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anti-Human CHD8 Antibodies:
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Human Polyclonal CHD8 Primary Antibody for ICC, IF - ABIN253036
Damaschke, Yang, Blute, Lin, Huang, Jarrard: Frequent disruption of chromodomain helicase DNA-binding protein 8 (CHD8) and functionally associated chromatin regulators in prostate cancer. in Neoplasia (New York, N.Y.) 2014
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Human Polyclonal CHD8 Primary Antibody for ELISA, WB - ABIN566153
Rodenberg, Hoggatt, Chen, Touw, Jones, Herring: Regulation of serum response factor activity and smooth muscle cell apoptosis by chromodomain helicase DNA-binding protein 8. in American journal of physiology. Cell physiology 2010
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Human Polyclonal CHD8 Primary Antibody for ChIP, ICC - ABIN253035
Sugathan, Biagioli, Golzio, Erdin, Blumenthal, Manavalan, Ragavendran, Brand, Lucente, Miles, Sheridan, Stortchevoi, Kellis, Haggarty, Katsanis, Gusella, Talkowski: CHD8 regulates neurodevelopmental pathways associated with autism spectrum disorder in neural progenitors. in Proceedings of the National Academy of Sciences of the United States of America 2014
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SHANK3 (show SHANK3 Antibodies), CHD8, and ADNP (show ADNP Antibodies) had distinctly higher scores than all other genes in the dataset describing the genes associated with autism spectrum disorders.
Data suggest that CHD6 (show CHD6 Antibodies) and CHD7 (show CHD7 Antibodies) both bind with high affinity to short linker DNA, whereas CHD8 requires longer DNA for binding; thus, CHD8 slides nucleosomes into positions with more flanking linker DNA than CHD7 (show CHD7 Antibodies); CHD6 (show CHD6 Antibodies) disrupts nucleosomes in a distinct non-sliding manner.
present observation and published data suggest that phenotype present in patients with duplication of 14q11.2 region, encompassing the SUPT16H (show SUPT16H Antibodies) and CHD8 genes, resemble in some extend features described in cases carrying microdeletion of that genomic region
Review of 16 other CHD8 mutation cases suggests that clinical features and their severity vary considerably across individuals; however, these data support a CHD8 mutation syndrome, further highlighting the importance of genomic medicine to guide clinical assessment and treatment
Our clinical case supports the hypothesis that CHD8 may play a central role in neuronal cell development and Autism spectrum disorders risk
Study provides evidence that links the CHD8 chromatin remodeler to the cancer maintenance functions of BRD4 (show BRD4 Antibodies) and NSD3 (show WHSC1L1 Antibodies).
Taken together our data demonstrate that CHD8 is involved in late stages of progesterone receptor (show PGR Antibodies) enhancers activation.
Loss of CHD8 contributes to autism spectrum disorder by perturbing an ancient gene regulatory network during human brain development.
CHD8 insufficiency results in altered gene expression of coding genes and noncoding RNAs. The changes among protein-coding genes involved genes that are enriched in neuronal development and in previously identified autism candidate genes.
In the first detailed analysis in cancer, a marked loss of CHD8 expression and increased BORIS (show CTCFL Antibodies)/CTCF (show CTCF Antibodies) ratio indicate frequent disruption of CTCF (show CTCF Antibodies) and its effector genes in PCa (show FLVCR1 Antibodies).
identified a co-expression module with peak expression in early brain development featuring dysregulation of RNA processing, chromatin remodeling and cell-cycle genes enriched for promoter binding by Chd8
these roles of Chd8 and the dynamics of Chd8 expression during development help negotiate the fine balance between neural progenitor proliferation and differentiation
find altered synaptic physiology in medium spiny neurons of the nucleus accumbens. Perturbation of Chd8 in adult mice recapitulates improved acquired motor learning behavior found in Chd8(+/-) animals, suggesting a role for CHD8 in adult striatal circuits. These results support a mechanism linking chromatin modification to striatal dysfunction and the molecular pathology of ASD (show GUSB Antibodies).
results are thus consistent with the notion that CHD8 haploinsufficiency is a highly penetrant risk factor for autism spectrum disorder, with disease pathogenesis probably resulting from a delay in neurodevelopment
The chromatin regulator CHD8 is a context-dependent mediator of cell survival in murine hematopoietic malignancies.
Chd8 promotes the association of beta-catenin (show CTNNB1 Antibodies) and histone H1 (show H1F0 Antibodies), with formation of the trimeric complex on chromatin being required for inhibition of beta-catenin (show CTNNB1 Antibodies)-dependent transactivation.
These data suggest that CHD8 plays a dual role in smooth muscle cells modulating SRF activity toward differentiation genes and promoting cell survival through interactions with both SRF and CTCF (show CTCF Antibodies) to regulate expression of Birc5 (show BIRC5 Antibodies) and CARD10 (show CARD10 Antibodies).
These observations reveal a mode of p53 (show TP53 Antibodies) regulation mediated by CHD8, which may set a threshold for induction of apoptosis during early embryogenesis by counteracting p53 (show TP53 Antibodies) function through recruitment of histone H1 (show H1F0 Antibodies).
CHD8 precipitates a network of gene-expression changes involved in neurodevelopmental pathways in which many autism spectrum disorder-associated genes may converge on shared mechanisms of pathogenesis
This gene encodes a DNA helicase that functions as a transcription repressor by remodeling chromatin structure. It binds beta-catenin and negatively regulates Wnt signaling pathway, which plays a pivotal role in vertebrate early development and morphogenesis. Mice lacking this gene exhibit early embryonic death. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
chromodomain helicase DNA binding protein 8
, chromodomain-helicase-DNA-binding protein 8
, ATP-dependent helicase CHD8
, chromodomain-helicase-DNA-binding protein 8-like
, axis duplication inhibitor
, helicase with SNF2 domain 1
, beta-catenin binding protein
, chromodomain helicase DNA binding protein family