recombinant mouse igf1  (R&D Systems)

Journal: bioRxiv

Article Title: A Wnt-responsive fibrocartilage progenitor system coordinates postnatal mandibular condylar cartilage growth

doi: 10.64898/2026.03.25.714159

Figure Lengend Snippet: (A) Differential gene expression analysis was performed comparing H2B–EGFP –positive and H2B–EGFP –negative cells within the MC-progenitor cluster identified by single-cell RNA sequencing. Genes are ranked by statistical significance. Foxm1 is significantly enriched in the H2B–EGFP –positive population, whereas Tgfb1 is enriched in the H2B–EGFP –negative population, indicating divergent transcriptional programs associated with Wnt activity. (B) Feature plots were generated to visualize expression of representative genes across mandibular condylar cartilage populations. Wnt-responsive cells show enriched expression of Foxm1 and IGF signaling–related genes ( Igf1 , Igf1r , Igfbp4 , Igfbp7 ), whereas Wnt-low populations express Tgfb1 and related factors ( Igf2r , Igfbp5 , Igfbp6 ), supporting distinct signaling states. (C) Western blot analysis was performed in isolated Wnt-responsive cells transfected with control vector or constitutively active β-catenin (S33Y). Cells were stimulated with recombinant IGF1 for the indicated time points. β-catenin activation enhances Foxm1 expression and downstream mitogenic signaling, including ERK and IGF1R phosphorylation, indicating that β-catenin promotes proliferative signaling responses. (D) Co-immunoprecipitation was performed to assess interaction between β-catenin and Foxm1. Cell lysates immunoprecipitated with anti–β-catenin antibody show enrichment of Foxm1 compared with control IgG, indicating a physical association between β-catenin and Foxm1. (E,F) Histological and immunofluorescence analyses were performed on mandibular condyles from control and Axin2 CreERT2 ;Ctnnb1 fl/+ ;Foxm1 fl/+ compound heterozygous mice at P42. H&E staining reveals reduced fibrocartilage thickness, and Ki67 staining shows decreased proliferative activity, indicating cooperative effects of β-catenin and Foxm1 in maintaining fibrocartilage proliferation. Scale bar, 100 μm. (G) Quantification of fibrocartilage thickness and Ki67-positive cells was performed. Compound heterozygous mice show reduced fibrocartilage thickness and decreased proliferation compared with controls. Data are presented as mean ± s.d. Each dot represents one biologically independent animal. (H,I) Histological and immunofluorescence analyses were performed on mandibular condyles from control and Axin2 CreERT2 ;Foxm1 fl/fl mice at P42. Foxm1 deletion results in marked condylar hypoplasia and reduced proliferative activity, indicating a critical role for Foxm1 in fibrocartilage growth. Scale bar, 100 μm. (J) Quantification of cartilage thickness and proliferative indices was performed in Foxm1 conditional knockout mice. Foxm1 deficiency significantly reduces cartilage growth and proliferation. Data are presented as mean ± s.d. Each dot represents one biologically independent animal. Statistical significance was assessed using two-tailed Student’s t-test. n.s., not significant; **P < 0.01; ****P < 0.0001. Abbreviations: sz, superficial zone; fc, fibrocartilage zone; cc, chondrocartilage zone.

Article Snippet: Cells were stimulated with recombinant mouse IGF1 (Cat No. 791-MG-050, R&D systems) for 0, 30, 60, or 180 min.

Techniques: Gene Expression, Single Cell, RNA Sequencing, Activity Assay, Generated, Expressing, Western Blot, Isolation, Transfection, Control, Plasmid Preparation, Recombinant, Activation Assay, Phospho-proteomics, Immunoprecipitation, Immunofluorescence, Staining, Knock-Out, Two Tailed Test

Journal: bioRxiv

Article Title: A Wnt-responsive fibrocartilage progenitor system coordinates postnatal mandibular condylar cartilage growth

doi: 10.64898/2026.03.25.714159

Figure Lengend Snippet: (A) RNAscope in situ hybridization showing Foxm1 transcript localization within the fibrocartilage compartment of the mandibular condyle. (B) RNAscope detection of Igf1 transcripts enriched in the superficial region of the fibrocartilage layer. (C) Violin plot comparing Foxm1 expression between H2B-EGFP –positive and H2B-EGFP –negative cells within the MC-progenitor cluster. Scale bars: 100 μm.

Article Snippet: Cells were stimulated with recombinant mouse IGF1 (Cat No. 791-MG-050, R&D systems) for 0, 30, 60, or 180 min.

Techniques: RNAscope, In Situ Hybridization, Expressing

Journal: Nature Communications

Article Title: Combinatory differentiation of human induced pluripotent stem cells generates functional thymic epithelium driving dendritic cell and CD4/CD8 T cell development

doi: 10.1038/s41467-026-68675-y

Figure Lengend Snippet: a Differentiation itinerary of the thymic epithelium showing DE (Definitive Endoderm), AFE (Anterior Foregut Endoderm), 3PPE (Third Pharyngeal Pouch Endoderm) and TEP (Thymic Epithelial Progenitor) stages (Created in BioRender. Guillonneau, C. (2025) https://BioRender.com/r5v7uln ). b Factors tested in DOE (abbreviations), their associated pathways and the timings corresponding to each tested stage transition (D5-D7: DE-to-AFE, D7-D11: AFE-to-3PPE and D11-D13: 3PPE-to-TEP). Plackett–Burman designs were used to estimate factor effects on differentiation at the three transitions, with two dose levels (−1/+1) per factor. c UMAP representations of early ( Left ) and late ( Right ) pharyngeal development scRNA-seq reference datasets, with clusters corresponding to stages of the thymic differentiation trajectory shown in color. Reference datasets: Han et al. (E8.5–E9.5) and Magaletta et al. (E9.5–E12.5). d Bulk RNA-seq results for each sample (vertical) treated with combinations of factors tested in DOE in four experiments (D5-D7, Han E8.5; D7-D11, Han and Magaletta E9.5; D11-D13, Magaletta E11.5/12.5) showing expression scores of marker genes for pharyngeal development clusters (horizontal). Cluster names corresponding to the thymic differentiation trajectory are highlighted in bold. The upper part of each heatmap shows the factor combinations applied, with high doses highlighted in orange. Statistical significance was assessed by ANOVA (Supplementary Fig. ). Significant factors are shown in red or blue, indicating those to be supplemented or excluded in the optimized protocol. Han et. al. dataset: D5 to D7: p = 0.02338 (Noggin); 4.246e-05 (IWR1); 0.05526 (LY3); 4.345.e-07 (RA)/D7 to D11: p = 5.233.e-05 (CHIR99); 0.0002875 (FLI06); 0.0015895 (IWR1). Magaletta et. al. dataset: D7 to D11: p = 1.877.e-05 (CHIR99); 1.877.e-05 (FLI06); 0.0003179 (IRW1)/D11 to D13: dots indicate suggestive p values, p = 0.089927 (BMP4); 0.079926 (IGF1); 0.086185 (RANKL). e Summary of pathway modulation: black, DOE-identified pathways to be activated (+) or inhibited (−); blue, pathways neutral in DOE but enhancing FOXN1 expression (BMP/FGF) or proliferation (FGF/EGF) at the TEP stage; green, the FGF pathway (not tested in DOE, post-DOE), activating FOXN1 at the TEP stage. DE Definitive Endoderm, AFE Anterior Foregut Endoderm, 3PPE Third Pharyngeal Pouch Endoderm, TEP Thymic Epithelial Progenitor. See corresponding factor names in ( b ) (Created in BioRender. Guillonneau, C. (2025) https://BioRender.com/ht4edy0 ). f Summary of the optimized protocol with full factor list, doses and exposure windows, DE Definitive Endoderm, AFE Anterior Foregut Endoderm, 3PPE Third Pharyngeal Pouch Endoderm, TEP Thymic Epithelial Progenitor.

Article Snippet: The supplementation included Activin A, CHIR99, BMP4 (Miltenyi, 130-111-167), retinoic acid (Sigma Aldrich, 302-79-4), FGF8 (BiotechneR&D, 423-F8), Noggin (Miltenyi 130-103-455), LY-364947 (Sigma Aldrich L6293-5MG), FGF10 (Miltenyi, 130-127-858), IGF1 (Miltenyi, 130-093-886), EGF (Miltenyi, 130-097-751), and RANK-L (BiotechneR&D: 6449-TEC).

Techniques: RNA Sequencing, Expressing, Marker

Journal: Development (Cambridge, England)

Article Title: Kupffer cells control neonatal hepatic metabolism via Igf1 signaling

doi: 10.1242/dev.204962

Figure Lengend Snippet: KC-hepatocyte crosstalk is altered in P0 KO Spi1 livers. (A) Bar plot showing the relative information flow of between WT Spi1 and KO Spi1 of inferred cell–cell communication using CellChat. (B) Comparison of the significant ligand–receptor pairs between WT Spi1 and KO Spi1 , which contribute to the signaling from KCs to the hepatocyte clusters. (C) Heatmap showing the relative importance of KC and hepatocyte clusters as sender, receiver, mediator and influencer, based on the computed four network centrality measures of IGF (top) and visfatin (bottom) signaling. (D) Box plot of variance stabilizing transformation-normalized Igf1 expression in hepatocytes and macrophages in WT Spi1 and KO Spi1 mice at P0. n =5 per genotype from 3 independent litters. Differential expression was tested using DESeq2 on raw counts. The whiskers represent the 5-95% percentile, the box extends from the 25th to 75th percentiles and the horizontal line represents the median. (E) Serum insulin levels measured by ELISA on WT Spi1 and KO Spi1 at P0. n =4-5 per genotype from 4 independent litters. Bar plot presented as mean±s.d. Unpaired Student's t -test. (F) Serum glucagon levels measured by ELISA on WT Spi1 and KO Spi1 at P0. n =6 per genotype from 3 independent litters. Bar plot presented as mean±s.d. Unpaired Student's t -test. (G) Enrichment analysis of downregulated phosphorylation sites showing the decreased and increased phosphorylation in KO Spi1 liver compared to WT Spi1 . n =4-6 per genotype from 5 independent litters.

Article Snippet: Recombinant Igf1 protein (R&D Systems, 791-MG) was added in the same way at a final concentration of 100 ng/ml.

Techniques: Comparison, Transformation Assay, Expressing, Quantitative Proteomics, Enzyme-linked Immunosorbent Assay, Phospho-proteomics

Journal: Development (Cambridge, England)

Article Title: Kupffer cells control neonatal hepatic metabolism via Igf1 signaling

doi: 10.1242/dev.204962

Figure Lengend Snippet: KC-derived Igf1 regulates glycogen homeostasis in hepatocytes at birth. (A) Percentage of (left) and normalized (right) Igf1 expression in the respective hepatic cell type during embryogenesis. (B) Breeding scheme to produce KO Igf1 mice and littermate controls ( WT Igf1 ). Created in BioRender by Mass, E., 2025. https://BioRender.com/jvsfc8p . This figure was sublicensed under CC-BY 4.0 terms. (C,D) Igf1 levels measured by ELISA on whole liver lysate (C) and serum (D) of WT Igf1 and KO Igf1 at P0. n =7-8 per genotype from 4 independent litters. Bar plots presented as mean±s.d. Unpaired Student's t -test. (E) Glycogen levels measured on whole liver lysates of WT Igf1 and KO Igf1 at P0. n =11-16 per genotype from 7 independent litters. Values were normalized per litter. The whiskers represent the 5-95% percentile, the box extends from the 25th to 75th percentiles and the horizontal line represents the median. Cross indicates the mean. Mann–Whitney test. (F) Representative transmission electron micrograph from WT Igf1 and KO Igf1 livers at P0. n =3-4 per genotype from 2 independent litters. GP, glycogen particle; N, nucleus. Scale bars: 8 µm. (G) Scheme indicating the quantification process of glycogen content in hepatocytes. (H) Hepatocyte glycogen content of KO Igf1 normalized to WT Igf1 littermates; each value represents one hepatocyte (ten hepatocytes were assessed per liver). n =3-4 per genotype from 2 independent litters. Mann–Whitney test. (I) Normalized total metabolite abundance in WT Igf1 and KO Igf1 livers following [U- 13 C 6 ]-glucose tracing at P0. n =5-6 per genotype from 2 independent litters. Unpaired Student's t -test. ns, not significant ( P >0.05). (J) Fractional enrichment of labeled metabolites following [U- 13 C 6 ]-glucose tracing at P0 with and without the addition of exogenous Igf1 protein. Liver samples with and without Igf1 from the same animal are connected with a line. n =5-6 per genotype from 2 independent litters. Wilcoxon test.

Article Snippet: Recombinant Igf1 protein (R&D Systems, 791-MG) was added in the same way at a final concentration of 100 ng/ml.

Techniques: Derivative Assay, Expressing, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY, Transmission Assay, Labeling

Journal: Development (Cambridge, England)

Article Title: Kupffer cells control neonatal hepatic metabolism via Igf1 signaling

doi: 10.1242/dev.204962

Figure Lengend Snippet: KC-hepatocyte crosstalk is altered in P0 KO Spi1 livers. (A) Bar plot showing the relative information flow of between WT Spi1 and KO Spi1 of inferred cell–cell communication using CellChat. (B) Comparison of the significant ligand–receptor pairs between WT Spi1 and KO Spi1 , which contribute to the signaling from KCs to the hepatocyte clusters. (C) Heatmap showing the relative importance of KC and hepatocyte clusters as sender, receiver, mediator and influencer, based on the computed four network centrality measures of IGF (top) and visfatin (bottom) signaling. (D) Box plot of variance stabilizing transformation-normalized Igf1 expression in hepatocytes and macrophages in WT Spi1 and KO Spi1 mice at P0. n =5 per genotype from 3 independent litters. Differential expression was tested using DESeq2 on raw counts. The whiskers represent the 5-95% percentile, the box extends from the 25th to 75th percentiles and the horizontal line represents the median. (E) Serum insulin levels measured by ELISA on WT Spi1 and KO Spi1 at P0. n =4-5 per genotype from 4 independent litters. Bar plot presented as mean±s.d. Unpaired Student's t -test. (F) Serum glucagon levels measured by ELISA on WT Spi1 and KO Spi1 at P0. n =6 per genotype from 3 independent litters. Bar plot presented as mean±s.d. Unpaired Student's t -test. (G) Enrichment analysis of downregulated phosphorylation sites showing the decreased and increased phosphorylation in KO Spi1 liver compared to WT Spi1 . n =4-6 per genotype from 5 independent litters.

Article Snippet: To determine the amount of Igf1 present in the perinatal liver and serum the Quantitative ELISA Mouse/Rat Igf1 Kit Liver Glycogen Assay Kit from R&D Systems (MG100) was used.

Techniques: Comparison, Transformation Assay, Expressing, Quantitative Proteomics, Enzyme-linked Immunosorbent Assay, Phospho-proteomics

Journal: Development (Cambridge, England)

Article Title: Kupffer cells control neonatal hepatic metabolism via Igf1 signaling

doi: 10.1242/dev.204962

Figure Lengend Snippet: KC-derived Igf1 regulates glycogen homeostasis in hepatocytes at birth. (A) Percentage of (left) and normalized (right) Igf1 expression in the respective hepatic cell type during embryogenesis. (B) Breeding scheme to produce KO Igf1 mice and littermate controls ( WT Igf1 ). Created in BioRender by Mass, E., 2025. https://BioRender.com/jvsfc8p . This figure was sublicensed under CC-BY 4.0 terms. (C,D) Igf1 levels measured by ELISA on whole liver lysate (C) and serum (D) of WT Igf1 and KO Igf1 at P0. n =7-8 per genotype from 4 independent litters. Bar plots presented as mean±s.d. Unpaired Student's t -test. (E) Glycogen levels measured on whole liver lysates of WT Igf1 and KO Igf1 at P0. n =11-16 per genotype from 7 independent litters. Values were normalized per litter. The whiskers represent the 5-95% percentile, the box extends from the 25th to 75th percentiles and the horizontal line represents the median. Cross indicates the mean. Mann–Whitney test. (F) Representative transmission electron micrograph from WT Igf1 and KO Igf1 livers at P0. n =3-4 per genotype from 2 independent litters. GP, glycogen particle; N, nucleus. Scale bars: 8 µm. (G) Scheme indicating the quantification process of glycogen content in hepatocytes. (H) Hepatocyte glycogen content of KO Igf1 normalized to WT Igf1 littermates; each value represents one hepatocyte (ten hepatocytes were assessed per liver). n =3-4 per genotype from 2 independent litters. Mann–Whitney test. (I) Normalized total metabolite abundance in WT Igf1 and KO Igf1 livers following [U- 13 C 6 ]-glucose tracing at P0. n =5-6 per genotype from 2 independent litters. Unpaired Student's t -test. ns, not significant ( P >0.05). (J) Fractional enrichment of labeled metabolites following [U- 13 C 6 ]-glucose tracing at P0 with and without the addition of exogenous Igf1 protein. Liver samples with and without Igf1 from the same animal are connected with a line. n =5-6 per genotype from 2 independent litters. Wilcoxon test.

Article Snippet: To determine the amount of Igf1 present in the perinatal liver and serum the Quantitative ELISA Mouse/Rat Igf1 Kit Liver Glycogen Assay Kit from R&D Systems (MG100) was used.

Techniques: Derivative Assay, Expressing, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY, Transmission Assay, Labeling

Journal: Nature Communications

Article Title: Airway immune profiles and therapeutic implications of IGF1 in eosinophilic granulomatosis with polyangiitis

doi: 10.1038/s41467-025-68104-6

Figure Lengend Snippet: a UMAP plots of 12 macrophage and DC subtypes from baseline and follow-up samples. IGF1 ⁺Macrophage cluster (cluster 3) highlighted. b Volcano plot of DEGs in IGF1 ⁺ macrophages between baseline and follow-up. Upregulated (red), downregulated (blue), stable (grey) genes shown. c Bar plots of top enriched Reactome pathways in IGF1 ⁺ macrophages from DEGs (two-sided Wilcoxon rank-sum test, adjusted P values). Pathway enrichment of top 20 upregulated genes via Enrichr (Reactome_Pathways_2024, hypergeometric test, unadjusted P values). d UMAP plots of key marker gene expression ( HP , IGF1 , RETN ) in macrophage subsets; color intensity reflects normalized UMI counts. e Violin plots of IGF1 , RETN , HP expression across disease phases (EGPA baseline, Cs-remission, Cs-relapse) in macrophages. f Immunofluorescent staining and quantification of IGF1⁺CD68⁺ macrophages in bronchial mucosae (biological replicates; EGPA n = 15, Cs-remission n = 3, Cs-relapse n = 5). Scale bars: 100 μm (upper), 20 μm (lower). g UMAP plots of 11 epithelial cell subsets from combined samples. h Heatmap of relative enrichment (observed/expected Ro/e) of epithelial subtypes across groups and sample types. i Dot plot of reciprocal epithelial ligand-receptor expression across subsets. Interaction pairs linked by color-coded lines; dot size reflects expression fraction, color intensity shows relative expression. j Violin plots of marker gene expression for goblet cell subsets (Goblet-1, Goblet−2) and ionocytes across groups. k Immunofluorescent staining and quantification of MUC5AC⁺ epithelial cells (biological replicates; EGPA n = 10, Cs-remission n = 3, Cs-relapse n = 5). Scale bar: 100 μm. Data presented as median with IQR. f , k Two-sided Kruskal–Wallis test with Dunn’s post-hoc and Bonferroni correction. * P < 0.05, ** P < 0.01, *** P < 0.001; NS, not significant. Exact P values in Supplementary Data . Cs-relapse corticosteroid relapse, Cs-remission corticosteroid remission, DC dendritic cell, DEGs differentially expressed genes, IGF1 insulin-like growth factor 1, MUC5AC mucin 5AC, Ro/e ratio of observed to expected.

Article Snippet: For human sputum IGF1 concentration detection, 100uL sputum supernatant was used (Multi Sciences, Cat# EK1131-96).

Techniques: Marker, Gene Expression, Expressing, Staining

Journal: Nature Communications

Article Title: Airway immune profiles and therapeutic implications of IGF1 in eosinophilic granulomatosis with polyangiitis

doi: 10.1038/s41467-025-68104-6

Figure Lengend Snippet: a Immunofluorescent staining and quantification of IGF1⁺ epithelial cells at bronchial mucosae from control ( n = 6), SEA ( n = 9), EGPA ( n = 10), Cs-remission ( n = 3), and Cs-relapse ( n = 5) groups (biological replicates). Scale bar: 100 μm. b Bar plots of IGF1 concentrations in sputum samples from Control ( n = 13), SEA ( n = 23), and EGPA ( n = 21) (biological replicates). c Schematic of EGPA airway epithelial cells in ALI culture stimulated with IL-13, IL-33, or medium (Control). Bar plots show relative expression of IGF1 , IGF1R , and IGFBP3 , and IGF1 concentrations under different conditions. Data from 3 independent experiments (biological replicates). d Schematic of ALI system with IGF1 stimulation versus control. Representative histological (HE, PAS) and immunofluorescent (MUC5AC with DAPI) staining demonstrate morphological changes and mucin production (goblet hyperplasia) in ALI cultures with medium (Control) or IGF1 stimulation. Scale bars: 50 μm (HE, PAS), 20 μm (MUC5AC). Bar plots of IL-25, IL-33, and TSLP concentrations in culture supernatant at time points (Day 9, 13, 17, 21). Data from 3 independent experiments (biological replicates). e Scatter plot showing positive correlation between eosinophil abundance and IGF1 concentration in sputum from EGPA patients ( n = 21). f Schematic of proposed mechanism where IGF1 promotes goblet hyperplasia and augments T2-mediated inflammation through IGF1-IL25 loop, contributing to disease exacerbation in asthma and EGPA. Data presented as mean ± SD. a – c Two-sided one-way ANOVA with Tukey’s post-hoc test. d Two-sided unpaired t -test. e Two-sided Pearson correlation test. * P < 0.05, ** P < 0.01, *** P < 0.001; NS, not significant. Exact P values in Supplementary Data . ALI air-liquid interface, HE hematoxylin and eosin, IGF1R insulin-like growth factor 1 receptor, IGFBP3 insulin-like growth factor binding protein 3, PAS periodic acid-Schiff, TSLP thymic stromal lymphopoietin.

Article Snippet: For human sputum IGF1 concentration detection, 100uL sputum supernatant was used (Multi Sciences, Cat# EK1131-96).

Techniques: Staining, Control, Expressing, Concentration Assay, Binding Assay

Journal: Nature Communications

Article Title: Airway immune profiles and therapeutic implications of IGF1 in eosinophilic granulomatosis with polyangiitis

doi: 10.1038/s41467-025-68104-6

Figure Lengend Snippet: a – e Anti-IGF1 treatment reduces eosinophilic inflammation and airway remodeling in IL-5 transgenic mice challenged with HDM and IL-33. Mice were divided into Control (PBS-treated), Model (HDM+IL-33 challenged), and Anti-IGF1 (HDM+IL-33+anti-IGF1 antibody) groups. a Total cell counts in bronchoalveolar lavage fluid (BALF) from control, model, and anti-IGF1-treated groups. b Eosinophil percentage in BALF. c Absolute eosinophil counts in BALF. d IL−25 levels in BALF quantified by ELISA. e Representative histological images of lung sections stained with hematoxylin and eosin (H&E, upper panels) and periodic acid-Schiff (PAS, lower panels), with corresponding inflammation and PAS score quantifications. Scale bar, 100 μm. f – h IGF1R deficiency modulates eosinophilic inflammation and airway remodeling via IL−25 in HDM+IL-33 challenged mice. f Total cell counts in BALF from wild-type (WT, Scgb1a1 -IRES-+/+ Igf1r f/f ), conditional knockout ( Scgb1a1 -IRES-Cre/+ Igf1r f/f , CKO), and CKO mice treated with recombinant IL-25 (rIL-25). All groups were challenged with HDM+IL-33. g Flow cytometric analysis of eosinophils (CD45 + Siglec-F + CD11c - ) in BALF. Representative plots and quantification of eosinophil percentages are shown. h Representative H&E (upper panels) and PAS (lower panels) staining of lung sections from WT, CKO, and CKO+rIL-25 groups, with quantification of inflammation and PAS scores. Scale bar, 100 μm. Statistical analysis: Data are presented as mean ± SD ( n = 5 mice per group). Statistical significance was determined using a two-sided one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001; NS, not significant. Exact P values and complete test statistics for a – h are provided in Supplementary Data . CKO conditional knockout, HDM house dust mite, rIL-25 recombinant IL-25, WT wild-type.

Article Snippet: For human sputum IGF1 concentration detection, 100uL sputum supernatant was used (Multi Sciences, Cat# EK1131-96).

Techniques: Transgenic Assay, Control, Enzyme-linked Immunosorbent Assay, Staining, Knock-Out, Recombinant