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Enhanced <t>SAA1</t> expression and NET formation in plasma of MS patients. (A) SAA1 protein expression was quantified by ELISA in plasma samples collected from MS patients and HC. (B) H3.1-nucleosome expression was quantified by ELISA in plasma samples collected from MS patients and HC
Human Saa1 Elisa Kit, supplied by R&D Systems, 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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Verification of potential biomarkers for AS. (A) Expression levels of <t>SAA1,</t> FERMT3, ILK, and TLN1 in plasma samples from active-stage AS patients, stable-stage AS patients, and healthy controls measured by proteomics. ROC curves for the individual protein (SAA1, FERMT3, ILK, and TLN1) as a predictor to classify AS patients from healthy controls (B), and active-stage AS patients from stable-stage AS patients (C). (D) ELISA analysis of SAA1, FERMT3, ILK, and TLN1 expressions in the plasma samples from an independent validation cohort of healthy controls (N, n = 24), active-stage AS (A, n = 27), and stable-stage AS patients (S, n = 28). Statistical analyses employed Wilcoxon rank-sum test for intergroup comparisons, with results reported as mean ± SEM. Significance thresholds based on BH-adjusted p -values were defined as: *, <0.05; **, <0.01; ***, <0.001.
Human Serum Amyloid A Saa1 Elisa Kit, supplied by Aviva 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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Mendeley Ltd rna seq matrices of adipose stromal vascular cells under saa1 or lps treatment
(A) Cell-cell communication analysis of SAA signaling pathway for the indicated depots and cells. Line colors and widths represent the sending cell and the strength of the signal, respectively. (B) Pseudobulk comparison of differentially expressed genes in epiploic vs. subcutaneous depots, highlighting the indicated signaling pathways. (C) Expression of <t>SAA1</t> mRNA upon stimulation with LPS (10 ng/mL), TNF-α (2.5 ng/mL), IL-1β (10 ng/mL), or IL-6 (10 ng/mL) for 24 h. Data are presented as fold change (FC) over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. (D) Relative expression of SAA1 (left) and SAA2 (right) mRNA in adipocytes, ASPCs, adipose-derived endothelial cells (adECs), and THP1-derived macrophages (THP1 M0). Significant (<0.05) p values compared with the cell-type-specific control from one-way ANOVA are shown. (E) Results from ELISA measurements of SAA in conditioned media from human adipocytes incubated without or with LPS for 72 h. Results are displayed as mean, error bars represent standard error of the mean, and statistical significance was calculated using Student’s t test. (F) Analyses of DNA methylation in the indicated cell classes for the promoter and gene body regions of SAA1 and SAA2 , respectively. Chromosomal localization and motifs for NFKB2/RELA/REL and STAT3 are indicated for both genes. (G) SAA1 and SAA2 mRNA expression in adipocytes treated with or without LPS in the presence or absence of different inhibitors described in the main text. Data are presented as FC over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. For (C), (D), and (G), data are displayed as geometric mean ± 95% confidence intervals with technical replicates displayed from three independent experiments. ASPC, adipose stromal and progenitor cell.
Rna Seq Matrices Of Adipose Stromal Vascular Cells Under Saa1 Or Lps Treatment, supplied by Mendeley Ltd, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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OriGene human recombinant saa1 protein
(A) Cell-cell communication analysis of SAA signaling pathway for the indicated depots and cells. Line colors and widths represent the sending cell and the strength of the signal, respectively. (B) Pseudobulk comparison of differentially expressed genes in epiploic vs. subcutaneous depots, highlighting the indicated signaling pathways. (C) Expression of <t>SAA1</t> mRNA upon stimulation with LPS (10 ng/mL), TNF-α (2.5 ng/mL), IL-1β (10 ng/mL), or IL-6 (10 ng/mL) for 24 h. Data are presented as fold change (FC) over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. (D) Relative expression of SAA1 (left) and SAA2 (right) mRNA in adipocytes, ASPCs, adipose-derived endothelial cells (adECs), and THP1-derived macrophages (THP1 M0). Significant (<0.05) p values compared with the cell-type-specific control from one-way ANOVA are shown. (E) Results from ELISA measurements of SAA in conditioned media from human adipocytes incubated without or with LPS for 72 h. Results are displayed as mean, error bars represent standard error of the mean, and statistical significance was calculated using Student’s t test. (F) Analyses of DNA methylation in the indicated cell classes for the promoter and gene body regions of SAA1 and SAA2 , respectively. Chromosomal localization and motifs for NFKB2/RELA/REL and STAT3 are indicated for both genes. (G) SAA1 and SAA2 mRNA expression in adipocytes treated with or without LPS in the presence or absence of different inhibitors described in the main text. Data are presented as FC over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. For (C), (D), and (G), data are displayed as geometric mean ± 95% confidence intervals with technical replicates displayed from three independent experiments. ASPC, adipose stromal and progenitor cell.
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Novoprotein recombinant human saa1
(A) Cell-cell communication analysis of SAA signaling pathway for the indicated depots and cells. Line colors and widths represent the sending cell and the strength of the signal, respectively. (B) Pseudobulk comparison of differentially expressed genes in epiploic vs. subcutaneous depots, highlighting the indicated signaling pathways. (C) Expression of <t>SAA1</t> mRNA upon stimulation with LPS (10 ng/mL), TNF-α (2.5 ng/mL), IL-1β (10 ng/mL), or IL-6 (10 ng/mL) for 24 h. Data are presented as fold change (FC) over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. (D) Relative expression of SAA1 (left) and SAA2 (right) mRNA in adipocytes, ASPCs, adipose-derived endothelial cells (adECs), and THP1-derived macrophages (THP1 M0). Significant (<0.05) p values compared with the cell-type-specific control from one-way ANOVA are shown. (E) Results from ELISA measurements of SAA in conditioned media from human adipocytes incubated without or with LPS for 72 h. Results are displayed as mean, error bars represent standard error of the mean, and statistical significance was calculated using Student’s t test. (F) Analyses of DNA methylation in the indicated cell classes for the promoter and gene body regions of SAA1 and SAA2 , respectively. Chromosomal localization and motifs for NFKB2/RELA/REL and STAT3 are indicated for both genes. (G) SAA1 and SAA2 mRNA expression in adipocytes treated with or without LPS in the presence or absence of different inhibitors described in the main text. Data are presented as FC over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. For (C), (D), and (G), data are displayed as geometric mean ± 95% confidence intervals with technical replicates displayed from three independent experiments. ASPC, adipose stromal and progenitor cell.
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Enhanced SAA1 expression and NET formation in plasma of MS patients. (A) SAA1 protein expression was quantified by ELISA in plasma samples collected from MS patients and HC. (B) H3.1-nucleosome expression was quantified by ELISA in plasma samples collected from MS patients and HC

Journal: Journal of Neuroinflammation

Article Title: Single-cell RNA sequencing uncovers neutrophil clusters associated with autoimmune neuroinflammation

doi: 10.1186/s12974-026-03772-9

Figure Lengend Snippet: Enhanced SAA1 expression and NET formation in plasma of MS patients. (A) SAA1 protein expression was quantified by ELISA in plasma samples collected from MS patients and HC. (B) H3.1-nucleosome expression was quantified by ELISA in plasma samples collected from MS patients and HC

Article Snippet: The human SAA1 ELISA kit (DY3019-05; R & D Systems, Minneapolis, MN) detected human SAA1 in plasma samples from MS patients and HC.

Techniques: Expressing, Clinical Proteomics, Enzyme-linked Immunosorbent Assay

Verification of potential biomarkers for AS. (A) Expression levels of SAA1, FERMT3, ILK, and TLN1 in plasma samples from active-stage AS patients, stable-stage AS patients, and healthy controls measured by proteomics. ROC curves for the individual protein (SAA1, FERMT3, ILK, and TLN1) as a predictor to classify AS patients from healthy controls (B), and active-stage AS patients from stable-stage AS patients (C). (D) ELISA analysis of SAA1, FERMT3, ILK, and TLN1 expressions in the plasma samples from an independent validation cohort of healthy controls (N, n = 24), active-stage AS (A, n = 27), and stable-stage AS patients (S, n = 28). Statistical analyses employed Wilcoxon rank-sum test for intergroup comparisons, with results reported as mean ± SEM. Significance thresholds based on BH-adjusted p -values were defined as: *, <0.05; **, <0.01; ***, <0.001.

Journal: Journal of Advanced Research

Article Title: Characterization of immune features and discovery of potential biomarkers for ankylosing spondylitis using deep plasma proteomics

doi: 10.1016/j.jare.2025.05.052

Figure Lengend Snippet: Verification of potential biomarkers for AS. (A) Expression levels of SAA1, FERMT3, ILK, and TLN1 in plasma samples from active-stage AS patients, stable-stage AS patients, and healthy controls measured by proteomics. ROC curves for the individual protein (SAA1, FERMT3, ILK, and TLN1) as a predictor to classify AS patients from healthy controls (B), and active-stage AS patients from stable-stage AS patients (C). (D) ELISA analysis of SAA1, FERMT3, ILK, and TLN1 expressions in the plasma samples from an independent validation cohort of healthy controls (N, n = 24), active-stage AS (A, n = 27), and stable-stage AS patients (S, n = 28). Statistical analyses employed Wilcoxon rank-sum test for intergroup comparisons, with results reported as mean ± SEM. Significance thresholds based on BH-adjusted p -values were defined as: *, <0.05; **, <0.01; ***, <0.001.

Article Snippet: The human serum amyloid A (SAA1) ELISA kit (#OKIA00083) was purchased from Aviva Systems Biology Company (San Diego, CA, USA).

Techniques: Expressing, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Biomarker Discovery

(A) Cell-cell communication analysis of SAA signaling pathway for the indicated depots and cells. Line colors and widths represent the sending cell and the strength of the signal, respectively. (B) Pseudobulk comparison of differentially expressed genes in epiploic vs. subcutaneous depots, highlighting the indicated signaling pathways. (C) Expression of SAA1 mRNA upon stimulation with LPS (10 ng/mL), TNF-α (2.5 ng/mL), IL-1β (10 ng/mL), or IL-6 (10 ng/mL) for 24 h. Data are presented as fold change (FC) over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. (D) Relative expression of SAA1 (left) and SAA2 (right) mRNA in adipocytes, ASPCs, adipose-derived endothelial cells (adECs), and THP1-derived macrophages (THP1 M0). Significant (<0.05) p values compared with the cell-type-specific control from one-way ANOVA are shown. (E) Results from ELISA measurements of SAA in conditioned media from human adipocytes incubated without or with LPS for 72 h. Results are displayed as mean, error bars represent standard error of the mean, and statistical significance was calculated using Student’s t test. (F) Analyses of DNA methylation in the indicated cell classes for the promoter and gene body regions of SAA1 and SAA2 , respectively. Chromosomal localization and motifs for NFKB2/RELA/REL and STAT3 are indicated for both genes. (G) SAA1 and SAA2 mRNA expression in adipocytes treated with or without LPS in the presence or absence of different inhibitors described in the main text. Data are presented as FC over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. For (C), (D), and (G), data are displayed as geometric mean ± 95% confidence intervals with technical replicates displayed from three independent experiments. ASPC, adipose stromal and progenitor cell.

Journal: Cell metabolism

Article Title: Cytoarchitectural multi-depot profiling reveals immune-metabolic crosstalk in human colon-associated adipose tissue

doi: 10.1016/j.cmet.2025.12.008

Figure Lengend Snippet: (A) Cell-cell communication analysis of SAA signaling pathway for the indicated depots and cells. Line colors and widths represent the sending cell and the strength of the signal, respectively. (B) Pseudobulk comparison of differentially expressed genes in epiploic vs. subcutaneous depots, highlighting the indicated signaling pathways. (C) Expression of SAA1 mRNA upon stimulation with LPS (10 ng/mL), TNF-α (2.5 ng/mL), IL-1β (10 ng/mL), or IL-6 (10 ng/mL) for 24 h. Data are presented as fold change (FC) over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. (D) Relative expression of SAA1 (left) and SAA2 (right) mRNA in adipocytes, ASPCs, adipose-derived endothelial cells (adECs), and THP1-derived macrophages (THP1 M0). Significant (<0.05) p values compared with the cell-type-specific control from one-way ANOVA are shown. (E) Results from ELISA measurements of SAA in conditioned media from human adipocytes incubated without or with LPS for 72 h. Results are displayed as mean, error bars represent standard error of the mean, and statistical significance was calculated using Student’s t test. (F) Analyses of DNA methylation in the indicated cell classes for the promoter and gene body regions of SAA1 and SAA2 , respectively. Chromosomal localization and motifs for NFKB2/RELA/REL and STAT3 are indicated for both genes. (G) SAA1 and SAA2 mRNA expression in adipocytes treated with or without LPS in the presence or absence of different inhibitors described in the main text. Data are presented as FC over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. For (C), (D), and (G), data are displayed as geometric mean ± 95% confidence intervals with technical replicates displayed from three independent experiments. ASPC, adipose stromal and progenitor cell.

Article Snippet: RNA-seq matrices of adipose stromal vascular cells under SAA1 or LPS treatment , This paper , Mendeley Data: https://doi.org/10.17632/8p7k6htgfm.1.

Techniques: Comparison, Protein-Protein interactions, Expressing, Derivative Assay, Control, Enzyme-linked Immunosorbent Assay, Incubation, DNA Methylation Assay

(A) Top Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways based on differentially expressed genes from comparisons of SAA1- or LPS-treated vs. control-treated adipose-derived stromal-vascular cells. (B) Network view of the six common SAA1- and LPS-regulated pathways showing shared and treatment-specific genes. (C) Expression scores for SAA1- (left) and LPS-responsive (right) genes following a 6-h incubation with either ligand in stromal-vascular cells from subcutaneous human WAT. Results are displayed on the uniform manifold approximation and projection panel from and violin plots for each indicated cell class. Note that adipocytes and mesothelial cells were removed as these are not present in the stromal-vascular fraction from the subcutaneous depot. (D) Representative immunostaining of epiploic adipose tissue using antibodies directed against markers for Adipo SAA (CES1) and macrophages (CD68). Hoechst33342 was used as the counterstain for nuclei. Scale bar, 100 μm. ASPC, adipose stromal and progenitor cell; NES, normalized enrichment score.

Journal: Cell metabolism

Article Title: Cytoarchitectural multi-depot profiling reveals immune-metabolic crosstalk in human colon-associated adipose tissue

doi: 10.1016/j.cmet.2025.12.008

Figure Lengend Snippet: (A) Top Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways based on differentially expressed genes from comparisons of SAA1- or LPS-treated vs. control-treated adipose-derived stromal-vascular cells. (B) Network view of the six common SAA1- and LPS-regulated pathways showing shared and treatment-specific genes. (C) Expression scores for SAA1- (left) and LPS-responsive (right) genes following a 6-h incubation with either ligand in stromal-vascular cells from subcutaneous human WAT. Results are displayed on the uniform manifold approximation and projection panel from and violin plots for each indicated cell class. Note that adipocytes and mesothelial cells were removed as these are not present in the stromal-vascular fraction from the subcutaneous depot. (D) Representative immunostaining of epiploic adipose tissue using antibodies directed against markers for Adipo SAA (CES1) and macrophages (CD68). Hoechst33342 was used as the counterstain for nuclei. Scale bar, 100 μm. ASPC, adipose stromal and progenitor cell; NES, normalized enrichment score.

Article Snippet: RNA-seq matrices of adipose stromal vascular cells under SAA1 or LPS treatment , This paper , Mendeley Data: https://doi.org/10.17632/8p7k6htgfm.1.

Techniques: Control, Derivative Assay, Expressing, Incubation, Immunostaining

(A) Cell-cell communication analysis of SAA signaling pathway for the indicated depots and cells. Line colors and widths represent the sending cell and the strength of the signal, respectively. (B) Pseudobulk comparison of differentially expressed genes in epiploic vs. subcutaneous depots, highlighting the indicated signaling pathways. (C) Expression of SAA1 mRNA upon stimulation with LPS (10 ng/mL), TNF-α (2.5 ng/mL), IL-1β (10 ng/mL), or IL-6 (10 ng/mL) for 24 h. Data are presented as fold change (FC) over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. (D) Relative expression of SAA1 (left) and SAA2 (right) mRNA in adipocytes, ASPCs, adipose-derived endothelial cells (adECs), and THP1-derived macrophages (THP1 M0). Significant (<0.05) p values compared with the cell-type-specific control from one-way ANOVA are shown. (E) Results from ELISA measurements of SAA in conditioned media from human adipocytes incubated without or with LPS for 72 h. Results are displayed as mean, error bars represent standard error of the mean, and statistical significance was calculated using Student’s t test. (F) Analyses of DNA methylation in the indicated cell classes for the promoter and gene body regions of SAA1 and SAA2 , respectively. Chromosomal localization and motifs for NFKB2/RELA/REL and STAT3 are indicated for both genes. (G) SAA1 and SAA2 mRNA expression in adipocytes treated with or without LPS in the presence or absence of different inhibitors described in the main text. Data are presented as FC over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. For (C), (D), and (G), data are displayed as geometric mean ± 95% confidence intervals with technical replicates displayed from three independent experiments. ASPC, adipose stromal and progenitor cell.

Journal: Cell metabolism

Article Title: Cytoarchitectural multi-depot profiling reveals immune-metabolic crosstalk in human colon-associated adipose tissue

doi: 10.1016/j.cmet.2025.12.008

Figure Lengend Snippet: (A) Cell-cell communication analysis of SAA signaling pathway for the indicated depots and cells. Line colors and widths represent the sending cell and the strength of the signal, respectively. (B) Pseudobulk comparison of differentially expressed genes in epiploic vs. subcutaneous depots, highlighting the indicated signaling pathways. (C) Expression of SAA1 mRNA upon stimulation with LPS (10 ng/mL), TNF-α (2.5 ng/mL), IL-1β (10 ng/mL), or IL-6 (10 ng/mL) for 24 h. Data are presented as fold change (FC) over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. (D) Relative expression of SAA1 (left) and SAA2 (right) mRNA in adipocytes, ASPCs, adipose-derived endothelial cells (adECs), and THP1-derived macrophages (THP1 M0). Significant (<0.05) p values compared with the cell-type-specific control from one-way ANOVA are shown. (E) Results from ELISA measurements of SAA in conditioned media from human adipocytes incubated without or with LPS for 72 h. Results are displayed as mean, error bars represent standard error of the mean, and statistical significance was calculated using Student’s t test. (F) Analyses of DNA methylation in the indicated cell classes for the promoter and gene body regions of SAA1 and SAA2 , respectively. Chromosomal localization and motifs for NFKB2/RELA/REL and STAT3 are indicated for both genes. (G) SAA1 and SAA2 mRNA expression in adipocytes treated with or without LPS in the presence or absence of different inhibitors described in the main text. Data are presented as FC over vehicle. Significant (<0.05) p values compared with the vehicle from one-way ANOVA are shown. For (C), (D), and (G), data are displayed as geometric mean ± 95% confidence intervals with technical replicates displayed from three independent experiments. ASPC, adipose stromal and progenitor cell.

Article Snippet: Human recombinant SAA1 protein , OriGene , Cat#TP310664.

Techniques: Comparison, Protein-Protein interactions, Expressing, Derivative Assay, Control, Enzyme-linked Immunosorbent Assay, Incubation, DNA Methylation Assay

(A) Top Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways based on differentially expressed genes from comparisons of SAA1- or LPS-treated vs. control-treated adipose-derived stromal-vascular cells. (B) Network view of the six common SAA1- and LPS-regulated pathways showing shared and treatment-specific genes. (C) Expression scores for SAA1- (left) and LPS-responsive (right) genes following a 6-h incubation with either ligand in stromal-vascular cells from subcutaneous human WAT. Results are displayed on the uniform manifold approximation and projection panel from and violin plots for each indicated cell class. Note that adipocytes and mesothelial cells were removed as these are not present in the stromal-vascular fraction from the subcutaneous depot. (D) Representative immunostaining of epiploic adipose tissue using antibodies directed against markers for Adipo SAA (CES1) and macrophages (CD68). Hoechst33342 was used as the counterstain for nuclei. Scale bar, 100 μm. ASPC, adipose stromal and progenitor cell; NES, normalized enrichment score.

Journal: Cell metabolism

Article Title: Cytoarchitectural multi-depot profiling reveals immune-metabolic crosstalk in human colon-associated adipose tissue

doi: 10.1016/j.cmet.2025.12.008

Figure Lengend Snippet: (A) Top Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways based on differentially expressed genes from comparisons of SAA1- or LPS-treated vs. control-treated adipose-derived stromal-vascular cells. (B) Network view of the six common SAA1- and LPS-regulated pathways showing shared and treatment-specific genes. (C) Expression scores for SAA1- (left) and LPS-responsive (right) genes following a 6-h incubation with either ligand in stromal-vascular cells from subcutaneous human WAT. Results are displayed on the uniform manifold approximation and projection panel from and violin plots for each indicated cell class. Note that adipocytes and mesothelial cells were removed as these are not present in the stromal-vascular fraction from the subcutaneous depot. (D) Representative immunostaining of epiploic adipose tissue using antibodies directed against markers for Adipo SAA (CES1) and macrophages (CD68). Hoechst33342 was used as the counterstain for nuclei. Scale bar, 100 μm. ASPC, adipose stromal and progenitor cell; NES, normalized enrichment score.

Article Snippet: Human recombinant SAA1 protein , OriGene , Cat#TP310664.

Techniques: Control, Derivative Assay, Expressing, Incubation, Immunostaining