Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA302275 | ENA |
REPOSITORIES: ENA
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Project description:LSD1 Corepressor Rcor2 Orchestrates Neurogenesis in the Developing Mouse Brain
| PRJNA302273 | ENA
Project description:LSD1 Corepressor Rcor2 Orchestrates Neurogenesis in the Developing Mouse Brain [RNA-Seq]
| PRJNA302276 | ENA
Project description:Pallial functional organization is mediated by the dynamic interplay of a broad spectrum of cellular and molecular cues that promote midline patterning, neurogenesis, axon guidance and neural connectivity. The regulators that orchestrate these seminal processes are still poorly understood. By employing a pallial conditional ablation model, we report that the transcriptional and epigenetic modulator, REST corepressor 2 (Rcor2) plays key roles in organizing the developing corticoseptal boundary. ChIP-seq and RNA-seq analyses reveal that Rcor2 modulates a diverse repertoire of classes of genes with essential roles in CC development, including pallial/subpallial patterning, cell fate specification and axon guidance.
2020-05-01 | GSE118751 | GEO
Project description:Precise control of transcriptional programs underlying metazoan development is modulated by enzymatically active co-regulatory complexes, coupled with epigenetic strategies, but how specific members of histone modification enzyme families such as histone methyltransferases and demethylases are utilized in vivo to simultaneously orchestrate distinct developmental gene activation and repression programs remains unclear. Here, we report that the initially-described histone lysine demethylase, LSD1, a component of the CoREST/CtBP corepressor complex, is required for late cell-lineage determination and differentiation during pituitary organogenesis. Surprisingly, LSD1 acts primarily on target gene activation programs, as well as in gene repression programs, based on recruitment of distinct LSD1-containing coactivator or corepressor complexes. Intriguingly, LSD1-dependent gene repression programs can be extended late in development with the induced expression of ZEB1, a Kr.pple-like repressor that can act as a molecular beacon for recruitment of the LSD1-containing CtBP/CoREST corepressor complex, causing repression of an additional cohort of genes, such as GH, that previously required LSD1 for activation.
2007-02-13 | E-TABM-223 | biostudies-arrayexpress
Project description:ChIP-seq analysis of CIC and H3K27Ac in the developing mouse brain
2020-04-15 | GSE131301 | GEO
Project description:ChIP-seq analysis using Flag M2, LSD1 and H3K4me2 antibodies respectively in Rcor2Flag embryonic brain.
2016-01-22 | GSE75039 | GEO
Project description:We performed ChIP-Seq in Lsd1-WT, Lsd1-GT and Kdm5c-WT mouse embryonic stem cells (mES).
2020-09-01 | GSE94552 | GEO
Project description:We report the application of single-molecule-based sequencing technology for REST and its cofactors genome wide binding sites in E14 cells.We then combine these binding sirtes with REST regulating gene profiling, to understand REST binding and regulation in E14 cells. Examination of REST and 5 cofactors(RCOR1, RCOR2,RCOR3,SIN3A,SIN3B) in E14 cells, REST and SIN3A endogenous antibody were used for ChIP experiment. The stable E14 cells expressing low level exogenous RCOR1, RCOR2, RCOR3,and SIN3B with V5 tag were used for ChIP experiment with V5 antibody to obtain individual ChIP DNA.
2011-04-01 | E-GEOD-28233 | biostudies-arrayexpress
Project description:Genomic amplification of OTUD7B is frequently found across human cancers. But its role in tumorigenesis is poorly understood. Lysine‐specific demethylase 1 (LSD1) is known to execute epigenetic regulation by forming corepressor complex with CoREST/histone deacetylases (HDACs). However, the molecular mechanisms by which cells maintain LSD1/CoREST complex integrity are unknown. Here, it is reported that LSD1 protein undergoes K63‐linked polyubiquitination. OTUD7B is responsible for LSD1 deubiquitination at K226/277 residues, resulting in dynamic control of LSD1 binding partner specificity and cellular homeostasis. OTUD7B deficiency increases K63‐linked ubiquitination of LSD1, which disrupts LSD1/CoREST complex formation and targets LSD1 for p62‐mediated proteolysis. Consequently, OTUD7B deficiency impairs genome‐wide LSD1 occupancy and enhances the methylation of H3K4/H3K9, therefore profoundly impacting global gene expression and abrogating breast cancer metastasis. Moreover, physiological fluctuation of OTUD7B modulates cell cycle‐dependent LSD1 oscillation, ensuring the G1/S transition. Both OTUD7B and LSD1 proteins are overpresented in high‐grade or metastatic human breast cancer, while dysregulation of either protein is associated with poor survival and metastasis. Thus, OTUD7B plays a unique partner‐switching role in maintaining the integrity of LSD1/CoREST corepressor complex, LSD1 turnover, and breast cancer metastasis.
2021-04-20 | GSE172369 | GEO
Project description:Genomic amplification of OTUD7B is frequently found across human cancers. But its role in tumorigenesis is poorly understood. Lysine‐specific demethylase 1 (LSD1) is known to execute epigenetic regulation by forming corepressor complex with CoREST/histone deacetylases (HDACs). However, the molecular mechanisms by which cells maintain LSD1/CoREST complex integrity are unknown. Here, it is reported that LSD1 protein undergoes K63‐linked polyubiquitination. OTUD7B is responsible for LSD1 deubiquitination at K226/277 residues, resulting in dynamic control of LSD1 binding partner specificity and cellular homeostasis. OTUD7B deficiency increases K63‐linked ubiquitination of LSD1, which disrupts LSD1/CoREST complex formation and targets LSD1 for p62‐mediated proteolysis. Consequently, OTUD7B deficiency impairs genome‐wide LSD1 occupancy and enhances the methylation of H3K4/H3K9, therefore profoundly impacting global gene expression and abrogating breast cancer metastasis. Moreover, physiological fluctuation of OTUD7B modulates cell cycle‐dependent LSD1 oscillation, ensuring the G1/S transition. Both OTUD7B and LSD1 proteins are overpresented in high‐grade or metastatic human breast cancer, while dysregulation of either protein is associated with poor survival and metastasis. Thus, OTUD7B plays a unique partner‐switching role in maintaining the integrity of LSD1/CoREST corepressor complex, LSD1 turnover, and breast cancer metastasis.
2021-04-20 | GSE172370 | GEO