isl1 antibody (Santa Cruz Biotechnology)

Santa Cruz Biotechnology isl1 antibody

Figure 3. <t>ISL1</t> Is a Potential Major Regulator of Differential Expression between A2780 and A2780cis Cells (A and D) Distribution of p53 in (A) and ISL1 and EGR1 in (D) ChIP-seq peaks in A2780 cells by chromatin patterns. (B) Illustrative scheme of a PageRank-based network. Lists of transcription factors and motifs with the highest PageRank scores in A2780 (in red) or A2780cis (in blue) cells. Analysis based on H3K27ac:GRO-seq and H3K4me2:GRO-seq data. *, motif assigned to M4 in the clustering analysis but colocalizing with M14 (see Figure 1D). (C) Radar plots depicting PageRank scores for ISL1 and EGR1. Arrows indicate (D) differences in PageRank scores. (E) Boxplots of GRO-seq signal enrichment (log2 scale) by cell and condition within different distances (50 kb to 3 Mb, as indicated) from ISL1 (top) or p53 (bottom) ChIP-seq peaks in A2780 cells. Conditions (in this order): A2780-vehicle, A2780-cisplatin, A2780cis-vehicle, and A2780cis-cisplatin. Welch two-sample t-test; *p % 0.005, **p % 103, *** p % 104, ****p % 105, *****p % 106. (F) Dispersed genes within different distances from ISL1, EGR1, or p53 ChIP-seq peaks. The names of representative genes are included. Modules with higher (in black) or lower (in gray italics) gene enrichment than randomly expected are indicated, as well as the percentage of the genes over the total in each module. c2

Isl1 Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/d5+rrid+ab+2314683/Islet-1+Antibody/pm32320655-378-35-43
Average 93 stars, based on 1 article reviews

isl1 antibody - by Bioz Stars, 2026-10

93/100 stars

Buy from Supplier

Image Search Results

Figure 3. ISL1 Is a Potential Major Regulator of Differential Expression between A2780 and A2780cis Cells (A and D) Distribution of p53 in (A) and ISL1 and EGR1 in (D) ChIP-seq peaks in A2780 cells by chromatin patterns. (B) Illustrative scheme of a PageRank-based network. Lists of transcription factors and motifs with the highest PageRank scores in A2780 (in red) or A2780cis (in blue) cells. Analysis based on H3K27ac:GRO-seq and H3K4me2:GRO-seq data. *, motif assigned to M4 in the clustering analysis but colocalizing with M14 (see Figure 1D). (C) Radar plots depicting PageRank scores for ISL1 and EGR1. Arrows indicate (D) differences in PageRank scores. (E) Boxplots of GRO-seq signal enrichment (log2 scale) by cell and condition within different distances (50 kb to 3 Mb, as indicated) from ISL1 (top) or p53 (bottom) ChIP-seq peaks in A2780 cells. Conditions (in this order): A2780-vehicle, A2780-cisplatin, A2780cis-vehicle, and A2780cis-cisplatin. Welch two-sample t-test; *p % 0.005, **p % 103, *** p % 104, ****p % 105, *****p % 106. (F) Dispersed genes within different distances from ISL1, EGR1, or p53 ChIP-seq peaks. The names of representative genes are included. Modules with higher (in black) or lower (in gray italics) gene enrichment than randomly expected are indicated, as well as the percentage of the genes over the total in each module. c2

Journal: Cell reports

Article Title: Super-Enhancer Redistribution as a Mechanism of Broad Gene Dysregulation in Repeatedly Drug-Treated Cancer Cells.

doi: 10.1016/j.celrep.2020.107532

Figure Lengend Snippet: Figure 3. ISL1 Is a Potential Major Regulator of Differential Expression between A2780 and A2780cis Cells (A and D) Distribution of p53 in (A) and ISL1 and EGR1 in (D) ChIP-seq peaks in A2780 cells by chromatin patterns. (B) Illustrative scheme of a PageRank-based network. Lists of transcription factors and motifs with the highest PageRank scores in A2780 (in red) or A2780cis (in blue) cells. Analysis based on H3K27ac:GRO-seq and H3K4me2:GRO-seq data. *, motif assigned to M4 in the clustering analysis but colocalizing with M14 (see Figure 1D). (C) Radar plots depicting PageRank scores for ISL1 and EGR1. Arrows indicate (D) differences in PageRank scores. (E) Boxplots of GRO-seq signal enrichment (log2 scale) by cell and condition within different distances (50 kb to 3 Mb, as indicated) from ISL1 (top) or p53 (bottom) ChIP-seq peaks in A2780 cells. Conditions (in this order): A2780-vehicle, A2780-cisplatin, A2780cis-vehicle, and A2780cis-cisplatin. Welch two-sample t-test; *p % 0.005, **p % 103, *** p % 104, ****p % 105, *****p % 106. (F) Dispersed genes within different distances from ISL1, EGR1, or p53 ChIP-seq peaks. The names of representative genes are included. Modules with higher (in black) or lower (in gray italics) gene enrichment than randomly expected are indicated, as well as the percentage of the genes over the total in each module. c2

Article Snippet: ChIPs were conducted as previously (Benner et al., 2013), using the following antibodies: H3K4me3 antibody (Millipore, Cat#07-473; RRID:AB_1977252), H3K4me2 antibody (Active Motif, Cat#39141; RRID:AB_2614985), H3K27ac antibody (Abcam, Cat#ab4729; RRID:AB_2118291), p53 antibody (Active Motif, Cat#39334; RRID:AB_2753148), ISL1 antibody (DHSB, Cat#39.4D5 s; RRID:AB_2314683), EGR1 antibody (Santa Cruz Biotechnology, Cat#sc-110; RRID:AB_2097174), and CTCF antibody (Active Motif, Cat#61932; RRID:AB_2614975).

Techniques: Quantitative Proteomics, ChIP-sequencing

$Figure 4. SEs Are Associated with Major Organizational and Expression Differences between A2780 and A2780cis Cells (A and E) From top to bottom, read-density tracks of the indicated ChIP-seq and GRO-seq signal in A2780 (A) and A2780cis (Acis) cells after 3-day vehicle (veh.) or cisplatin (cis.) treatment. The y axis indicates sequencing read density. Green bars indicate dense areas of ISL1 peaks, blue bars indicate candidate SEs, and the red bar highlights a 2.9-Mb-wide region with low signal in A2780cis cells. Above in (A), shown are 6-kb bins of variable patterns in the same order as depicted in Figure 2B, corresponding to the peach- and purple-colored regions. (B) The top two panels show distribution of SEs by clusters and treatment in A2780/A2780cis cells. The bottom two panels show differential of the relative fraction of SEs over the total by chromatin pattern between A2780 and A2780cis cells and between biological replicates, as indicated. (C) Differential in H3K27ac accumulation (fold change, log10) at the set of ROSE-deﬁned SEs in the following comparisons (SEs ranked by H3K27ac signal in vehicle A2780 cells): 3-day vehicle- versus cisplatin-treated A2780 cells (in blue), cisplatin responsiveness in A2780 versus A2780cis cells (in orange), and combined 3-day vehicle/cisplatin-treated signal in A2780 versus A2780cis cells (in green). (D) Differential GRO-seq signal around each of the 14 variable patterns (distances: 50-kb, 500-kb, and 5-Mb regions) in 3-day cisplatin-treated A2780 and 3-day vehicle- and cisplatin-treated A2780cis cells relative to 3-day vehicle-treated A2780 cells. Arrows highlight the ﬁve cases with the strongest effects. See also Figure S4.$

Journal: Cell reports

Article Title: Super-Enhancer Redistribution as a Mechanism of Broad Gene Dysregulation in Repeatedly Drug-Treated Cancer Cells.

doi: 10.1016/j.celrep.2020.107532

Figure Lengend Snippet: Figure 4. SEs Are Associated with Major Organizational and Expression Differences between A2780 and A2780cis Cells (A and E) From top to bottom, read-density tracks of the indicated ChIP-seq and GRO-seq signal in A2780 (A) and A2780cis (Acis) cells after 3-day vehicle (veh.) or cisplatin (cis.) treatment. The y axis indicates sequencing read density. Green bars indicate dense areas of ISL1 peaks, blue bars indicate candidate SEs, and the red bar highlights a 2.9-Mb-wide region with low signal in A2780cis cells. Above in (A), shown are 6-kb bins of variable patterns in the same order as depicted in Figure 2B, corresponding to the peach- and purple-colored regions. (B) The top two panels show distribution of SEs by clusters and treatment in A2780/A2780cis cells. The bottom two panels show differential of the relative fraction of SEs over the total by chromatin pattern between A2780 and A2780cis cells and between biological replicates, as indicated. (C) Differential in H3K27ac accumulation (fold change, log10) at the set of ROSE-deﬁned SEs in the following comparisons (SEs ranked by H3K27ac signal in vehicle A2780 cells): 3-day vehicle- versus cisplatin-treated A2780 cells (in blue), cisplatin responsiveness in A2780 versus A2780cis cells (in orange), and combined 3-day vehicle/cisplatin-treated signal in A2780 versus A2780cis cells (in green). (D) Differential GRO-seq signal around each of the 14 variable patterns (distances: 50-kb, 500-kb, and 5-Mb regions) in 3-day cisplatin-treated A2780 and 3-day vehicle- and cisplatin-treated A2780cis cells relative to 3-day vehicle-treated A2780 cells. Arrows highlight the ﬁve cases with the strongest effects. See also Figure S4.

Techniques: Expressing, ChIP-sequencing, Sequencing

Figure 6. ISL1 Dysregulation after Chronic Cisplatin Treatment (A–C) Singlet distribution of forward scatter A (FSC-A; x axis) versus FITC-A signal (Alexa Fluor-488; y axis) identiﬁed by FACS analysis in ﬁxed A2780 and A2780cis (A), in CRISPRi/a-modiﬁed cells (B), and in A2780 cells treated for 3 days with cisplatin IC50 (C) and adding no additional time, 2 days, or 2 weeks (in duplicate) of recovery without drug. As reference, dashed lines indicate the position of the predominant subpopulation and maximum and minimum margins for panels in (A). Each analysis corresponds to n = 100,000 sorting events. (D) FACS sorting of n = 1.7 million ﬁxed low-ISL1-expressing and n = 1.7 million ﬁxed high-ISL1-expressing cells, decrosslinking, and RNA-seq analysis. Panel shows FACS analysis of the ﬁrst n = 10,000 sorting events. Tracks show RNA-seq signal along the ISL1 and RPL27 (as reference) loci. Other genomic regions shown in Figure S6D. Hierarchical clustering of high-ISL1- and low-ISL1-expressing A2780 cells, bulk A2780 cells, and A2780cis cells. (E) H3K4me3, H3K4me2, and H3K27ac ChIP-seq signal along the ISL1 locus in A2780 and A2780cis cells after 3-day of vehicle (veh.) or cisplatin (cis.) treatment. (F) Time-course analysis of ISL1 protein abundance at the indicated time point after the end of a 2-day cisplatin treatment (2.0 mM) examined by western blot in A2780 cells (two different exposures). (G) Dose-titration analysis of ISL1 protein abundance at the end of a 2-day cisplatin treatment followed by 2 days or 2 weeks of recovery without drug in A2780 cells. C, nonrecovery control. (H) Dose-response curve of cisplatin in A2780/A2780cis and CRISPRi/a-modiﬁed cells (2-day treatment). Lines represent median values. Biological duplicates (n = 2) with six technical replicates each (n = 6). As reference, A2780 and A2780cis data are identically shown in both panels.

Journal: Cell reports

Article Title: Super-Enhancer Redistribution as a Mechanism of Broad Gene Dysregulation in Repeatedly Drug-Treated Cancer Cells.

doi: 10.1016/j.celrep.2020.107532

Figure Lengend Snippet: Figure 6. ISL1 Dysregulation after Chronic Cisplatin Treatment (A–C) Singlet distribution of forward scatter A (FSC-A; x axis) versus FITC-A signal (Alexa Fluor-488; y axis) identiﬁed by FACS analysis in ﬁxed A2780 and A2780cis (A), in CRISPRi/a-modiﬁed cells (B), and in A2780 cells treated for 3 days with cisplatin IC50 (C) and adding no additional time, 2 days, or 2 weeks (in duplicate) of recovery without drug. As reference, dashed lines indicate the position of the predominant subpopulation and maximum and minimum margins for panels in (A). Each analysis corresponds to n = 100,000 sorting events. (D) FACS sorting of n = 1.7 million ﬁxed low-ISL1-expressing and n = 1.7 million ﬁxed high-ISL1-expressing cells, decrosslinking, and RNA-seq analysis. Panel shows FACS analysis of the ﬁrst n = 10,000 sorting events. Tracks show RNA-seq signal along the ISL1 and RPL27 (as reference) loci. Other genomic regions shown in Figure S6D. Hierarchical clustering of high-ISL1- and low-ISL1-expressing A2780 cells, bulk A2780 cells, and A2780cis cells. (E) H3K4me3, H3K4me2, and H3K27ac ChIP-seq signal along the ISL1 locus in A2780 and A2780cis cells after 3-day of vehicle (veh.) or cisplatin (cis.) treatment. (F) Time-course analysis of ISL1 protein abundance at the indicated time point after the end of a 2-day cisplatin treatment (2.0 mM) examined by western blot in A2780 cells (two different exposures). (G) Dose-titration analysis of ISL1 protein abundance at the end of a 2-day cisplatin treatment followed by 2 days or 2 weeks of recovery without drug in A2780 cells. C, nonrecovery control. (H) Dose-response curve of cisplatin in A2780/A2780cis and CRISPRi/a-modiﬁed cells (2-day treatment). Lines represent median values. Biological duplicates (n = 2) with six technical replicates each (n = 6). As reference, A2780 and A2780cis data are identically shown in both panels.

Techniques: Expressing, RNA Sequencing, ChIP-sequencing, Quantitative Proteomics, Western Blot, Titration, Control

d5 rrid ab 2314683 Search Results

Image Search Results