Review

g401 (ATCC)

ATCC is a verified supplier

ATCC manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

ATCC g401

( A ) Violin plots of gene dependency for n = 1077 cell lines (DepMap) for genes targeted by FDA-approved targeted therapies (blue) or chemotherapies (red). Genes inhibited by multiprotein-targeted inhibitors were excluded. Individual cell lines (points) are shown when ≤−1.0 (not shown when median gene dependency ≤−0.5). ( B ) Box plot of median dependencies for 17,453 genes, separated into FDA-approved classes (A) or other genes. P values, two-sided Wilcoxon rank-sum test. n.s., not significant. ( C ) Box plot of z -scores for the GPD ξ value for each gene’s dependency distribution as a measure of selective dependency. Genes above the top quartile of the targeted therapy group (1.98%; n = 346) were selected for further analysis. ( D ) Workflow to identify pHTI genes using selective dependency (C), human and mouse genetics, and normal tissue (GTEx) expression. ( E ) Box plot of IRS4 dependency scores by cancer type. ( F ) Correlation between IRS4 mRNA (CCLE RNA-seq) and dependency scores. r , Pearson correlation. ( G ) Western blot of indicated cell lines. ( H ) Western blot 3 days posttransduction with control or gene-targeted lentiviral sgRNAs at 10 MOI (for combination, each sgRNA at 5 MOI). Puromycin began 1 day posttransduction. ( I to L ) Viability (CellTiter-Glo) after lentiviral transduction in IRS4-absent (I and K) and IRS4-expressing (J and L) cell lines. Cells were transduced at 10 MOI (TC797, PER-624, <t>G401,</t> and HCC2429) or 20 MOI (all others), puromycin selected for 1 or 2 days, and plated with six technical replicates per time point (or three for PER-704). Eight to 14 hours after plating at day 0, measurement was performed for normalization. For TC797, PER-624, G401, and HCC2429, a combination of two IRS4 or PLK1 sgRNAs was given; puromycin was maintained during days 0 to 3 for each of these, except G401. For other cell lines, sgRNAs were administered individually without puromycin maintenance postplating. Points, mean values; errors bars, standard deviation.

G401, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 237 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/g401/product/ATCC
Average 95 stars, based on 237 article reviews

g401 - by Bioz Stars, 2026-06

95/100 stars

Images

1) Product Images from "IRS4 is a PI3K-activating cancer dependency up-regulated through DNA rearrangements or epigenetic mechanisms in multiple solid tumors"

Article Title: IRS4 is a PI3K-activating cancer dependency up-regulated through DNA rearrangements or epigenetic mechanisms in multiple solid tumors

Journal: Science Advances

doi: 10.1126/sciadv.aeb3503

Figure Legend Snippet: ( A ) Violin plots of gene dependency for n = 1077 cell lines (DepMap) for genes targeted by FDA-approved targeted therapies (blue) or chemotherapies (red). Genes inhibited by multiprotein-targeted inhibitors were excluded. Individual cell lines (points) are shown when ≤−1.0 (not shown when median gene dependency ≤−0.5). ( B ) Box plot of median dependencies for 17,453 genes, separated into FDA-approved classes (A) or other genes. P values, two-sided Wilcoxon rank-sum test. n.s., not significant. ( C ) Box plot of z -scores for the GPD ξ value for each gene’s dependency distribution as a measure of selective dependency. Genes above the top quartile of the targeted therapy group (1.98%; n = 346) were selected for further analysis. ( D ) Workflow to identify pHTI genes using selective dependency (C), human and mouse genetics, and normal tissue (GTEx) expression. ( E ) Box plot of IRS4 dependency scores by cancer type. ( F ) Correlation between IRS4 mRNA (CCLE RNA-seq) and dependency scores. r , Pearson correlation. ( G ) Western blot of indicated cell lines. ( H ) Western blot 3 days posttransduction with control or gene-targeted lentiviral sgRNAs at 10 MOI (for combination, each sgRNA at 5 MOI). Puromycin began 1 day posttransduction. ( I to L ) Viability (CellTiter-Glo) after lentiviral transduction in IRS4-absent (I and K) and IRS4-expressing (J and L) cell lines. Cells were transduced at 10 MOI (TC797, PER-624, G401, and HCC2429) or 20 MOI (all others), puromycin selected for 1 or 2 days, and plated with six technical replicates per time point (or three for PER-704). Eight to 14 hours after plating at day 0, measurement was performed for normalization. For TC797, PER-624, G401, and HCC2429, a combination of two IRS4 or PLK1 sgRNAs was given; puromycin was maintained during days 0 to 3 for each of these, except G401. For other cell lines, sgRNAs were administered individually without puromycin maintenance postplating. Points, mean values; errors bars, standard deviation.

Techniques Used: Expressing, RNA Sequencing, Western Blot, Control, Transduction, Standard Deviation

Image Search Results

Journal: Science Advances

Article Title: IRS4 is a PI3K-activating cancer dependency up-regulated through DNA rearrangements or epigenetic mechanisms in multiple solid tumors

doi: 10.1126/sciadv.aeb3503

Figure Lengend Snippet: ( A ) Violin plots of gene dependency for n = 1077 cell lines (DepMap) for genes targeted by FDA-approved targeted therapies (blue) or chemotherapies (red). Genes inhibited by multiprotein-targeted inhibitors were excluded. Individual cell lines (points) are shown when ≤−1.0 (not shown when median gene dependency ≤−0.5). ( B ) Box plot of median dependencies for 17,453 genes, separated into FDA-approved classes (A) or other genes. P values, two-sided Wilcoxon rank-sum test. n.s., not significant. ( C ) Box plot of z -scores for the GPD ξ value for each gene’s dependency distribution as a measure of selective dependency. Genes above the top quartile of the targeted therapy group (1.98%; n = 346) were selected for further analysis. ( D ) Workflow to identify pHTI genes using selective dependency (C), human and mouse genetics, and normal tissue (GTEx) expression. ( E ) Box plot of IRS4 dependency scores by cancer type. ( F ) Correlation between IRS4 mRNA (CCLE RNA-seq) and dependency scores. r , Pearson correlation. ( G ) Western blot of indicated cell lines. ( H ) Western blot 3 days posttransduction with control or gene-targeted lentiviral sgRNAs at 10 MOI (for combination, each sgRNA at 5 MOI). Puromycin began 1 day posttransduction. ( I to L ) Viability (CellTiter-Glo) after lentiviral transduction in IRS4-absent (I and K) and IRS4-expressing (J and L) cell lines. Cells were transduced at 10 MOI (TC797, PER-624, G401, and HCC2429) or 20 MOI (all others), puromycin selected for 1 or 2 days, and plated with six technical replicates per time point (or three for PER-704). Eight to 14 hours after plating at day 0, measurement was performed for normalization. For TC797, PER-624, G401, and HCC2429, a combination of two IRS4 or PLK1 sgRNAs was given; puromycin was maintained during days 0 to 3 for each of these, except G401. For other cell lines, sgRNAs were administered individually without puromycin maintenance postplating. Points, mean values; errors bars, standard deviation.

Article Snippet: G401, RPMI2650, BT474, and SKBR3 cells were obtained from American Type Culture Collection.

Techniques: Expressing, RNA Sequencing, Western Blot, Control, Transduction, Standard Deviation

( A ) Diagram of IRS family protein signaling based largely on IRS1 and IRS2 studies. PH, PTB, and tail represent IRS4 domains. Red “P”, phosphotyrosine. The bottom shows the structure of the IRS1 PH and PTB domains (1QQG), with a small-molecule binding pocket indicated. ( B ) Left: IRS4 domain variants with deleted regions shown as absent or dotted lines. Right: Western blot of BT474 cells transduced with IRS4 domain variants (C-terminally FLAG tagged). The IRS4 antibody binding location is indicated. ( C ) MTT assay after 4 days of lapatinib treatment in BT474 or SKBR3 cells expressing indicated domain variants (performed in two batches; fig. S18). ( D ) Western blot of BT474 cells expressing indicated domain variants after 4 hours of lapatinib treatment. “Short” and “long” indicate exposure times. ( E ) Top: siRNA binding locations in IRS4 mRNA, indicating domain variants affected. HCC2429 cells were transduced with indicated IRS4 domain variants, followed by siRNA transfection. Proliferation was measured by the MTT assay (middle) 4 days after transfection (which occurred on days 0 and 2), and Western blotting (bottom) was performed 3 days after transfection. The bar plot shows the means and standard deviation of 10 technical replicates, which are shown as individual points. P values, two-sided t test. ( F ) CellTiter-Glo assay in TTC1240 IRS4-dTAG knockin cells after 4 days of dTAG V -1 treatment, after transduction with indicated IRS4 domain variants. Means and standard deviations are shown. ( G ) IP-Western blot of BT474 cells transduced as indicated. IP was performed using an α-IRS4 antibody (binding to the IRS4 C terminus) or IgG control. Left three lanes show input protein. ( H ) BT474 cells were stably transduced with GFP, IRS4 WT-GFP, or IRS4 ΔPH/PTB-GFP (latter two with GFP as a C-terminal tag). Cells were stained with NucRed Live 647, and live cell imaging was then performed using a Zeiss Apotome microscope.

Journal: Science Advances

Article Title: IRS4 is a PI3K-activating cancer dependency up-regulated through DNA rearrangements or epigenetic mechanisms in multiple solid tumors

doi: 10.1126/sciadv.aeb3503

Figure Lengend Snippet: ( A ) Diagram of IRS family protein signaling based largely on IRS1 and IRS2 studies. PH, PTB, and tail represent IRS4 domains. Red “P”, phosphotyrosine. The bottom shows the structure of the IRS1 PH and PTB domains (1QQG), with a small-molecule binding pocket indicated. ( B ) Left: IRS4 domain variants with deleted regions shown as absent or dotted lines. Right: Western blot of BT474 cells transduced with IRS4 domain variants (C-terminally FLAG tagged). The IRS4 antibody binding location is indicated. ( C ) MTT assay after 4 days of lapatinib treatment in BT474 or SKBR3 cells expressing indicated domain variants (performed in two batches; fig. S18). ( D ) Western blot of BT474 cells expressing indicated domain variants after 4 hours of lapatinib treatment. “Short” and “long” indicate exposure times. ( E ) Top: siRNA binding locations in IRS4 mRNA, indicating domain variants affected. HCC2429 cells were transduced with indicated IRS4 domain variants, followed by siRNA transfection. Proliferation was measured by the MTT assay (middle) 4 days after transfection (which occurred on days 0 and 2), and Western blotting (bottom) was performed 3 days after transfection. The bar plot shows the means and standard deviation of 10 technical replicates, which are shown as individual points. P values, two-sided t test. ( F ) CellTiter-Glo assay in TTC1240 IRS4-dTAG knockin cells after 4 days of dTAG V -1 treatment, after transduction with indicated IRS4 domain variants. Means and standard deviations are shown. ( G ) IP-Western blot of BT474 cells transduced as indicated. IP was performed using an α-IRS4 antibody (binding to the IRS4 C terminus) or IgG control. Left three lanes show input protein. ( H ) BT474 cells were stably transduced with GFP, IRS4 WT-GFP, or IRS4 ΔPH/PTB-GFP (latter two with GFP as a C-terminal tag). Cells were stained with NucRed Live 647, and live cell imaging was then performed using a Zeiss Apotome microscope.

Article Snippet: G401, RPMI2650, BT474, and SKBR3 cells were obtained from American Type Culture Collection.

Techniques: Binding Assay, Western Blot, Transduction, MTT Assay, Expressing, Transfection, Standard Deviation, Glo Assay, Knock-In, Control, Stable Transfection, Staining, Live Cell Imaging, Microscopy

(A) Fold-change plot of differentially expressed genes (DEGs) is shown with log2 fold change values and p-value color coding from RNA-seq analysis comparing early versus late L6 nymph in the PG. (B) Representative confocal images and quantification (C) of HSL protein levels in mouse Leydig cells from young (5 weeks), adult (6 months), and tumor-bearing mice. Scale bar: 20 μm. (D) qPCR analysis of relative leptin mRNA levels in HEK293T cells compared to G401 cells, showing significant upregulation of leptin signaling in the tumor context. (E) Bodipy staining (green) of steroidogenic tissues in control (6 months) and tumor-bearing mice (4 months). (F) Quantitative analysis of LD area in Leydig cells based on image E. (G) A schematic model illustrating the mechanism across D. melanogaster , B. germanica , and M. musculus . The leptin/Upd-JAK/STAT-HSL axis acts as a universal spatiotemporal switch, coordinating lipid mobilization to transition steroidogenic cells from a quiescent (LD-poor) to an activated (LD-rich) state during development or tumor-induced stress. Data are presented as mean ± s.e.m.. Statistical significance was determined by one-way ANOVA followed by multiple comparisons. **p < 0.01, ****p < 0.0001.

Journal: bioRxiv

Article Title: Leptin Acts as a Peripheral Tropic Signal to Tune Steroidogenesis

doi: 10.64898/2026.04.13.718290

Figure Lengend Snippet: (A) Fold-change plot of differentially expressed genes (DEGs) is shown with log2 fold change values and p-value color coding from RNA-seq analysis comparing early versus late L6 nymph in the PG. (B) Representative confocal images and quantification (C) of HSL protein levels in mouse Leydig cells from young (5 weeks), adult (6 months), and tumor-bearing mice. Scale bar: 20 μm. (D) qPCR analysis of relative leptin mRNA levels in HEK293T cells compared to G401 cells, showing significant upregulation of leptin signaling in the tumor context. (E) Bodipy staining (green) of steroidogenic tissues in control (6 months) and tumor-bearing mice (4 months). (F) Quantitative analysis of LD area in Leydig cells based on image E. (G) A schematic model illustrating the mechanism across D. melanogaster , B. germanica , and M. musculus . The leptin/Upd-JAK/STAT-HSL axis acts as a universal spatiotemporal switch, coordinating lipid mobilization to transition steroidogenic cells from a quiescent (LD-poor) to an activated (LD-rich) state during development or tumor-induced stress. Data are presented as mean ± s.e.m.. Statistical significance was determined by one-way ANOVA followed by multiple comparisons. **p < 0.01, ****p < 0.0001.

Article Snippet: G401 cells were cultured in McCoy’s 5A medium (ATCC, 30-2007TM) supplemented with 10% FBS.

Techniques: RNA Sequencing, Staining, Control

a Heatmap of ChIP-seq signal for PHIP (blue, n = 3), and posttranslational modifications (PTMs) marking active promoters, i.e., H3K4me3 (orange, n = 3), H3K27ac (green, n = 3), and H3K14ac (salmon, n = 3) at PHIP peaks ( n = 17,230) in G401 cells, sorted by H3K27ac intensity. Also shown are the enhancer marker H3K4me1 (cyan, n = 2) and the repressive/bivalent marker H3K27me3 (red). Volcano plot of differentially expressed genes after knocking down ( b ) or overexpressing ( c ) PHIP in G401 RT cells ( n = 3). Statistical analysis was performed using a two-sided empirical Bayes moderated t- test using the limma package. The dashed line indicates the adjusted P = 0.05. For significantly downregulated genes (blue): adjusted P < 0.05, log2FC < − 1; for significantly upregulated genes (red): adjusted P < 0.05, log2FC > 1. d Heatmap of RNA-seq signal for PHIP target genes ( n = 2077) in control (black), PHIP-overexpressing (red), PHIP-knockdown (purple), and PHIP-rescue (gray) G401 cells. e Western blots showing acetylation of H3K14, H3K27, and H4K12 in histone lysates from siCtrl-treated and siPHIP-treated RT cell lines (G401, A204, and BT16). Blots are representative of n = 3 biological replicates for all cell lines. H3 and HSP90 are loading controls. f Evaluation of the effects of PHIP knockdown on histone acetylation. Heatmap of ChIP-seq signal for PHIP (blue, n = 3) in G401 cells and for H4ac (cherry, n = 3), H3K27ac (green, n = 3), H3K14ac (salmon, n = 3), and H3K4me3 (orange, n = 3) in siCtrl-treated and siPHIP-treated G401 cells at active TSSs (H4ac + , n = 9058). Sorted by H3K27ac. g Heatmap of H3K27ac ChIP-seq signal at sites where H3K27ac is lost after PHIP loss ( n = 22,193) in control (black), PHIP-overexpressing (red), PHIP-knockdown (purple), and PHIP-rescue (gray) G401 cells. Source data are provided as a file.

Journal: Nature Communications

Article Title: PHIP suppresses NuRD to enable the growth of SWI/SNF-mutant cancers

doi: 10.1038/s41467-026-70699-3

Figure Lengend Snippet: a Heatmap of ChIP-seq signal for PHIP (blue, n = 3), and posttranslational modifications (PTMs) marking active promoters, i.e., H3K4me3 (orange, n = 3), H3K27ac (green, n = 3), and H3K14ac (salmon, n = 3) at PHIP peaks ( n = 17,230) in G401 cells, sorted by H3K27ac intensity. Also shown are the enhancer marker H3K4me1 (cyan, n = 2) and the repressive/bivalent marker H3K27me3 (red). Volcano plot of differentially expressed genes after knocking down ( b ) or overexpressing ( c ) PHIP in G401 RT cells ( n = 3). Statistical analysis was performed using a two-sided empirical Bayes moderated t- test using the limma package. The dashed line indicates the adjusted P = 0.05. For significantly downregulated genes (blue): adjusted P < 0.05, log2FC < − 1; for significantly upregulated genes (red): adjusted P < 0.05, log2FC > 1. d Heatmap of RNA-seq signal for PHIP target genes ( n = 2077) in control (black), PHIP-overexpressing (red), PHIP-knockdown (purple), and PHIP-rescue (gray) G401 cells. e Western blots showing acetylation of H3K14, H3K27, and H4K12 in histone lysates from siCtrl-treated and siPHIP-treated RT cell lines (G401, A204, and BT16). Blots are representative of n = 3 biological replicates for all cell lines. H3 and HSP90 are loading controls. f Evaluation of the effects of PHIP knockdown on histone acetylation. Heatmap of ChIP-seq signal for PHIP (blue, n = 3) in G401 cells and for H4ac (cherry, n = 3), H3K27ac (green, n = 3), H3K14ac (salmon, n = 3), and H3K4me3 (orange, n = 3) in siCtrl-treated and siPHIP-treated G401 cells at active TSSs (H4ac + , n = 9058). Sorted by H3K27ac. g Heatmap of H3K27ac ChIP-seq signal at sites where H3K27ac is lost after PHIP loss ( n = 22,193) in control (black), PHIP-overexpressing (red), PHIP-knockdown (purple), and PHIP-rescue (gray) G401 cells. Source data are provided as a file.

Article Snippet: G401 (ATCC-CRL1441), A204 (ATCC-HTB-82), and HEK293T (ATCC-CRL-3216) cell lines were obtained from ATCC.

Techniques: ChIP-sequencing, Marker, RNA Sequencing, Control, Knockdown, Western Blot

Review

Structured Review

Images

1) Product Images from "IRS4 is a PI3K-activating cancer dependency up-regulated through DNA rearrangements or epigenetic mechanisms in multiple solid tumors"

Similar Products

Image Search Results