups or one-way ANOVA with Tukey’s post-hoc test for multi-group comparisons. n represents independent biological experiments. Ctrl control group, POD postoperative day, MFI mean fluorescence intensity. Control groups received vehicle. Source data are provided as a file.

    Journal: Nature Communications

    Article Title: Spatiotemporally controlled restoration of GAS6 signaling via mRNA therapy promotes scarless healing in preclinical models

    doi: 10.1038/s41467-026-69540-8

    Figure Lengend Snippet: TAM receptor (TYRO3, AXL, MERTK) and ligand (PROS1, GAS6) expression in: a keloid-prone ( n = 8, K) versus healthy ( n = 6, N) individual wounds ( GSE113619 ; 1st and 2nd: initial and 42-day biopsies); b normal human skin ( n = 24, NS), early (≤7 days, n = 22, EW), late (8 days–1 month, n = 29, LW), and chronic (>1 month, n = 3, CW) wounds ( GSE178411 ); c normal ( n = 5, NS), acute ( n = 5, AW), type I ( n = 5, DW Ⅰ), and type II diabetic ( n = 3, DW Ⅱ) mouse wounds ( GSE283228 ); d IFN-γ/LPS-stimulated macrophages ( n = 4; GSE53986 ). Conserved GAS6 downregulation in datasets e GSE113619 , f GSE178411 , g GSE283228 , and h GSE53986 (mean ± SD; n values as in a – d ). i – l Single-cell RNA-seq analysis of human wounds ( GSE241132 ; n = 3). i UMAP plot colored by cell type. j GAS6 expression over time. k FeaturePlot visualization of GAS6 expression at representative times. l GAS6 expression across cell types. m – o In vivo analysis of RU-301-treated mice. m Representative wound images (POD0, 3, 7, 10, 14) and H&E-stained scar (POD30); scale bars, 1 mm, 500 µm. n Relative wound area over time (Ctrl, n = 6; RU-301, n = 7). o Scar length on POD30 (Ctrl, n = 3; RU-301, n = 3). p , r Apoptosis in POD3 wounds. p Quantification of Cleaved caspase 3 MFI (Control, n = 6; RU-301, n = 5). r Representative immunofluorescence images; scale bars, 500 µm, 100 µm. q , s Macrophage migration towards POD3 dermal samples. q Quantification of migrated macrophages ( n = 3). s Representative Transwell images; scale bars, 100 µm. All quantitative data are presented as mean ± SD. Statistical significance was determined using two-tailed unpaired t-tests for comparisons between two groups or one-way ANOVA with Tukey’s post-hoc test for multi-group comparisons. n represents independent biological experiments. Ctrl control group, POD postoperative day, MFI mean fluorescence intensity. Control groups received vehicle. Source data are provided as a file.

    Article Snippet: For the LNP-GAS6 mRNA therapeutic evaluation, the groups included: i. saline (I), ii. Gel (II), iii. LNP@Gel (III), iv. GAS6 mRNA-LNP@Gel (50 μg/ml) (IV), v. recombinant GAS6 protein (10 μg/ml, MedChemExpress) (V).

    Techniques: Expressing, Single Cell, RNA Sequencing, In Vivo, Staining, Control, Immunofluorescence, Migration, Two Tailed Test, Fluorescence

    a Schematic of LNP-GAS6 mRNA design for targeted TAM receptor agonism. b – g Physicochemical characterization of LNPs and LNP-GAS6 mRNA. b – d Diameter, polydispersity index (PDI), and zeta potential measured by dynamic light scattering (DLS) ( n = 5). Encapsulation efficiency ( e ) and encapsulated mRNA concentration ( f ) quantified using the Quant-iT RiboGreen RNA Assay Kit ( n = 5). g Representative transmission electron microscopy (TEM) image; scale bars, 200 nm, 50 nm. h GAS6 protein secretion quantified by ELISA in fibroblasts and macrophages at 24, 48, and 72 h post-treatment with LNP-GAS6 mRNA ( n = 3). i – k Intracellular GAS6 protein expression assessed by immunofluorescence. i Representative images of fibroblasts and macrophages; Blue, DAPI (nuclei); green, GAS6; scale bars, 100 µm. Quantification of GAS6 MFI in fibroblasts ( j ) and macrophages ( k ) ( n = 3). All quantitative data are presented as mean ± SD. Statistical significance was determined using two-tailed unpaired t-tests for comparisons between two groups or one-way ANOVA with Tukey’s post-hoc test for multi-group comparisons. n represents independent biological experiments. MFI mean fluorescence intensity; I, LNP; II, LNP-GAS6 mRNA. Source data are provided as a file.

    Journal: Nature Communications

    Article Title: Spatiotemporally controlled restoration of GAS6 signaling via mRNA therapy promotes scarless healing in preclinical models

    doi: 10.1038/s41467-026-69540-8

    Figure Lengend Snippet: a Schematic of LNP-GAS6 mRNA design for targeted TAM receptor agonism. b – g Physicochemical characterization of LNPs and LNP-GAS6 mRNA. b – d Diameter, polydispersity index (PDI), and zeta potential measured by dynamic light scattering (DLS) ( n = 5). Encapsulation efficiency ( e ) and encapsulated mRNA concentration ( f ) quantified using the Quant-iT RiboGreen RNA Assay Kit ( n = 5). g Representative transmission electron microscopy (TEM) image; scale bars, 200 nm, 50 nm. h GAS6 protein secretion quantified by ELISA in fibroblasts and macrophages at 24, 48, and 72 h post-treatment with LNP-GAS6 mRNA ( n = 3). i – k Intracellular GAS6 protein expression assessed by immunofluorescence. i Representative images of fibroblasts and macrophages; Blue, DAPI (nuclei); green, GAS6; scale bars, 100 µm. Quantification of GAS6 MFI in fibroblasts ( j ) and macrophages ( k ) ( n = 3). All quantitative data are presented as mean ± SD. Statistical significance was determined using two-tailed unpaired t-tests for comparisons between two groups or one-way ANOVA with Tukey’s post-hoc test for multi-group comparisons. n represents independent biological experiments. MFI mean fluorescence intensity; I, LNP; II, LNP-GAS6 mRNA. Source data are provided as a file.

    Article Snippet: For the LNP-GAS6 mRNA therapeutic evaluation, the groups included: i. saline (I), ii. Gel (II), iii. LNP@Gel (III), iv. GAS6 mRNA-LNP@Gel (50 μg/ml) (IV), v. recombinant GAS6 protein (10 μg/ml, MedChemExpress) (V).

    Techniques: Zeta Potential Analyzer, Encapsulation, Concentration Assay, Transmission Assay, Electron Microscopy, Enzyme-linked Immunosorbent Assay, Expressing, Immunofluorescence, Two Tailed Test, Fluorescence

    a Il10 expression in macrophages after GAS6 siRNA treatment, assessed by RT‑qPCR ( n = 3). Expression of Csf1 ( b ) and Cxcl12 ( c ) in fibroblasts treated with conditioned medium (CM) from the indicated macrophage groups ( n = 3). d Percentage of macrophages that engulfed apoptotic cells (CFDA‑SE⁺), assessed by flow cytometry ( n = 3). Expression of Nos2 ( e ) and Arg1 ( f ) in macrophages ( n = 3). g – i Efferocytosis analysis in macrophages. g Percentage of CFDA‑SE⁺ macrophages. h MFI of CFDA‑SE within phagocytes, reflecting the number of apoptotic cells ingested per macrophage ( n = 4). i Representative flow cytometry plots. j Schematic of the macrophage‑fibroblast paracrine signaling model. Created in BioRender. Hanxiao, S. (2026) https://BioRender.com/snsu6jk . Expression of Tnf ( k ), Il1b ( l ), and Il10 ( m ) in macrophages ( n = 3). Expression of Csf1 ( n ) and Cxcl12 ( o ) in fibroblasts ( n = 3). LPS CM: conditioned medium from LPS‑treated macrophages; LNP‑GAS6 mRNA CM: conditioned medium from LNP‑GAS6 mRNA‑treated macrophages. Expression of Csf1 ( p ) and Cxcl12 ( q ) in fibroblasts under the indicated treatments ( n = 3). All quantitative data are presented as mean ± SD. Statistical significance was determined using two‑tailed unpaired t‑tests for comparisons between two groups or one‑way ANOVA with Tukey’s post‑hoc test for multi‑group comparisons. CM conditioned medium, MFI mean fluorescence intensity. Source data are provided as a file.

    Journal: Nature Communications

    Article Title: Spatiotemporally controlled restoration of GAS6 signaling via mRNA therapy promotes scarless healing in preclinical models

    doi: 10.1038/s41467-026-69540-8

    Figure Lengend Snippet: a Il10 expression in macrophages after GAS6 siRNA treatment, assessed by RT‑qPCR ( n = 3). Expression of Csf1 ( b ) and Cxcl12 ( c ) in fibroblasts treated with conditioned medium (CM) from the indicated macrophage groups ( n = 3). d Percentage of macrophages that engulfed apoptotic cells (CFDA‑SE⁺), assessed by flow cytometry ( n = 3). Expression of Nos2 ( e ) and Arg1 ( f ) in macrophages ( n = 3). g – i Efferocytosis analysis in macrophages. g Percentage of CFDA‑SE⁺ macrophages. h MFI of CFDA‑SE within phagocytes, reflecting the number of apoptotic cells ingested per macrophage ( n = 4). i Representative flow cytometry plots. j Schematic of the macrophage‑fibroblast paracrine signaling model. Created in BioRender. Hanxiao, S. (2026) https://BioRender.com/snsu6jk . Expression of Tnf ( k ), Il1b ( l ), and Il10 ( m ) in macrophages ( n = 3). Expression of Csf1 ( n ) and Cxcl12 ( o ) in fibroblasts ( n = 3). LPS CM: conditioned medium from LPS‑treated macrophages; LNP‑GAS6 mRNA CM: conditioned medium from LNP‑GAS6 mRNA‑treated macrophages. Expression of Csf1 ( p ) and Cxcl12 ( q ) in fibroblasts under the indicated treatments ( n = 3). All quantitative data are presented as mean ± SD. Statistical significance was determined using two‑tailed unpaired t‑tests for comparisons between two groups or one‑way ANOVA with Tukey’s post‑hoc test for multi‑group comparisons. CM conditioned medium, MFI mean fluorescence intensity. Source data are provided as a file.

    Article Snippet: For the LNP-GAS6 mRNA therapeutic evaluation, the groups included: i. saline (I), ii. Gel (II), iii. LNP@Gel (III), iv. GAS6 mRNA-LNP@Gel (50 μg/ml) (IV), v. recombinant GAS6 protein (10 μg/ml, MedChemExpress) (V).

    Techniques: Expressing, Flow Cytometry, Fluorescence

    a , b Thermosensitive properties of LNP-GAS6 mRNA@Gel. a In vitro sol‑gel transition in vitro at 4 °C (liquid) and 37 °C (gel) (representative images, n = 3). b In vivo gelation upon application to acute and diabetic murine wounds (representative images, n = 3). c Distribution of PKH26‑labeled LNPs within the hydrogel matrix, detected by confocal microscopy (representative image, n = 3). d – f Bioluminescence imaging of luciferase expression. d Representative images of wounds after treatment with LNP‑Fluc mRNA (5 μg/wound) by injection or hydrogel. e Longitudinal quantification of bioluminescence flux in individual mice over time ( n = 4). f Comparative analysis of total signal intensity between LNP‑Fluc mRNA and LNP‑Fluc mRNA@Gel groups ( n = 4). g – k In vivo experiment of LNP-mRNA@Hydrogel concentration screening. g Representative immunofluorescence images for GAS6 (green) and DAPI (blue) in POD3 acute wounds; scale bars, 1 mm. Quantification of GAS6 MFI in deep and superficial skin layers at the wound center ( h ) and edge ( i ) ( n = 4). Wound width ( j ) and granulation tissue thickness ( k ) after treatment ( n = 4). All quantitative data are presented as mean ± SD. Statistical significance was determined using two‑tailed unpaired t‑tests for comparisons between two groups or one‑way ANOVA with Tukey’s post‑hoc test for multi‑group comparisons. n represents independent biological experiments. MFI mean fluorescence intensity, POD postoperative day. Source data are provided as a file.

    Journal: Nature Communications

    Article Title: Spatiotemporally controlled restoration of GAS6 signaling via mRNA therapy promotes scarless healing in preclinical models

    doi: 10.1038/s41467-026-69540-8

    Figure Lengend Snippet: a , b Thermosensitive properties of LNP-GAS6 mRNA@Gel. a In vitro sol‑gel transition in vitro at 4 °C (liquid) and 37 °C (gel) (representative images, n = 3). b In vivo gelation upon application to acute and diabetic murine wounds (representative images, n = 3). c Distribution of PKH26‑labeled LNPs within the hydrogel matrix, detected by confocal microscopy (representative image, n = 3). d – f Bioluminescence imaging of luciferase expression. d Representative images of wounds after treatment with LNP‑Fluc mRNA (5 μg/wound) by injection or hydrogel. e Longitudinal quantification of bioluminescence flux in individual mice over time ( n = 4). f Comparative analysis of total signal intensity between LNP‑Fluc mRNA and LNP‑Fluc mRNA@Gel groups ( n = 4). g – k In vivo experiment of LNP-mRNA@Hydrogel concentration screening. g Representative immunofluorescence images for GAS6 (green) and DAPI (blue) in POD3 acute wounds; scale bars, 1 mm. Quantification of GAS6 MFI in deep and superficial skin layers at the wound center ( h ) and edge ( i ) ( n = 4). Wound width ( j ) and granulation tissue thickness ( k ) after treatment ( n = 4). All quantitative data are presented as mean ± SD. Statistical significance was determined using two‑tailed unpaired t‑tests for comparisons between two groups or one‑way ANOVA with Tukey’s post‑hoc test for multi‑group comparisons. n represents independent biological experiments. MFI mean fluorescence intensity, POD postoperative day. Source data are provided as a file.

    Article Snippet: For the LNP-GAS6 mRNA therapeutic evaluation, the groups included: i. saline (I), ii. Gel (II), iii. LNP@Gel (III), iv. GAS6 mRNA-LNP@Gel (50 μg/ml) (IV), v. recombinant GAS6 protein (10 μg/ml, MedChemExpress) (V).

    Techniques: In Vitro, In Vivo, Confocal Microscopy, Imaging, Luciferase, Expressing, Injection, Concentration Assay, Immunofluorescence, Fluorescence

    a Experimental design: full-thickness wounds in mice treated with PBS, Gel, LNP@Gel, LNP-GAS6 mRNA@Gel, or GAS6 recombinant protein. Created in BioRender. Hanxiao, S. (2026) https://BioRender.com/78012r9 . b – d Wound closure analysis. b Representative wound images on POD0, 3, 7, 10, 14, and 30. c Quantification of relative wound area over time ( n = 8). d Heatmap of wound closure dynamics ( n = 8). e – g Scar analysis on POD30. e Representative H&E (scale bars, 1 mm, 200 µm) and Masson’s trichrome (scale bars, 1 mm, 250 µm, 50 µm) staining. f Scar length ( n = 6). g CVF ratio (scar area CVF/normal skin CVF) ( n = 6). h , i Apoptosis in POD3 wounds. ( h ) Representative images of immunofluorescence for Cleaved caspase 3; scale bars, 200 µm, 100 µm. i Quantification of Cleaved caspase 3 MFI ( n = 3). Blue, DAPI; Green, F4/80; Red, Cleaved Caspase 3. j , k Macrophage migration toward POD3 dermal samples ( n = 3). j Representative images of Transwell assay; scale bars, 100 µm. k Quantification of migrated macrophages ( n = 3). All quantitative data are presented as mean ± SD. Statistical significance was determined using two‑tailed unpaired t‑tests for comparisons between two groups or one‑way ANOVA with Tukey’s post‑hoc test for multi‑group comparisons. n represents independent biological experiments. CVF collagen volume fraction, MFI mean fluorescence intensity, POD postoperative day. Ⅰ, Control; Ⅱ, Gel; Ⅲ, LNP@Gel, Ⅳ, LNP-GAS6 mRNA@Gel; Ⅴ, GAS6 Recombinant Protein. Source data are provided as a file.

    Journal: Nature Communications

    Article Title: Spatiotemporally controlled restoration of GAS6 signaling via mRNA therapy promotes scarless healing in preclinical models

    doi: 10.1038/s41467-026-69540-8

    Figure Lengend Snippet: a Experimental design: full-thickness wounds in mice treated with PBS, Gel, LNP@Gel, LNP-GAS6 mRNA@Gel, or GAS6 recombinant protein. Created in BioRender. Hanxiao, S. (2026) https://BioRender.com/78012r9 . b – d Wound closure analysis. b Representative wound images on POD0, 3, 7, 10, 14, and 30. c Quantification of relative wound area over time ( n = 8). d Heatmap of wound closure dynamics ( n = 8). e – g Scar analysis on POD30. e Representative H&E (scale bars, 1 mm, 200 µm) and Masson’s trichrome (scale bars, 1 mm, 250 µm, 50 µm) staining. f Scar length ( n = 6). g CVF ratio (scar area CVF/normal skin CVF) ( n = 6). h , i Apoptosis in POD3 wounds. ( h ) Representative images of immunofluorescence for Cleaved caspase 3; scale bars, 200 µm, 100 µm. i Quantification of Cleaved caspase 3 MFI ( n = 3). Blue, DAPI; Green, F4/80; Red, Cleaved Caspase 3. j , k Macrophage migration toward POD3 dermal samples ( n = 3). j Representative images of Transwell assay; scale bars, 100 µm. k Quantification of migrated macrophages ( n = 3). All quantitative data are presented as mean ± SD. Statistical significance was determined using two‑tailed unpaired t‑tests for comparisons between two groups or one‑way ANOVA with Tukey’s post‑hoc test for multi‑group comparisons. n represents independent biological experiments. CVF collagen volume fraction, MFI mean fluorescence intensity, POD postoperative day. Ⅰ, Control; Ⅱ, Gel; Ⅲ, LNP@Gel, Ⅳ, LNP-GAS6 mRNA@Gel; Ⅴ, GAS6 Recombinant Protein. Source data are provided as a file.

    Article Snippet: For the LNP-GAS6 mRNA therapeutic evaluation, the groups included: i. saline (I), ii. Gel (II), iii. LNP@Gel (III), iv. GAS6 mRNA-LNP@Gel (50 μg/ml) (IV), v. recombinant GAS6 protein (10 μg/ml, MedChemExpress) (V).

    Techniques: Recombinant, Staining, Immunofluorescence, Migration, Transwell Assay, Fluorescence, Control

    a Administration protocol for LNP-GAS6 mRNA@Gel with or without AXL or MERTK receptor inhibitors. b , c Wound closure analysis. b Quantification of relative wound area over time ( n = 4). c Representative wound images on POD0, 3, 7, 10, and 14. d – h Transcriptomic analysis of treatment effects ( n = 3). d KEGG and e GSEA enrichment plots highlighting OXPHOS as a top-ranked pathway. Venn diagram ( f ), heatmap ( g ), and volcano plot ( h ) showing expression changes of OXPHOS-related genes (45 upregulated, 3 downregulated). i – l OXPHOS functional validation in macrophages ( n = 3). Expression of Ndufa3 ( i ), Uqcrb ( j ), and Cox5a ( k ) by RT‑qPCR following GAS6 siRNA treatment ( n = 3). l Relative ATP levels in macrophages after treatment with GAS6 siRNA or LNP‑GAS6 mRNA. All quantitative data are presented as mean ± SD. Statistical significance was determined using two‑tailed unpaired t‑tests for comparisons between two groups or one‑way ANOVA with Tukey’s post‑hoc test for multi‑group comparisons. n represents independent biological experiments. Ctrl control, AXL i AXL inhibitor, MERTK i MERTK inhibitor, OXPHOS oxidative phosphorylation, POD postoperative day. Source data are provided as a file.

    Journal: Nature Communications

    Article Title: Spatiotemporally controlled restoration of GAS6 signaling via mRNA therapy promotes scarless healing in preclinical models

    doi: 10.1038/s41467-026-69540-8

    Figure Lengend Snippet: a Administration protocol for LNP-GAS6 mRNA@Gel with or without AXL or MERTK receptor inhibitors. b , c Wound closure analysis. b Quantification of relative wound area over time ( n = 4). c Representative wound images on POD0, 3, 7, 10, and 14. d – h Transcriptomic analysis of treatment effects ( n = 3). d KEGG and e GSEA enrichment plots highlighting OXPHOS as a top-ranked pathway. Venn diagram ( f ), heatmap ( g ), and volcano plot ( h ) showing expression changes of OXPHOS-related genes (45 upregulated, 3 downregulated). i – l OXPHOS functional validation in macrophages ( n = 3). Expression of Ndufa3 ( i ), Uqcrb ( j ), and Cox5a ( k ) by RT‑qPCR following GAS6 siRNA treatment ( n = 3). l Relative ATP levels in macrophages after treatment with GAS6 siRNA or LNP‑GAS6 mRNA. All quantitative data are presented as mean ± SD. Statistical significance was determined using two‑tailed unpaired t‑tests for comparisons between two groups or one‑way ANOVA with Tukey’s post‑hoc test for multi‑group comparisons. n represents independent biological experiments. Ctrl control, AXL i AXL inhibitor, MERTK i MERTK inhibitor, OXPHOS oxidative phosphorylation, POD postoperative day. Source data are provided as a file.

    Article Snippet: For the LNP-GAS6 mRNA therapeutic evaluation, the groups included: i. saline (I), ii. Gel (II), iii. LNP@Gel (III), iv. GAS6 mRNA-LNP@Gel (50 μg/ml) (IV), v. recombinant GAS6 protein (10 μg/ml, MedChemExpress) (V).

    Techniques: Expressing, Functional Assay, Biomarker Discovery, Control, Phospho-proteomics

    a Experimental design: full-thickness wounds on rabbit ears treated with PBS, Gel, LNP@Gel, or LNP-GAS6 mRNA@Gel. Created in BioRender. Hanxiao, S. (2026) https://BioRender.com/eh3yqdy . b Representative wound images on POD0, 3, 7, 14, 21, 28, and 60. c , e Hypertrophic scar assessment on POD60 by Masson’s trichrome staining. c Representative images, each containing scar and adjacent normal skin ( n = 6); scale bars, 1 mm, 500 µm. e Quantification of the SEI, calculated as scar height/normal skin height ( n = 6). d , f Collagen composition analysis on POD60 by Sirius red staining under polarized light. d Representative images (scar and normal skin) ( n = 3); scale bars, 200 µm, 20 µm. f Quantification of the collagen I/III ratio ( n = 3). Under polarized light, thick type I collagen fibers appear red/orange-red; thin type III collagen fibers appear green. All quantitative data are presented as mean ± SD. Statistical significance was determined using two‑tailed unpaired t‑tests for comparisons between two groups or one‑way ANOVA with Tukey’s post‑hoc test for multi‑group comparisons. n represents independent biological experiments. SEI scar elevation index, POD postoperative day. Ⅰ, Control; Ⅱ, Gel; Ⅲ, LNP@Gel, Ⅳ, LNP-GAS6 mRNA@Gel; Ⅴ, Normal Skin. Source data are provided as a file.

    Journal: Nature Communications

    Article Title: Spatiotemporally controlled restoration of GAS6 signaling via mRNA therapy promotes scarless healing in preclinical models

    doi: 10.1038/s41467-026-69540-8

    Figure Lengend Snippet: a Experimental design: full-thickness wounds on rabbit ears treated with PBS, Gel, LNP@Gel, or LNP-GAS6 mRNA@Gel. Created in BioRender. Hanxiao, S. (2026) https://BioRender.com/eh3yqdy . b Representative wound images on POD0, 3, 7, 14, 21, 28, and 60. c , e Hypertrophic scar assessment on POD60 by Masson’s trichrome staining. c Representative images, each containing scar and adjacent normal skin ( n = 6); scale bars, 1 mm, 500 µm. e Quantification of the SEI, calculated as scar height/normal skin height ( n = 6). d , f Collagen composition analysis on POD60 by Sirius red staining under polarized light. d Representative images (scar and normal skin) ( n = 3); scale bars, 200 µm, 20 µm. f Quantification of the collagen I/III ratio ( n = 3). Under polarized light, thick type I collagen fibers appear red/orange-red; thin type III collagen fibers appear green. All quantitative data are presented as mean ± SD. Statistical significance was determined using two‑tailed unpaired t‑tests for comparisons between two groups or one‑way ANOVA with Tukey’s post‑hoc test for multi‑group comparisons. n represents independent biological experiments. SEI scar elevation index, POD postoperative day. Ⅰ, Control; Ⅱ, Gel; Ⅲ, LNP@Gel, Ⅳ, LNP-GAS6 mRNA@Gel; Ⅴ, Normal Skin. Source data are provided as a file.

    Article Snippet: For the LNP-GAS6 mRNA therapeutic evaluation, the groups included: i. saline (I), ii. Gel (II), iii. LNP@Gel (III), iv. GAS6 mRNA-LNP@Gel (50 μg/ml) (IV), v. recombinant GAS6 protein (10 μg/ml, MedChemExpress) (V).

    Techniques: Staining, Control

    a Experimental design: full-thickness dorsal wounds treated with Gel, LNP@Gel, LNP-GAS6 mRNA@Gel, or human EGF gel. Created in BioRender. Hanxiao, S. (2026) https://BioRender.com/a0axfcg . b – e Wound closure analysis. b Representative wound images on POD0, 7, 14, 21, 28, and 35. c Quantification of relative wound area over time ( n = 6). d Heatmap of closure dynamics ( n = 6). e Schematic simulation of wound area changes during healing. f – h Scar analysis on POD14 and 35. f Representative Masson’s trichrome staining; scale bars, 1 mm, 200 µm. g Scar length quantification ( n = 6). h CVF ratio (scar area CVF/normal skin CVF) ( n = 6). All quantitative data are presented as mean ± SD. Statistical significance was determined using two‑tailed unpaired t‑tests for comparisons between two groups or one‑way ANOVA with Tukey’s post‑hoc test for multi‑group comparisons. n represents independent biological experiments. CVF collagen volume fraction, POD postoperative day. Ⅰ, Gel; Ⅱ, LNP@Gel; Ⅲ, LNP-GAS6 mRNA@Gel, Ⅳ, h-EGF Gel (Human-Epidermal Growth Factor Gel). Source data are provided as a file.

    Journal: Nature Communications

    Article Title: Spatiotemporally controlled restoration of GAS6 signaling via mRNA therapy promotes scarless healing in preclinical models

    doi: 10.1038/s41467-026-69540-8

    Figure Lengend Snippet: a Experimental design: full-thickness dorsal wounds treated with Gel, LNP@Gel, LNP-GAS6 mRNA@Gel, or human EGF gel. Created in BioRender. Hanxiao, S. (2026) https://BioRender.com/a0axfcg . b – e Wound closure analysis. b Representative wound images on POD0, 7, 14, 21, 28, and 35. c Quantification of relative wound area over time ( n = 6). d Heatmap of closure dynamics ( n = 6). e Schematic simulation of wound area changes during healing. f – h Scar analysis on POD14 and 35. f Representative Masson’s trichrome staining; scale bars, 1 mm, 200 µm. g Scar length quantification ( n = 6). h CVF ratio (scar area CVF/normal skin CVF) ( n = 6). All quantitative data are presented as mean ± SD. Statistical significance was determined using two‑tailed unpaired t‑tests for comparisons between two groups or one‑way ANOVA with Tukey’s post‑hoc test for multi‑group comparisons. n represents independent biological experiments. CVF collagen volume fraction, POD postoperative day. Ⅰ, Gel; Ⅱ, LNP@Gel; Ⅲ, LNP-GAS6 mRNA@Gel, Ⅳ, h-EGF Gel (Human-Epidermal Growth Factor Gel). Source data are provided as a file.

    Article Snippet: For the LNP-GAS6 mRNA therapeutic evaluation, the groups included: i. saline (I), ii. Gel (II), iii. LNP@Gel (III), iv. GAS6 mRNA-LNP@Gel (50 μg/ml) (IV), v. recombinant GAS6 protein (10 μg/ml, MedChemExpress) (V).

    Techniques: Staining

    A qPCR analysis of GAS6 expression in Calu-3 and MKN7 parent cells treated with nonspecific (control) or GAS6-specific siRNAs for 48 h. * P < 0.05 (unpaired t-tests). B MTT assays evaluating cell viability of Calu-3 and MKN7 cells treated with nonspecific or GAS6-specific siRNAs were incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 72 h. These cell lines were incubated in an RPMI 1640 medium with 0.1% fetal bovine serum, penicillin (100 U/mL), and streptomycin (100 μg/mL) in a humidified 5% CO2 incubator at 37 °C for 72 h (* P < 0.05, one-way ANOVA). C Western blotting analysis of Calu-3 and MKN7 cells transfected with nonspecific or GAS6-specific siRNAs for 48 h, followed by treatment with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h. D Calu-3 and MKN7 cells with nonspecific siRNA or AXL-specific siRNAs were treated for 72 h with or without mobocertinib (0.01 or 0.1 μmol/L) and/or GAS6 (50 ng/mL). Cell growth was determined using MTT assays. * P < 0.05 (two-way ANOVA). E Western blotting of Calu-3 and MKN7 cells transfected with nonspecific or AXL-specific siRNAs and treated with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h and GAS6 (50 ng/mL) for 15 min. F MKN7 cells treated with or without mobocertinib (Mobo, 0.1 μmol/L) for 24 h were detected by western blotting with immunoprecipitation of the indicated proteins.

    Journal: NPJ Precision Oncology

    Article Title: AXL–SHC1 signaling axis mediates adaptive resistance to HER2-targeted tyrosine kinase inhibitors in HER2-aberrant lung and gastric cancers

    doi: 10.1038/s41698-026-01385-2

    Figure Lengend Snippet: A qPCR analysis of GAS6 expression in Calu-3 and MKN7 parent cells treated with nonspecific (control) or GAS6-specific siRNAs for 48 h. * P < 0.05 (unpaired t-tests). B MTT assays evaluating cell viability of Calu-3 and MKN7 cells treated with nonspecific or GAS6-specific siRNAs were incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 72 h. These cell lines were incubated in an RPMI 1640 medium with 0.1% fetal bovine serum, penicillin (100 U/mL), and streptomycin (100 μg/mL) in a humidified 5% CO2 incubator at 37 °C for 72 h (* P < 0.05, one-way ANOVA). C Western blotting analysis of Calu-3 and MKN7 cells transfected with nonspecific or GAS6-specific siRNAs for 48 h, followed by treatment with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h. D Calu-3 and MKN7 cells with nonspecific siRNA or AXL-specific siRNAs were treated for 72 h with or without mobocertinib (0.01 or 0.1 μmol/L) and/or GAS6 (50 ng/mL). Cell growth was determined using MTT assays. * P < 0.05 (two-way ANOVA). E Western blotting of Calu-3 and MKN7 cells transfected with nonspecific or AXL-specific siRNAs and treated with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h and GAS6 (50 ng/mL) for 15 min. F MKN7 cells treated with or without mobocertinib (Mobo, 0.1 μmol/L) for 24 h were detected by western blotting with immunoprecipitation of the indicated proteins.

    Article Snippet: Recombinant human GAS6 was obtained from R&D Systems (Minneapolis, MN, USA).

    Techniques: Expressing, Control, Incubation, Western Blot, Transfection, Immunoprecipitation

    A Combination of mobocertinib and knockdown of several adapter proteins in Calu-3. and MKN7 cells. Calu-3 and MKN7 cells treated with nonspecific control, FYN, GRB2, PTPN11, Shc1, or SRC-specific siRNAs were incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 72 h, and cell viability was detected using MTT assays. * P < 0.05 compared with nonspecific control siRNA (two-way ANOVA). Data are represented as the mean ± S.D. B Western blotting of Calu-3 and MKN7 cells treated with nonspecific control siRNA or Shc1-specific siRNA and incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 24 h. C Calu-3 and MKN7 cells treated with or without mobocertinib (Mobo; 0.01 or 0.1 μmol/L) for 24 h were detected by western blotting with immunoprecipitation of the indicated proteins. D Western blotting showing nuclear localization of ShcBP1 in Calu-3 and MKN7 cells treated with mobocertinib (0.01 or 0.1 μmol/L) for 72 h. E Immunofluorescence showing nuclear localization of ShcBP1 in Calu-3 and MKN7 cells treated with mobocertinib (0.01 or 0.1 μmol/L) for 72 h. F MTT assays assessing cell viability of Calu-3 and MKN7 treated with nonspecific siRNA or ShcBP1-specific siRNAs, and incubated with or without mobocertinib * P < 0.05 (one-way ANOVA). G Schematic diagram illustrating the drug tolerance mechanisms, including GAS6–AXL activation through the SHC1BP–SHC1 complex, in HER2-aberrant cancer cells.

    Journal: NPJ Precision Oncology

    Article Title: AXL–SHC1 signaling axis mediates adaptive resistance to HER2-targeted tyrosine kinase inhibitors in HER2-aberrant lung and gastric cancers

    doi: 10.1038/s41698-026-01385-2

    Figure Lengend Snippet: A Combination of mobocertinib and knockdown of several adapter proteins in Calu-3. and MKN7 cells. Calu-3 and MKN7 cells treated with nonspecific control, FYN, GRB2, PTPN11, Shc1, or SRC-specific siRNAs were incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 72 h, and cell viability was detected using MTT assays. * P < 0.05 compared with nonspecific control siRNA (two-way ANOVA). Data are represented as the mean ± S.D. B Western blotting of Calu-3 and MKN7 cells treated with nonspecific control siRNA or Shc1-specific siRNA and incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 24 h. C Calu-3 and MKN7 cells treated with or without mobocertinib (Mobo; 0.01 or 0.1 μmol/L) for 24 h were detected by western blotting with immunoprecipitation of the indicated proteins. D Western blotting showing nuclear localization of ShcBP1 in Calu-3 and MKN7 cells treated with mobocertinib (0.01 or 0.1 μmol/L) for 72 h. E Immunofluorescence showing nuclear localization of ShcBP1 in Calu-3 and MKN7 cells treated with mobocertinib (0.01 or 0.1 μmol/L) for 72 h. F MTT assays assessing cell viability of Calu-3 and MKN7 treated with nonspecific siRNA or ShcBP1-specific siRNAs, and incubated with or without mobocertinib * P < 0.05 (one-way ANOVA). G Schematic diagram illustrating the drug tolerance mechanisms, including GAS6–AXL activation through the SHC1BP–SHC1 complex, in HER2-aberrant cancer cells.

    Article Snippet: Recombinant human GAS6 was obtained from R&D Systems (Minneapolis, MN, USA).

    Techniques: Knockdown, Control, Incubation, Western Blot, Immunoprecipitation, Immunofluorescence, Activation Assay

    PCB126 elevated levels of GAS6/ESR2 axis to enhance ESR2 activity. (A, B) GAS6 mRNA levels in IHEECs (A) and IHESCs (B) following treatment with various doses of PCB126 or vehicle. (C, D) ESR2 mRNA levels in IHEECs (C) and IHESCs (D) after treatment with increasing doses of PCB126 or vehicle. (E) Assessment of the intrinsic transcriptional activity of ESR2 induced by GAS6. HeLa cells were transiently transfected with an ESR2 expression vector and an ERE-luciferase reporter, followed by treatment with varying concentrations of GAS6 or vehicle for 48 hours. Relative luciferase activity was calculated as the fold change in GAS6-treated vs vehicle-treated cells. * P < .05; ** P < .01; *** P < .001. Abbreviations: ERE, estrogen response element; ESR2, estrogen receptor β; GAS6, growth arrest–specific 6; IHEEC, immortalized human endometrial epithelial cell; IHESC, immortalized human endometrial stromal cell; NS, nonspecific.

    Journal: Endocrinology

    Article Title: Polychlorinated Biphenyls Alter Estrogen Receptor β-mediated Epigenetic Regulation, Promoting Endometriosis

    doi: 10.1210/endocr/bqaf146

    Figure Lengend Snippet: PCB126 elevated levels of GAS6/ESR2 axis to enhance ESR2 activity. (A, B) GAS6 mRNA levels in IHEECs (A) and IHESCs (B) following treatment with various doses of PCB126 or vehicle. (C, D) ESR2 mRNA levels in IHEECs (C) and IHESCs (D) after treatment with increasing doses of PCB126 or vehicle. (E) Assessment of the intrinsic transcriptional activity of ESR2 induced by GAS6. HeLa cells were transiently transfected with an ESR2 expression vector and an ERE-luciferase reporter, followed by treatment with varying concentrations of GAS6 or vehicle for 48 hours. Relative luciferase activity was calculated as the fold change in GAS6-treated vs vehicle-treated cells. * P < .05; ** P < .01; *** P < .001. Abbreviations: ERE, estrogen response element; ESR2, estrogen receptor β; GAS6, growth arrest–specific 6; IHEEC, immortalized human endometrial epithelial cell; IHESC, immortalized human endometrial stromal cell; NS, nonspecific.

    Article Snippet: Three days after transfection, cells were treated with varying concentrations (0-100 ng/mL) of GAS6 protein (R&D Systems, catalog number: 885-GSB).

    Techniques: Activity Assay, Transfection, Expressing, Plasmid Preparation, Luciferase

    PCB126 indirectly elevated DNMT3A through the AXL/GAS6/ESR2 axis, enhancing endometriosis progression by altering the immune response. PCB126 exposure elevated GAS6 levels in endometriotic lesions, leading to the activation of AXL signaling. Activated AXL enhanced ESR2 activity, which in turn upregulated DNMT3A expression. Elevated DNMT3A contributed to developing endometriosis-associated inflammatory and immune microenvironment, promoting disease progression. Abbreviations: DNMT3A, DNA methyltransferase 3A; ESR2, estrogen receptor β; GAS6, growth arrest–specific 6.

    Journal: Endocrinology

    Article Title: Polychlorinated Biphenyls Alter Estrogen Receptor β-mediated Epigenetic Regulation, Promoting Endometriosis

    doi: 10.1210/endocr/bqaf146

    Figure Lengend Snippet: PCB126 indirectly elevated DNMT3A through the AXL/GAS6/ESR2 axis, enhancing endometriosis progression by altering the immune response. PCB126 exposure elevated GAS6 levels in endometriotic lesions, leading to the activation of AXL signaling. Activated AXL enhanced ESR2 activity, which in turn upregulated DNMT3A expression. Elevated DNMT3A contributed to developing endometriosis-associated inflammatory and immune microenvironment, promoting disease progression. Abbreviations: DNMT3A, DNA methyltransferase 3A; ESR2, estrogen receptor β; GAS6, growth arrest–specific 6.

    Article Snippet: Three days after transfection, cells were treated with varying concentrations (0-100 ng/mL) of GAS6 protein (R&D Systems, catalog number: 885-GSB).

    Techniques: Activation Assay, Activity Assay, Expressing, Biomarker Discovery