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mouse il 1 beta quantikine elisa kit  (R&D Systems)


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    R&D Systems mouse il 1 beta quantikine elisa kit
    Mouse Il 1 Beta Quantikine Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 34 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse il 1 beta quantikine elisa kit/product/R&D Systems
    Average 94 stars, based on 34 article reviews
    mouse il 1 beta quantikine elisa kit - by Bioz Stars, 2026-06
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    Multi Sciences (Lianke) Biotech Co Ltd mouse elisa kit
    rhIL-37 delays preterm delivery by reducing LPS-induced inflammatory effects and NLRP3 inflammasome activation in mice. ( A ) Orbital blood was collected from the control mice ( n = 6), LPS-induced preterm mice (LPS; n = 6), and rhIL-37 + LPS-co-treated preterm mice (rhIL-37 + LPS; n = 6).Serum levels of IL-1β, IL-6 <t>and</t> <t>TNF-α</t> were detected via <t>ELISA.</t> ( B ) Foetal membrane and placental tissues were collected from mice ( n = 6 per group) immediately before labour,, and the mRNA expression levels of NLRP3, Caspase-1 and ASC were detected via qRT-PCR. ( C ) Foetal membrane and placental tissues were collected from the mice in each group ( n = 3 per group), and the protein levels of NLRP3, Caspase-1, Pro-caspase-1 and ASC were analyzed by western blotting. ( D ) Western blot Results were normalised to β-actin. Bar graphs show statistical quantification of the western blot data. All data met the assumption of homogeneity of variance. Data are presented as mean ± s.e.m. Results are representative of at least three independent experiments. * p < 0.05; ** p < 0.01;*** p < 0.001;**** p < 0.0001 (one-way ANOVA).
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    R&D Systems mouse il 1 beta quantikine elisa kit
    rhIL-37 delays preterm delivery by reducing LPS-induced inflammatory effects and NLRP3 inflammasome activation in mice. ( A ) Orbital blood was collected from the control mice ( n = 6), LPS-induced preterm mice (LPS; n = 6), and rhIL-37 + LPS-co-treated preterm mice (rhIL-37 + LPS; n = 6).Serum levels of IL-1β, IL-6 <t>and</t> <t>TNF-α</t> were detected via <t>ELISA.</t> ( B ) Foetal membrane and placental tissues were collected from mice ( n = 6 per group) immediately before labour,, and the mRNA expression levels of NLRP3, Caspase-1 and ASC were detected via qRT-PCR. ( C ) Foetal membrane and placental tissues were collected from the mice in each group ( n = 3 per group), and the protein levels of NLRP3, Caspase-1, Pro-caspase-1 and ASC were analyzed by western blotting. ( D ) Western blot Results were normalised to β-actin. Bar graphs show statistical quantification of the western blot data. All data met the assumption of homogeneity of variance. Data are presented as mean ± s.e.m. Results are representative of at least three independent experiments. * p < 0.05; ** p < 0.01;*** p < 0.001;**** p < 0.0001 (one-way ANOVA).
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    R&D Systems mouse quantikine elisa kit
    rhIL-37 delays preterm delivery by reducing LPS-induced inflammatory effects and NLRP3 inflammasome activation in mice. ( A ) Orbital blood was collected from the control mice ( n = 6), LPS-induced preterm mice (LPS; n = 6), and rhIL-37 + LPS-co-treated preterm mice (rhIL-37 + LPS; n = 6).Serum levels of IL-1β, IL-6 <t>and</t> <t>TNF-α</t> were detected via <t>ELISA.</t> ( B ) Foetal membrane and placental tissues were collected from mice ( n = 6 per group) immediately before labour,, and the mRNA expression levels of NLRP3, Caspase-1 and ASC were detected via qRT-PCR. ( C ) Foetal membrane and placental tissues were collected from the mice in each group ( n = 3 per group), and the protein levels of NLRP3, Caspase-1, Pro-caspase-1 and ASC were analyzed by western blotting. ( D ) Western blot Results were normalised to β-actin. Bar graphs show statistical quantification of the western blot data. All data met the assumption of homogeneity of variance. Data are presented as mean ± s.e.m. Results are representative of at least three independent experiments. * p < 0.05; ** p < 0.01;*** p < 0.001;**** p < 0.0001 (one-way ANOVA).
    Mouse Quantikine Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems mouse quantikine elisa kits
    ( a-b ) NT LNPs and tLNPs containing FLuc mRNA were administered intravenously via retroorbital injection into pregnant and nonpregnant mice at a dose of 12 µg mRNA per mouse. After 6 h, mice were euthanized, and serum was collected. Serum levels of C3a, TNF, IFN-γ, IL-6, ALT, and AST were quantified in ( a ) pregnant and ( b ) nonpregnant mice via <t>ELISA.</t> Measurements are reported mean ± SD from n = 3–4 biological replicates. One-way ANOVA with post hoc Student’s t-tests using the Holm–Sídak correction for multiple comparisons was used to compare cytokine levels across treatment groups. ( c–e ) Spearman correlations for ( c ) TNF, ( d ) IFN-γ, and ( e ) IL-6 serum levels in pregnant (top) and nonpregnant (bottom) mice using the physicochemical parameters from traditional characterization methods, static SAXS analyses, and AF4-UV-DLS-MALS-SAXS analyses. ( f ) Heatmap representing the entire dataset. For Spearman correlation graphs, dotted lines represent r = –0.6 and 0.6.
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    R&D Systems mlif elisa kit
    (A) lif expression in the scRNA-seq from mouse livers with acetaminophen (APAP)-induced injury at the indicated time points. (B) lif expression in the scRNA-seq across cell types in the livers of mouse with APAP injury at the indicated time points. (C) lif expression in spatial transcriptomics of liver samples from healthy (HEA2) and APAP injury (APAP1_S2) humans. (D&E) Serum <t>mLIF</t> levels at 24, 48, and 72 h after partial hepatectomy (PHx) in mice treated with IgG (D) or anti-LIF neutralizing antibody (E). (F) Resected liver-to-body weight ratio in mice treated with anti-LIF antibody or control IgG. (G) Liver-to-body weight ratio at 24, 48, 72 h and 1-week post-PHx in mice treated with anti-LIF antibody or control IgG. (H) Immunofluorescence staining of liver sections at 48 h post-PHx from mice treated with anti-LIF antibody or control IgG. DAPI (blue), PCNA (red), CK19 (purple). Scale bars: 100 μm. (I) Quantification of PCNA-positive hepatocytes ratio at 48 h post-PHx in mice treated with anti-LIF antibody or control IgG.
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    R&D Systems mouse lif
    Cancer cell intrinsic CREB transcriptionally regulates <t>LIF</t> expression, driving macrophage-modulatory signaling in PDAC. (A) Experimental schematic demonstrating RNA sequencing (RNA-seq) analysis conducted in KPC mouse CREB WT and CREB KO tumor cells. (B) Bubble plot visualizing differentially regulated pathways (using molecular signature databases) in CREB KO transcriptomics compared with CREB WT tumor cells (n=3). (C) Ridge plot showing normalized enrichment scores for the hallmark JAK–STAT3 signaling pathway across different cellular constituents in the human HTAN pancreatic cancer dataset from treatment-naïve patients. (D) Western blot image depicting pSTAT3 activation, along with tSTAT3, vinculin and vimentin in mouse RAW macrophage 264.7 cell line treated with either recombinant (r) LIF alone (1 µg/mL) or in combination with EC359 (LIFR blockade, 0.2µM). (E) Chromatin Immunoprecipitation sequencing (ChIP-seq) peak signals visualized as heat maps which depict CREB binding sites across genomic regions in KPC mouse pancreatic tumor cells. The adjacent call out boxes with the heat maps showing essential genes regulated via CREB as its downstream mediators. (F) Integrative Genome Viewer (IGV) plot visualizing occupancy of CREB binding peaks in ChIP-seq data at the site of mouse Lif promoter gene regulatory sequences. (G-H) Violin dot plots showing downregulation of LIF expression via qPCR <t>and</t> <t>ELISA</t> in bulk tumor lysates of CREB KO KPC orthotopic PDAC tumors as compared to CREB WT with n=3-7 mice per group. (I) Representative photomicrographs of whole pancreas along with its corresponding quantification depicting significantly reduced LIF expression via IHC in age matched KPC C -/- as compared to KPC mice. Individual data points with mean ± SEM are shown and compared by two-tailed unpaired t test. *p<0.05; **p<0.01; ns non-significant (p>0.05).
    Mouse Lif, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cancer cell intrinsic CREB transcriptionally regulates <t>LIF</t> expression, driving macrophage-modulatory signaling in PDAC. (A) Experimental schematic demonstrating RNA sequencing (RNA-seq) analysis conducted in KPC mouse CREB WT and CREB KO tumor cells. (B) Bubble plot visualizing differentially regulated pathways (using molecular signature databases) in CREB KO transcriptomics compared with CREB WT tumor cells (n=3). (C) Ridge plot showing normalized enrichment scores for the hallmark JAK–STAT3 signaling pathway across different cellular constituents in the human HTAN pancreatic cancer dataset from treatment-naïve patients. (D) Western blot image depicting pSTAT3 activation, along with tSTAT3, vinculin and vimentin in mouse RAW macrophage 264.7 cell line treated with either recombinant (r) LIF alone (1 µg/mL) or in combination with EC359 (LIFR blockade, 0.2µM). (E) Chromatin Immunoprecipitation sequencing (ChIP-seq) peak signals visualized as heat maps which depict CREB binding sites across genomic regions in KPC mouse pancreatic tumor cells. The adjacent call out boxes with the heat maps showing essential genes regulated via CREB as its downstream mediators. (F) Integrative Genome Viewer (IGV) plot visualizing occupancy of CREB binding peaks in ChIP-seq data at the site of mouse Lif promoter gene regulatory sequences. (G-H) Violin dot plots showing downregulation of LIF expression via qPCR <t>and</t> <t>ELISA</t> in bulk tumor lysates of CREB KO KPC orthotopic PDAC tumors as compared to CREB WT with n=3-7 mice per group. (I) Representative photomicrographs of whole pancreas along with its corresponding quantification depicting significantly reduced LIF expression via IHC in age matched KPC C -/- as compared to KPC mice. Individual data points with mean ± SEM are shown and compared by two-tailed unpaired t test. *p<0.05; **p<0.01; ns non-significant (p>0.05).
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    R&D Systems mouse leukemia inhibitory factor lif
    Cancer cell intrinsic CREB transcriptionally regulates <t>LIF</t> expression, driving macrophage-modulatory signaling in PDAC. (A) Experimental schematic demonstrating RNA sequencing (RNA-seq) analysis conducted in KPC mouse CREB WT and CREB KO tumor cells. (B) Bubble plot visualizing differentially regulated pathways (using molecular signature databases) in CREB KO transcriptomics compared with CREB WT tumor cells (n=3). (C) Ridge plot showing normalized enrichment scores for the hallmark JAK–STAT3 signaling pathway across different cellular constituents in the human HTAN pancreatic cancer dataset from treatment-naïve patients. (D) Western blot image depicting pSTAT3 activation, along with tSTAT3, vinculin and vimentin in mouse RAW macrophage 264.7 cell line treated with either recombinant (r) LIF alone (1 µg/mL) or in combination with EC359 (LIFR blockade, 0.2µM). (E) Chromatin Immunoprecipitation sequencing (ChIP-seq) peak signals visualized as heat maps which depict CREB binding sites across genomic regions in KPC mouse pancreatic tumor cells. The adjacent call out boxes with the heat maps showing essential genes regulated via CREB as its downstream mediators. (F) Integrative Genome Viewer (IGV) plot visualizing occupancy of CREB binding peaks in ChIP-seq data at the site of mouse Lif promoter gene regulatory sequences. (G-H) Violin dot plots showing downregulation of LIF expression via qPCR <t>and</t> <t>ELISA</t> in bulk tumor lysates of CREB KO KPC orthotopic PDAC tumors as compared to CREB WT with n=3-7 mice per group. (I) Representative photomicrographs of whole pancreas along with its corresponding quantification depicting significantly reduced LIF expression via IHC in age matched KPC C -/- as compared to KPC mice. Individual data points with mean ± SEM are shown and compared by two-tailed unpaired t test. *p<0.05; **p<0.01; ns non-significant (p>0.05).
    Mouse Leukemia Inhibitory Factor Lif, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cancer cell intrinsic CREB transcriptionally regulates <t>LIF</t> expression, driving macrophage-modulatory signaling in PDAC. (A) Experimental schematic demonstrating RNA sequencing (RNA-seq) analysis conducted in KPC mouse CREB WT and CREB KO tumor cells. (B) Bubble plot visualizing differentially regulated pathways (using molecular signature databases) in CREB KO transcriptomics compared with CREB WT tumor cells (n=3). (C) Ridge plot showing normalized enrichment scores for the hallmark JAK–STAT3 signaling pathway across different cellular constituents in the human HTAN pancreatic cancer dataset from treatment-naïve patients. (D) Western blot image depicting pSTAT3 activation, along with tSTAT3, vinculin and vimentin in mouse RAW macrophage 264.7 cell line treated with either recombinant (r) LIF alone (1 µg/mL) or in combination with EC359 (LIFR blockade, 0.2µM). (E) Chromatin Immunoprecipitation sequencing (ChIP-seq) peak signals visualized as heat maps which depict CREB binding sites across genomic regions in KPC mouse pancreatic tumor cells. The adjacent call out boxes with the heat maps showing essential genes regulated via CREB as its downstream mediators. (F) Integrative Genome Viewer (IGV) plot visualizing occupancy of CREB binding peaks in ChIP-seq data at the site of mouse Lif promoter gene regulatory sequences. (G-H) Violin dot plots showing downregulation of LIF expression via qPCR <t>and</t> <t>ELISA</t> in bulk tumor lysates of CREB KO KPC orthotopic PDAC tumors as compared to CREB WT with n=3-7 mice per group. (I) Representative photomicrographs of whole pancreas along with its corresponding quantification depicting significantly reduced LIF expression via IHC in age matched KPC C -/- as compared to KPC mice. Individual data points with mean ± SEM are shown and compared by two-tailed unpaired t test. *p<0.05; **p<0.01; ns non-significant (p>0.05).
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    rhIL-37 delays preterm delivery by reducing LPS-induced inflammatory effects and NLRP3 inflammasome activation in mice. ( A ) Orbital blood was collected from the control mice ( n = 6), LPS-induced preterm mice (LPS; n = 6), and rhIL-37 + LPS-co-treated preterm mice (rhIL-37 + LPS; n = 6).Serum levels of IL-1β, IL-6 and TNF-α were detected via ELISA. ( B ) Foetal membrane and placental tissues were collected from mice ( n = 6 per group) immediately before labour,, and the mRNA expression levels of NLRP3, Caspase-1 and ASC were detected via qRT-PCR. ( C ) Foetal membrane and placental tissues were collected from the mice in each group ( n = 3 per group), and the protein levels of NLRP3, Caspase-1, Pro-caspase-1 and ASC were analyzed by western blotting. ( D ) Western blot Results were normalised to β-actin. Bar graphs show statistical quantification of the western blot data. All data met the assumption of homogeneity of variance. Data are presented as mean ± s.e.m. Results are representative of at least three independent experiments. * p < 0.05; ** p < 0.01;*** p < 0.001;**** p < 0.0001 (one-way ANOVA).

    Journal: Scientific Reports

    Article Title: IL-37 alleviates inflammatory effects and NLRP3 inflammasome activation in LPS-induced preterm birth

    doi: 10.1038/s41598-025-34506-1

    Figure Lengend Snippet: rhIL-37 delays preterm delivery by reducing LPS-induced inflammatory effects and NLRP3 inflammasome activation in mice. ( A ) Orbital blood was collected from the control mice ( n = 6), LPS-induced preterm mice (LPS; n = 6), and rhIL-37 + LPS-co-treated preterm mice (rhIL-37 + LPS; n = 6).Serum levels of IL-1β, IL-6 and TNF-α were detected via ELISA. ( B ) Foetal membrane and placental tissues were collected from mice ( n = 6 per group) immediately before labour,, and the mRNA expression levels of NLRP3, Caspase-1 and ASC were detected via qRT-PCR. ( C ) Foetal membrane and placental tissues were collected from the mice in each group ( n = 3 per group), and the protein levels of NLRP3, Caspase-1, Pro-caspase-1 and ASC were analyzed by western blotting. ( D ) Western blot Results were normalised to β-actin. Bar graphs show statistical quantification of the western blot data. All data met the assumption of homogeneity of variance. Data are presented as mean ± s.e.m. Results are representative of at least three independent experiments. * p < 0.05; ** p < 0.01;*** p < 0.001;**** p < 0.0001 (one-way ANOVA).

    Article Snippet: For mouse samples, IL-1β, IL-6, and TNF-α levels in orbital blood serum/plasma supernatants were assayed using a mouse ELISA kit (LiankeBio, Hangzhou, China).

    Techniques: Activation Assay, Control, Enzyme-linked Immunosorbent Assay, Membrane, Expressing, Quantitative RT-PCR, Western Blot

    IL-37 knockdown enhances LPS-induced inflammatory and NLRP3 inflammasome activation in HTR-8/Svneo cells. ( A ) Cell supernatants were collected from control, si_NC- or si_IL37-treated cells following LPS exposure, and IL-37 expression level were detected by ELISA, qRT-PCR and Western blotting. ( B ) IL-1β, IL-6 and TNF-α levels in the cell supernatants were detected by ELISA. ( C ) The mRNA expression levels of NLRP3, Caspase-1 and ASC after cell treatment with LPS ( n = 5) were measured by qRT-PCR analysis. ( D ) NLRP3,pro-caspase-1, caspase-1 and ASC protein levels were detected by Western blotting, and the results were normalised to β-actin. All data exhibited equal variance.The data are shown as the mean ± s.e.m. The results are representative of at least three independent experiments. * p < 0.05; ** p < 0.01;*** p < 0.001;**** p < 0.0001 (One-way ANOVA).

    Journal: Scientific Reports

    Article Title: IL-37 alleviates inflammatory effects and NLRP3 inflammasome activation in LPS-induced preterm birth

    doi: 10.1038/s41598-025-34506-1

    Figure Lengend Snippet: IL-37 knockdown enhances LPS-induced inflammatory and NLRP3 inflammasome activation in HTR-8/Svneo cells. ( A ) Cell supernatants were collected from control, si_NC- or si_IL37-treated cells following LPS exposure, and IL-37 expression level were detected by ELISA, qRT-PCR and Western blotting. ( B ) IL-1β, IL-6 and TNF-α levels in the cell supernatants were detected by ELISA. ( C ) The mRNA expression levels of NLRP3, Caspase-1 and ASC after cell treatment with LPS ( n = 5) were measured by qRT-PCR analysis. ( D ) NLRP3,pro-caspase-1, caspase-1 and ASC protein levels were detected by Western blotting, and the results were normalised to β-actin. All data exhibited equal variance.The data are shown as the mean ± s.e.m. The results are representative of at least three independent experiments. * p < 0.05; ** p < 0.01;*** p < 0.001;**** p < 0.0001 (One-way ANOVA).

    Article Snippet: For mouse samples, IL-1β, IL-6, and TNF-α levels in orbital blood serum/plasma supernatants were assayed using a mouse ELISA kit (LiankeBio, Hangzhou, China).

    Techniques: Knockdown, Activation Assay, Control, Expressing, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Western Blot

    Nigericin reversed the anti-inflammatory effects and effects of rhIL-37 and its inhibition of NF-κB p65 activation in LPS-induced PTB.t ( A ) Cell supernatants were collected from HTR-8/Svneo cells co-treated with rhIL-37 and LPS, then either left untreated or treated with nigericin.The mRNA expression of NLRP3, caspase-1, and ASC was detected. ( B ) Cells were collected, and the protein expression of NLRP3, caspase-1, pro-caspase-1, and ASC was detected by western blotting. Results were normalised to β-actin and statistically analyzed.( C ) HTR-8/Svneo cell supernatants were collected after co-treatment with rhIL-37 and LPS (with or without nigericin), and the expression levels of IL-1β, IL-6, and TNF-α were detected by ELISA. ( D ) HTR-8/Svneo cells co-treated with rhIL-37 and LPS (with or without nigericin) were collected. The mRNA expression of p65 was detected by qRT-PCR, and protein expression of p65 and p-p65 was detected by western blotting. Densitometric quantification of p-p65 relative to p65 was performed. Statistical analysis of the western blot results was performed.All data exhibited equal variance.The data are shown as the means ± s.e.m. The results are representative of at least three independent experiments..

    Journal: Scientific Reports

    Article Title: IL-37 alleviates inflammatory effects and NLRP3 inflammasome activation in LPS-induced preterm birth

    doi: 10.1038/s41598-025-34506-1

    Figure Lengend Snippet: Nigericin reversed the anti-inflammatory effects and effects of rhIL-37 and its inhibition of NF-κB p65 activation in LPS-induced PTB.t ( A ) Cell supernatants were collected from HTR-8/Svneo cells co-treated with rhIL-37 and LPS, then either left untreated or treated with nigericin.The mRNA expression of NLRP3, caspase-1, and ASC was detected. ( B ) Cells were collected, and the protein expression of NLRP3, caspase-1, pro-caspase-1, and ASC was detected by western blotting. Results were normalised to β-actin and statistically analyzed.( C ) HTR-8/Svneo cell supernatants were collected after co-treatment with rhIL-37 and LPS (with or without nigericin), and the expression levels of IL-1β, IL-6, and TNF-α were detected by ELISA. ( D ) HTR-8/Svneo cells co-treated with rhIL-37 and LPS (with or without nigericin) were collected. The mRNA expression of p65 was detected by qRT-PCR, and protein expression of p65 and p-p65 was detected by western blotting. Densitometric quantification of p-p65 relative to p65 was performed. Statistical analysis of the western blot results was performed.All data exhibited equal variance.The data are shown as the means ± s.e.m. The results are representative of at least three independent experiments..

    Article Snippet: For mouse samples, IL-1β, IL-6, and TNF-α levels in orbital blood serum/plasma supernatants were assayed using a mouse ELISA kit (LiankeBio, Hangzhou, China).

    Techniques: Inhibition, Activation Assay, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR

    ( a-b ) NT LNPs and tLNPs containing FLuc mRNA were administered intravenously via retroorbital injection into pregnant and nonpregnant mice at a dose of 12 µg mRNA per mouse. After 6 h, mice were euthanized, and serum was collected. Serum levels of C3a, TNF, IFN-γ, IL-6, ALT, and AST were quantified in ( a ) pregnant and ( b ) nonpregnant mice via ELISA. Measurements are reported mean ± SD from n = 3–4 biological replicates. One-way ANOVA with post hoc Student’s t-tests using the Holm–Sídak correction for multiple comparisons was used to compare cytokine levels across treatment groups. ( c–e ) Spearman correlations for ( c ) TNF, ( d ) IFN-γ, and ( e ) IL-6 serum levels in pregnant (top) and nonpregnant (bottom) mice using the physicochemical parameters from traditional characterization methods, static SAXS analyses, and AF4-UV-DLS-MALS-SAXS analyses. ( f ) Heatmap representing the entire dataset. For Spearman correlation graphs, dotted lines represent r = –0.6 and 0.6.

    Journal: bioRxiv

    Article Title: Resolving heterogeneity of targeted lipid nanoparticles through solution-based biophysical analyses

    doi: 10.64898/2026.03.31.715590

    Figure Lengend Snippet: ( a-b ) NT LNPs and tLNPs containing FLuc mRNA were administered intravenously via retroorbital injection into pregnant and nonpregnant mice at a dose of 12 µg mRNA per mouse. After 6 h, mice were euthanized, and serum was collected. Serum levels of C3a, TNF, IFN-γ, IL-6, ALT, and AST were quantified in ( a ) pregnant and ( b ) nonpregnant mice via ELISA. Measurements are reported mean ± SD from n = 3–4 biological replicates. One-way ANOVA with post hoc Student’s t-tests using the Holm–Sídak correction for multiple comparisons was used to compare cytokine levels across treatment groups. ( c–e ) Spearman correlations for ( c ) TNF, ( d ) IFN-γ, and ( e ) IL-6 serum levels in pregnant (top) and nonpregnant (bottom) mice using the physicochemical parameters from traditional characterization methods, static SAXS analyses, and AF4-UV-DLS-MALS-SAXS analyses. ( f ) Heatmap representing the entire dataset. For Spearman correlation graphs, dotted lines represent r = –0.6 and 0.6.

    Article Snippet: Mouse Quantikine ELISA kits (R&D systems) were used to evaluate C3a, IL-6, TNF, and IFN-γ levels in serum per the manufacturer’s instructions.

    Techniques: Injection, Enzyme-linked Immunosorbent Assay

    (A) lif expression in the scRNA-seq from mouse livers with acetaminophen (APAP)-induced injury at the indicated time points. (B) lif expression in the scRNA-seq across cell types in the livers of mouse with APAP injury at the indicated time points. (C) lif expression in spatial transcriptomics of liver samples from healthy (HEA2) and APAP injury (APAP1_S2) humans. (D&E) Serum mLIF levels at 24, 48, and 72 h after partial hepatectomy (PHx) in mice treated with IgG (D) or anti-LIF neutralizing antibody (E). (F) Resected liver-to-body weight ratio in mice treated with anti-LIF antibody or control IgG. (G) Liver-to-body weight ratio at 24, 48, 72 h and 1-week post-PHx in mice treated with anti-LIF antibody or control IgG. (H) Immunofluorescence staining of liver sections at 48 h post-PHx from mice treated with anti-LIF antibody or control IgG. DAPI (blue), PCNA (red), CK19 (purple). Scale bars: 100 μm. (I) Quantification of PCNA-positive hepatocytes ratio at 48 h post-PHx in mice treated with anti-LIF antibody or control IgG.

    Journal: bioRxiv

    Article Title: The LIF-LIFR Axis Promotes Liver Regeneration via Modulation of Angiogenesis and HGF Release from LSECs

    doi: 10.64898/2026.02.24.707802

    Figure Lengend Snippet: (A) lif expression in the scRNA-seq from mouse livers with acetaminophen (APAP)-induced injury at the indicated time points. (B) lif expression in the scRNA-seq across cell types in the livers of mouse with APAP injury at the indicated time points. (C) lif expression in spatial transcriptomics of liver samples from healthy (HEA2) and APAP injury (APAP1_S2) humans. (D&E) Serum mLIF levels at 24, 48, and 72 h after partial hepatectomy (PHx) in mice treated with IgG (D) or anti-LIF neutralizing antibody (E). (F) Resected liver-to-body weight ratio in mice treated with anti-LIF antibody or control IgG. (G) Liver-to-body weight ratio at 24, 48, 72 h and 1-week post-PHx in mice treated with anti-LIF antibody or control IgG. (H) Immunofluorescence staining of liver sections at 48 h post-PHx from mice treated with anti-LIF antibody or control IgG. DAPI (blue), PCNA (red), CK19 (purple). Scale bars: 100 μm. (I) Quantification of PCNA-positive hepatocytes ratio at 48 h post-PHx in mice treated with anti-LIF antibody or control IgG.

    Article Snippet: The following steps were carried out according to the manufacturer’s protocols from mLIF ELISA kit (R&D system, MLF00).

    Techniques: Expressing, Spatial Transcriptomics, Control, Immunofluorescence, Staining

    (A-C) Body weight (A), liver weight (B) and liver-to-body weight ratio (C) of mice injected with AAV8-TBG-mLIF at the indicated titers. (D) Serum mLIF levels in mice injected with AAV8-TBG-mLIF at the indicated titers. (E&F) CD31 immunofluorescence staining of liver sections from mice injected with low-doses AAV8-TBG-mLIF (1×10⁸ or 2.5×10⁸ GC/mouse) (E) and quantified in (F). Scale bar=50 μm. (G) Serum HGF levels in mice injected with AAV8-TBG-mLIF at the indicated titers. (H) Liver-to-body weight ratio at the indicated time points post-PHx in mice injected with low-doses AAV8-TBG-mLIF (1×10⁸ or 2.5×10⁸ GC/mouse). (I&J) Serum mLIF (H) and HGF (I) levels at 24, 48 and 72 h post-PHx in mice injected with low-doses AAV8-TBG-mLIF (1×10⁸ or 2.5×10⁸ GC/mouse).

    Journal: bioRxiv

    Article Title: The LIF-LIFR Axis Promotes Liver Regeneration via Modulation of Angiogenesis and HGF Release from LSECs

    doi: 10.64898/2026.02.24.707802

    Figure Lengend Snippet: (A-C) Body weight (A), liver weight (B) and liver-to-body weight ratio (C) of mice injected with AAV8-TBG-mLIF at the indicated titers. (D) Serum mLIF levels in mice injected with AAV8-TBG-mLIF at the indicated titers. (E&F) CD31 immunofluorescence staining of liver sections from mice injected with low-doses AAV8-TBG-mLIF (1×10⁸ or 2.5×10⁸ GC/mouse) (E) and quantified in (F). Scale bar=50 μm. (G) Serum HGF levels in mice injected with AAV8-TBG-mLIF at the indicated titers. (H) Liver-to-body weight ratio at the indicated time points post-PHx in mice injected with low-doses AAV8-TBG-mLIF (1×10⁸ or 2.5×10⁸ GC/mouse). (I&J) Serum mLIF (H) and HGF (I) levels at 24, 48 and 72 h post-PHx in mice injected with low-doses AAV8-TBG-mLIF (1×10⁸ or 2.5×10⁸ GC/mouse).

    Article Snippet: The following steps were carried out according to the manufacturer’s protocols from mLIF ELISA kit (R&D system, MLF00).

    Techniques: Injection, Immunofluorescence, Staining

    Cancer cell intrinsic CREB transcriptionally regulates LIF expression, driving macrophage-modulatory signaling in PDAC. (A) Experimental schematic demonstrating RNA sequencing (RNA-seq) analysis conducted in KPC mouse CREB WT and CREB KO tumor cells. (B) Bubble plot visualizing differentially regulated pathways (using molecular signature databases) in CREB KO transcriptomics compared with CREB WT tumor cells (n=3). (C) Ridge plot showing normalized enrichment scores for the hallmark JAK–STAT3 signaling pathway across different cellular constituents in the human HTAN pancreatic cancer dataset from treatment-naïve patients. (D) Western blot image depicting pSTAT3 activation, along with tSTAT3, vinculin and vimentin in mouse RAW macrophage 264.7 cell line treated with either recombinant (r) LIF alone (1 µg/mL) or in combination with EC359 (LIFR blockade, 0.2µM). (E) Chromatin Immunoprecipitation sequencing (ChIP-seq) peak signals visualized as heat maps which depict CREB binding sites across genomic regions in KPC mouse pancreatic tumor cells. The adjacent call out boxes with the heat maps showing essential genes regulated via CREB as its downstream mediators. (F) Integrative Genome Viewer (IGV) plot visualizing occupancy of CREB binding peaks in ChIP-seq data at the site of mouse Lif promoter gene regulatory sequences. (G-H) Violin dot plots showing downregulation of LIF expression via qPCR and ELISA in bulk tumor lysates of CREB KO KPC orthotopic PDAC tumors as compared to CREB WT with n=3-7 mice per group. (I) Representative photomicrographs of whole pancreas along with its corresponding quantification depicting significantly reduced LIF expression via IHC in age matched KPC C -/- as compared to KPC mice. Individual data points with mean ± SEM are shown and compared by two-tailed unpaired t test. *p<0.05; **p<0.01; ns non-significant (p>0.05).

    Journal: bioRxiv

    Article Title: Targeting CREB remodels the immune microenvironment to enhance immunotherapy responses in pancreatic cancer

    doi: 10.64898/2025.12.04.691935

    Figure Lengend Snippet: Cancer cell intrinsic CREB transcriptionally regulates LIF expression, driving macrophage-modulatory signaling in PDAC. (A) Experimental schematic demonstrating RNA sequencing (RNA-seq) analysis conducted in KPC mouse CREB WT and CREB KO tumor cells. (B) Bubble plot visualizing differentially regulated pathways (using molecular signature databases) in CREB KO transcriptomics compared with CREB WT tumor cells (n=3). (C) Ridge plot showing normalized enrichment scores for the hallmark JAK–STAT3 signaling pathway across different cellular constituents in the human HTAN pancreatic cancer dataset from treatment-naïve patients. (D) Western blot image depicting pSTAT3 activation, along with tSTAT3, vinculin and vimentin in mouse RAW macrophage 264.7 cell line treated with either recombinant (r) LIF alone (1 µg/mL) or in combination with EC359 (LIFR blockade, 0.2µM). (E) Chromatin Immunoprecipitation sequencing (ChIP-seq) peak signals visualized as heat maps which depict CREB binding sites across genomic regions in KPC mouse pancreatic tumor cells. The adjacent call out boxes with the heat maps showing essential genes regulated via CREB as its downstream mediators. (F) Integrative Genome Viewer (IGV) plot visualizing occupancy of CREB binding peaks in ChIP-seq data at the site of mouse Lif promoter gene regulatory sequences. (G-H) Violin dot plots showing downregulation of LIF expression via qPCR and ELISA in bulk tumor lysates of CREB KO KPC orthotopic PDAC tumors as compared to CREB WT with n=3-7 mice per group. (I) Representative photomicrographs of whole pancreas along with its corresponding quantification depicting significantly reduced LIF expression via IHC in age matched KPC C -/- as compared to KPC mice. Individual data points with mean ± SEM are shown and compared by two-tailed unpaired t test. *p<0.05; **p<0.01; ns non-significant (p>0.05).

    Article Snippet: Conditioned medium was collected from cells, cleared by centrifugation, and analyzed using a commercially available sandwich ELISA kit for mouse LIF (# MLF00; R&D systems), mouse IFN-ψ (# MIF00-1; R&D systems) according to the manufacturer’s instructions.

    Techniques: Expressing, RNA Sequencing, Western Blot, Activation Assay, Recombinant, ChIP-sequencing, Binding Assay, Enzyme-linked Immunosorbent Assay, Two Tailed Test