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The Drosophila melanogaster CHD1 chromatin remodeling factor (show ASH1L ELISA Kits) modulates global chromosome structure and counteracts HP1a (show CBX5 ELISA Kits) and H3K9me2.
Intestinal resistance against infection by P. aeruginosa is linked to maintaining proper balance of gut (show GUSB ELISA Kits)-microbe interactions and the chromatin remodeler CHD1 is involved in regulating this aspect.
our results emphasize a role for Chd1 in histone replacement in both budding yeast and Drosophila melanogaster, and surprisingly they show that the major effects of Chd1 on turnover occur at the 3' ends of genes.
results suggest a role for CHD1 in the assembly of active chromatin and a function of ACF (show A1CF ELISA Kits) in the assembly of repressive chromatin
findings establish CHD1 as a major factor in replacement histone metabolism in the nucleus and reveal a critical role for CHD1 in the earliest developmental instances of genome-scale, replication-independent nucleosome assembly.
These results clarify the roles of chromatin remodelers in transcription and provide novel insights into CHD1 function.
Increased CHD1L (show CHD1L ELISA Kits) protein expression was significantly associated with poor overall survival in pancreatic cancer patients.
CHD1 facilitates substrate handover from XPC (show XPC ELISA Kits) to the downstream TFIIH (show GTF2H1 ELISA Kits) (transcription factor IIH).
CHD1 is required for the induction of osteoblast-specific gene expression, extracellular-matrix mineralization and ectopic bone formation in vivo. Genome-wide occupancy analyses revealed increased CHD1 occupancy around the transcriptional start site of differentiation-activated genes.
examined the role of CHD1 in DNA double-strand break (DSB) repair in prostate cancer cells; findings show that CHD1 is required for the recruitment of CtIP (show RBBP8 ELISA Kits) to chromatin and subsequent end resection during DNA DSB repair; data support a role for CHD1 in opening the chromatin around the DSB to facilitate the recruitment of homologous recombination (HR) proteins
In PTEN-deficient prostate and breast cancers, CHD1 depletion profoundly and specifically suppressed cell proliferation, cell survival and tumorigenic potential.
The authors have identified an additional conserved domain C-terminal to the SANT-SLIDE domain and determined its structure by multidimensional heteronuclear NMR spectroscopy. They have termed this domain the CHD1 helical C-terminal (CHCT) domain as it is comprised of five alpha-helices arranged in a variant helical bundle topology.
These results indicate that CHD1 is a positive regulator of influenza virus multiplication and suggest a role for chromatin remodeling in the control of the influenza virus life cycle.
These data link the assembly of methylated KDM1A (show KDM1A ELISA Kits) and CHD1 with AR-dependent transcription and genomic translocations, thereby providing mechanistic insight into the formation of TMPRSS2 (show TMPRSS2 ELISA Kits)-ERG (show ERG ELISA Kits) gene fusions during prostate-tumor evolution.
We have identified CHD1 as the RUNX1 (show RUNX1 ELISA Kits) fusion partner in acute myeloid leukemia (show BCL11A ELISA Kits) with t(5;21)(q21;q22).
The double chromodomains of CHD1 adopt an 'open pocket' to interact with the free N-terminal amine of H3K4, and the open pocket permits the NS1 mimic to bind in a distinct conformation.
These results underscore the importance of Chd1 for the regulation of pluripotency in ESCs (show NR2E3 ELISA Kits) and provide evidence for a hitherto unrecognized critical role of the phosphorylated N-terminal SRR (show SRR ELISA Kits) for full functionality of Chd1.
find that Chd1 evicts nucleosomes downstream of the promoter in order to overcome the nucleosomal barrier and enable PolII promoter escape, thus providing mechanistic insight into the role of Chd1 in transcription and pluripotency
These findings indicate that CHD1 plays important roles in mouse early embryogenesis via activation of Hmgpi at zygotic gene activation.
Chd1-driven elevation in transcriptional output is essential for the developmental transition from endothelium to definitive hematopoiesis in the mouse embryo.
Chd1 promotes a globally elevated transcriptional output required to sustain the distinctly rapid growth of the mouse epiblast.
CHD1 and Mediator are recruited to an inducible gene, and genome-wide binding of the two proteins correlates well with active gene transcription in mouse ES cells
results indicate that Chd1 is essential for open chromatin and pluripotency of embryonic stem cells, and for somatic cell reprogramming to the pluripotent state
CHD1 is a critical factor for proper development of the follicular epithelium in terms of whole-cell chromatin arrangement.
The CHD family of proteins is characterized by the presence of chromo (chromatin organization modifier) domains and SNF2-related helicase/ATPase domains. CHD genes alter gene expression possibly by modification of chromatin structure thus altering access of the transcriptional apparatus to its chromosomal DNA template.
, Chromodomain-helicase-DNA-binding protein
, chromo-ATPase/helicase-DNA-binding domain
, chromo-ATPase/helicase-DNA-binding protein 1
, lethal (2) 23Cd
, chromodomain-helicase DNA-binding protein
, chromodomain helicase DNA binding protein 1
, ATP-dependent helicase CHD1
, chromodomain-helicase-DNA-binding protein 1
, chromo-helicase-DNA-binding on the Z chromosome protein
, chromo-helicase/ATPase-DNA binding protein 1