No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human CHD1 Antibodies:
anti-Mouse (Murine) CHD1 Antibodies:
anti-Rat (Rattus) CHD1 Antibodies:
Go to our pre-filtered search.
Human Polyclonal CHD1 Primary Antibody for ChIP, IP - ABIN253029
Tao, Xi, Briones, Muegge: Lsh mediated RNA polymerase II stalling at HoxC6 and HoxC8 involves DNA methylation. in PLoS ONE 2010
Show all 5 Pubmed References
Human Polyclonal CHD1 Primary Antibody for ELISA, WB - ABIN514371
Gallastegui, Millán-Zambrano, Terme, Chávez, Jordan: Chromatin reassembly factors are involved in transcriptional interference promoting HIV latency. in Journal of virology 2011
Dog (Canine) Polyclonal CHD1 Primary Antibody for ELISA - ABIN548168
Eissenberg, Lee, Schneider, Ilvarsonn, Shiekhattar, Shilatifard: The trithorax-group gene in Drosophila little imaginal discs encodes a trimethylated histone H3 Lys4 demethylase. in Nature structural & molecular biology 2007
Human Polyclonal CHD1 Primary Antibody for IP, WB - ABIN253028
Huang, Gulzar, Salari, Lapointe, Brooks, Pollack: Recurrent deletion of CHD1 in prostate cancer with relevance to cell invasiveness. in Oncogene 2012
Human Monoclonal CHD1 Primary Antibody for ICC, IF - ABIN2668517
Yoshimura, Harada, Odawara, Azuma, Okada, Nakamura, Ohkawa, Tachibana: Rat monoclonal antibody specific for the chromatin remodeling factor, CHD1. in Hybridoma (2005) 2010
Human Polyclonal CHD1 Primary Antibody for WB - ABIN2668525
Skene, Hernandez, Groudine, Henikoff: The nucleosomal barrier to promoter escape by RNA polymerase II is overcome by the chromatin remodeler Chd1. in eLife 2014
Our results suggest that variants in CHD1 can lead to diverse phenotypic outcomes; however, the neurodevelopmental phenotype appears to be limited to patients with missense variants, which is compatible with a dominant negative mechanism of disease.
Identified a unique N-terminal region of CHD1 that inhibits the DNA binding, ATPase, and chromatin assembly and remodeling activities of CHD1. CHD1 lacking the N terminus was more active in rescuing the defects in gammaH2AX formation and CtIP recruitment in CHD1-KO cells than full-length CHD1, suggesting the N terminus is a negative regulator in cells.
CHD1 loss is associated with an increased sensitivity to PARP inhibition and anti-cancer drugs that induce DNA intercross-strand links in prostate tumors.
Increased CHD1L protein expression was significantly associated with poor overall survival in pancreatic cancer patients.
CHD1 facilitates substrate handover from XPC to the downstream TFIIH (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 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 and CHD1 with AR-dependent transcription and genomic translocations, thereby providing mechanistic insight into the formation of TMPRSS2-ERG gene fusions during prostate-tumor evolution.
We have identified CHD1 as the RUNX1 fusion partner in acute myeloid leukemia 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.
identify coordinate loss of MAP3K7 and CHD1 as a unique driver of aggressive prostate cancer development
CHD1 and CHD2 act as positive regulators of HIV-1 gene expression.
results demonstrate the ability of confocal microscopy and FISH to identify the cell-to-cell differences in common gene fusions such as TMPRSS2-ERG that may arise independently within the same tumor focus
Data indicate that chromodomain-helicase-DNA-binding protein CHD1, neoplasm protein GREB1 and karyopherin alpha 2 protein KPNA2 as critical mediators of miR-26a and miR-26b elicited cell growth.
CHD1 is the 5q21 tumor suppressor gene in prostate cancer
findings suggest that CHD1 deletion may underlie cell invasiveness in a subset of prostate cancers, and indicate a possible novel role of altered chromatin remodeling in prostate tumorigenesis
findings collectively suggest that distinct CHD1-associated alterations of genomic structure evolve during and are required for the development of prostate cancer
CHD1 is a critical factor for proper development of the follicular epithelium in terms of whole-cell chromatin arrangement.
These results underscore the importance of Chd1 for the regulation of pluripotency in ESCs and provide evidence for a hitherto unrecognized critical role of the phosphorylated N-terminal SRR 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
An effect of Chd1 null mutation can be increased by deficiency of one of the genes, encoding variant histone H3.3, His 3.3 B, suggesting that the role of CHD1 in the control of male X chromosome organization can be mediated by CHD1 activity in H3.3 histone deposition and exchange.
The Drosophila melanogaster CHD1 chromatin remodeling factor modulates global chromosome structure and counteracts HP1a and H3K9me2.
Intestinal resistance against infection by P. aeruginosa is linked to maintaining proper balance of gut-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 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.
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.
ATP-dependent helicase CHD1
, chromodomain-helicase-DNA-binding protein 1
, chromo-helicase/ATPase-DNA binding protein 1
, chromodomain helicase DNA binding protein 1
, Chromodomain-helicase-DNA-binding protein
, chromo-ATPase/helicase-DNA-binding domain
, chromo-ATPase/helicase-DNA-binding protein 1
, lethal (2) 23Cd
, LOW QUALITY PROTEIN: chromodomain-helicase-DNA-binding protein 1