22765 Search Results


c varia atcc 22765 type  (ATCC)
90
ATCC c varia atcc 22765 type
C Varia Atcc 22765 Type, supplied by ATCC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/c varia atcc 22765 type/product/ATCC
Average 90 stars, based on 1 article reviews
c varia atcc 22765 type - by Bioz Stars, 2026-03
90/100 stars
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spry4  (Proteintech)
93
Proteintech spry4
(A) Genomic distribution of H3K27ac, H3K4me1, and H3K4me3 peaks in A2780-P and A2780-R cells. (B) Plot of the average level of H3K27ac, H3K4me1, and H3K4me3 peaks centered at the TSS in A2780-P or A2780-R cells. (C) Venn diagram showing the number and overlaps of enhancers and promoters between A2780-P and A2780-R cells overlapped by MAnorm (https://github.com/shao-lab/MAnorm). Common peaks merged. (D and E) Distribution of histone markers surrounding the summit of H3K27ac peaks, in gained or lost enhancer regions (D) and promoter regions (E). Black borders, A2780-P; dark red borders, A2780-R. Only one of the duplicates was plotted, as consistent results were observed in the other replicate. Each row represents 1 peak centered at the midpoint between two 2-kb flanking regions. (F) Scatterplot of the correlation between H3K27ac mark intensity and fold change of corresponding gene expressions. The horizontal axis illustrates the differences between resistant and parental cell lines, measured in counts per million mapped reads (CPM). Only genes of at least 4-fold change and H3K27ac changes of 500 CPM are shown. (G) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis enriched by downregulated genes in A2780-R (relative to A2780-P) showed that the MAPK pathway was significantly enriched. NES, normalized enrichment score. (H) Relative mRNA levels of ERK transcriptional targets in A2780-P/R cells (left) and OVCAR5-P/R cells (right). Results are represented as mean ± SD of 3 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 by unpaired Student’s t test. (I) ChIP-Seq profiles show the ChIP-Seq signal (y axis, reads per million) for H3K27ac, H3K4me1, and H3K4me3 at genomic loci of DUSP6, ETV4, and <t>SPRY4.</t> (J) The results showed relative mRNA level of DUSP6 in 9 commercial cell lines and 7 patient-derived cells. Results are represented as mean ± SD of 4 independent experiments.
Spry4, supplied by Proteintech, 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/result/spry4/product/Proteintech
Average 93 stars, based on 1 article reviews
spry4 - by Bioz Stars, 2026-03
93/100 stars
  Buy from Supplier

Image Search Results


(A) Genomic distribution of H3K27ac, H3K4me1, and H3K4me3 peaks in A2780-P and A2780-R cells. (B) Plot of the average level of H3K27ac, H3K4me1, and H3K4me3 peaks centered at the TSS in A2780-P or A2780-R cells. (C) Venn diagram showing the number and overlaps of enhancers and promoters between A2780-P and A2780-R cells overlapped by MAnorm (https://github.com/shao-lab/MAnorm). Common peaks merged. (D and E) Distribution of histone markers surrounding the summit of H3K27ac peaks, in gained or lost enhancer regions (D) and promoter regions (E). Black borders, A2780-P; dark red borders, A2780-R. Only one of the duplicates was plotted, as consistent results were observed in the other replicate. Each row represents 1 peak centered at the midpoint between two 2-kb flanking regions. (F) Scatterplot of the correlation between H3K27ac mark intensity and fold change of corresponding gene expressions. The horizontal axis illustrates the differences between resistant and parental cell lines, measured in counts per million mapped reads (CPM). Only genes of at least 4-fold change and H3K27ac changes of 500 CPM are shown. (G) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis enriched by downregulated genes in A2780-R (relative to A2780-P) showed that the MAPK pathway was significantly enriched. NES, normalized enrichment score. (H) Relative mRNA levels of ERK transcriptional targets in A2780-P/R cells (left) and OVCAR5-P/R cells (right). Results are represented as mean ± SD of 3 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 by unpaired Student’s t test. (I) ChIP-Seq profiles show the ChIP-Seq signal (y axis, reads per million) for H3K27ac, H3K4me1, and H3K4me3 at genomic loci of DUSP6, ETV4, and SPRY4. (J) The results showed relative mRNA level of DUSP6 in 9 commercial cell lines and 7 patient-derived cells. Results are represented as mean ± SD of 4 independent experiments.

Journal: The Journal of Clinical Investigation

Article Title: Targeting enhancer reprogramming to mitigate MEK inhibitor resistance in preclinical models of advanced ovarian cancer

doi: 10.1172/JCI145035

Figure Lengend Snippet: (A) Genomic distribution of H3K27ac, H3K4me1, and H3K4me3 peaks in A2780-P and A2780-R cells. (B) Plot of the average level of H3K27ac, H3K4me1, and H3K4me3 peaks centered at the TSS in A2780-P or A2780-R cells. (C) Venn diagram showing the number and overlaps of enhancers and promoters between A2780-P and A2780-R cells overlapped by MAnorm (https://github.com/shao-lab/MAnorm). Common peaks merged. (D and E) Distribution of histone markers surrounding the summit of H3K27ac peaks, in gained or lost enhancer regions (D) and promoter regions (E). Black borders, A2780-P; dark red borders, A2780-R. Only one of the duplicates was plotted, as consistent results were observed in the other replicate. Each row represents 1 peak centered at the midpoint between two 2-kb flanking regions. (F) Scatterplot of the correlation between H3K27ac mark intensity and fold change of corresponding gene expressions. The horizontal axis illustrates the differences between resistant and parental cell lines, measured in counts per million mapped reads (CPM). Only genes of at least 4-fold change and H3K27ac changes of 500 CPM are shown. (G) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis enriched by downregulated genes in A2780-R (relative to A2780-P) showed that the MAPK pathway was significantly enriched. NES, normalized enrichment score. (H) Relative mRNA levels of ERK transcriptional targets in A2780-P/R cells (left) and OVCAR5-P/R cells (right). Results are represented as mean ± SD of 3 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 by unpaired Student’s t test. (I) ChIP-Seq profiles show the ChIP-Seq signal (y axis, reads per million) for H3K27ac, H3K4me1, and H3K4me3 at genomic loci of DUSP6, ETV4, and SPRY4. (J) The results showed relative mRNA level of DUSP6 in 9 commercial cell lines and 7 patient-derived cells. Results are represented as mean ± SD of 4 independent experiments.

Article Snippet: The primary antibodies used were as follows: ERK1/2 (1:2000; 4696S), p-ERK1/2 (1:2000; 4370S), MEK (1:1000; 9126S), p-MEK (1:1000; 9154S), β-actin (1:2000; 8456S), and SPRY2 (1:1000; 14954S) were purchased from Cell Signaling Technology; DUSP6 (1:1000, pa5-15552; or 1:1000, ab76310) was obtained from Invitrogen or Abcam and ETV5 (1:1000; ab102010) was from Abcam; and SPRY4 (1:2000; 22765-1-AP) was from Proteintech.

Techniques: ChIP-sequencing, Derivative Assay