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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.

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
https://www.bioz.com/product/885+gsb/pmc13046926-240-0-6?v=R%26D+Systems
Average 95 stars, based on 95 article reviews

recombinant human gas6 - by Bioz Stars, 2026-08

95/100 stars

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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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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

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

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