Chromatin Immunoprecipitation sequencing (ChIP-seq) for SBNO1 and TAF4
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE311231 | GEO | 2026/04/15
REPOSITORIES: GEO
Similar Datasets
Project description:Chromatin Immunoprecipitation sequencing (ChIP-seq) for SBNO1 and TAF4
| PRJNA1368824 | ENA
Project description:TAF4 directed immunoprecipitation of the the Pre-initiation complex from mouse embryonic stem cells with or without depletion of TATA-box binding protein (TBP).
2022-05-27 | MSV000089562 | MassIVE
Project description:We investigates gene expression profiles in double conditional knockout mice for Sbno1 and Trp53. To generate these knockouts in the developing forebrain, Sbno1 floxed mice, Trp53 floxed mice, and the Emx1-Cre driver line were utilized. RNA-seq was performed on the telencephalon at embryonic day 12.5 (E12.5) and the cerebral cortex at embryonic day 18.5 (E18.5) to elucidate the roles of Sbno1 and Trp53 in neural development.
2025-12-23 | GSE307883 | GEO
Project description:Aberrant Notch signaling has been identified as a possible catalyst for hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA) development. Genetic studies in Drosophila observed that the knockout of strawberry notch (sno) mimics loss of notch. Here, we elucidated the role of the mammalian Strawberry Notch 1 (SBNO1) in HCC and CCA development.
2026-04-15 | GSE277271 | GEO
Project description:The multisubunit TFIID plays a direct role in transcription initiation by binding to core promoter elements and directing preinitiation complex assembly. Although TFIID may also function as a coactivator through direct interactions with promoter-bound activators, mechanistic aspects of this poorly defined function remain unclear. Here biochemical studies show a direct TFIID-E protein interaction that (i) is mediated through interaction of a novel E protein activation domain (AD3) with the TAF homology (TAFH) domain of TAF4, (ii) is critical for activation of a natural target gene by an E protein and (iii) mechanistically, acts by enhancing TFIID binding to the core promoter. Complementary assays establish a gene-specific role for the TAFH domain in TFIID recruitment and gene activation in vivo. These results firmly establish TAF4 as a bona fide E protein coactivator, as well as a mechanism involving facilitated TFIID binding through direct interaction with an E protein activation domain. Genome-wide profiling of mRNA levels in MEF lines with Taf4 loxp/- (ctrl), Taf4 -/- (ko), Taf4 -/- Tg:hTAF4 wt, and Taf4 -/- Tg: hTAF4 ? (TAFH-deleted).
2013-06-06 | E-GEOD-46807 | biostudies-arrayexpress
Project description:Aberrant Notch signaling has been identified as a possible catalyst for hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA) development. Genetic studies in Drosophila observed that the knockout of strawberry notch (sno) mimics loss of notch. Here, we elucidated the role of the mammalian Strawberry Notch 1 (SBNO1) in HCC and CCA development.
2026-04-15 | GSE277244 | GEO
Project description:Taf4 (TATA-box binding protein-associated factor 4) is a subunit of the general transcription factor TFIID, a component of the RNA polymerase II pre-initiation complex that interacts with tissue-specific transcription factors to regulate gene expression. Properly regulated gene expression is particularly important in the intestinal epithelium that is constantly renewed from stem cells. We investigated the role of Taf4 in the murine intestinal epithelium using tissue-specific inactivation. Taf4 inactivation during embryogenesis compromised gut morphogenesis and the emergence of adult-type stem cells, ultimately leading to death. In adults, Taf4 loss perturbed the stem cell compartment and the associated Paneth cells in the stem cell niche, epithelial turnover and differentiation of mature cells, thus exacerbating the response to inflammatory challenge and potentiating Apc-driven tumorigenesis. In addition, Taf4 inactivation ex vivo in organoids prevented budding formation and maintenance. Combining immunohistology with bulk RNA-seq, ATAC-seq and single-cell RNA-seq, showed that Taf4 loss caused broad chromatin remodeling, and a strong reduction in the numbers of stem and progenitor cells with a concomitant increase in an undifferentiated cell population that displayed high activity of the Ezh2 and Suz12 components of Polycomb Repressive Complex 2 (PRC2). In line with this observation, treatment of Taf4-mutant organoids with a specific Ezh2 inhibitor restored buddings, cell proliferation and the stem/progenitor compartment. Our results reveal the critical role of Taf4 in intestinal development and homeostasis and a novel mechanism by which Taf4 acts to maintain the stem/progenitor compartment by counteracting PRC2 repression of the stem cell gene expression program.
2023-01-05 | GSE205329 | GEO
Project description:Taf4 (TATA-box binding protein-associated factor 4) is a subunit of the general transcription factor TFIID, a component of the RNA polymerase II pre-initiation complex that interacts with tissue-specific transcription factors to regulate gene expression. Properly regulated gene expression is particularly important in the intestinal epithelium that is constantly renewed from stem cells. We investigated the role of Taf4 in the murine intestinal epithelium using tissue-specific inactivation. Taf4 inactivation during embryogenesis compromised gut morphogenesis and the emergence of adult-type stem cells, ultimately leading to death. In adults, Taf4 loss perturbed the stem cell compartment and the associated Paneth cells in the stem cell niche, epithelial turnover and differentiation of mature cells, thus exacerbating the response to inflammatory challenge and potentiating Apc-driven tumorigenesis. In addition, Taf4 inactivation ex vivo in organoids prevented budding formation and maintenance. Combining immunohistology with bulk RNA-seq, ATAC-seq and single-cell RNA-seq, showed that Taf4 loss caused broad chromatin remodeling, and a strong reduction in the numbers of stem and progenitor cells with a concomitant increase in an undifferentiated cell population that displayed high activity of the Ezh2 and Suz12 components of Polycomb Repressive Complex 2 (PRC2). In line with this observation, treatment of Taf4-mutant organoids with a specific Ezh2 inhibitor restored buddings, cell proliferation and the stem/progenitor compartment. Our results reveal the critical role of Taf4 in intestinal development and homeostasis and a novel mechanism by which Taf4 acts to maintain the stem/progenitor compartment by counteracting PRC2 repression of the stem cell gene expression program.
2023-01-05 | GSE205326 | GEO
Project description:Taf4 (TATA-box binding protein-associated factor 4) is a subunit of the general transcription factor TFIID, a component of the RNA polymerase II pre-initiation complex that interacts with tissue-specific transcription factors to regulate gene expression. Properly regulated gene expression is particularly important in the intestinal epithelium that is constantly renewed from stem cells. We investigated the role of Taf4 in the murine intestinal epithelium using tissue-specific inactivation. Taf4 inactivation during embryogenesis compromised gut morphogenesis and the emergence of adult-type stem cells, ultimately leading to death. In adults, Taf4 loss perturbed the stem cell compartment and the associated Paneth cells in the stem cell niche, epithelial turnover and differentiation of mature cells, thus exacerbating the response to inflammatory challenge and potentiating Apc-driven tumorigenesis. In addition, Taf4 inactivation ex vivo in organoids prevented budding formation and maintenance. Combining immunohistology with bulk RNA-seq, ATAC-seq and single-cell RNA-seq, showed that Taf4 loss caused broad chromatin remodeling, and a strong reduction in the numbers of stem and progenitor cells with a concomitant increase in an undifferentiated cell population that displayed high activity of the Ezh2 and Suz12 components of Polycomb Repressive Complex 2 (PRC2). In line with this observation, treatment of Taf4-mutant organoids with a specific Ezh2 inhibitor restored buddings, cell proliferation and the stem/progenitor compartment. Our results reveal the critical role of Taf4 in intestinal development and homeostasis and a novel mechanism by which Taf4 acts to maintain the stem/progenitor compartment by counteracting PRC2 repression of the stem cell gene expression program.
2023-01-05 | GSE205441 | GEO
Project description:We determined the Taf4 dependent differential expression of RNAs in WT as well as KO cells at day 9 of the differentiation into the cardiac lineage.
2016-03-20 | GSE70723 | GEO