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anti-Human CHD8 Antikörper:
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Human Polyclonal CHD8 Primary Antibody für 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 für 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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Human Polyclonal CHD8 Primary Antibody für 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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rare CNVR at 14q11 encompassing the chromatin modifier CHD8 was significantly associated with sporadic CRC risk. Copy number loss at CHD8 altered expressions of genes implicated in colorectal tumourigenesis.
We suggested that this constituted a new multiple congenital anomaly-intellectual disability syndrome due to defects in CHD8 and/or SUPT16H..The identification of multiple patients with the same genetic defect and characteristic clinical phenotype, confirms our suggestion that this is a syndromic disorder caused by haploinsufficiency or heterozygous loss of function of CHD8.
The Autism spectrum disorder candidate genes SATB2, CHD8 and EHMT1 show enriched expression in neurons, especially inhibitory neurons
SHANK3, CHD8, and ADNP had distinctly higher scores than all other genes in the dataset describing the genes associated with autism spectrum disorders.
Data suggest that CHD6 and CHD7 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; CHD6 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 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 and NSD3.
Taken together our data demonstrate that CHD8 is involved in late stages of progesterone receptor 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/CTCF ratio indicate frequent disruption of CTCF and its effector genes in PCa.
Recurrent approximately 100 Kb microdeletion in the chromosomal region 14q11.2, involving CHD8 gene, is associated with autism and macrocephaly.
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
indings suggest that CHD8 disruptions represent a specific pathway in the development of Autism spectrum disorder (ASD) and define a distinct ASD subtype. Common phenotypic features include increased head size; a facial phenotype marked by prominent forehead, wide-set eyes, and pointed chin; as well as increased rates of GI complaints and marked sleep dysfunction.
CHD8 is required for E2F-dependent transcription activation of S-phase genes
Loss of CHD8 expression is associated with aggressiveness in gastric cancer.
Genes that regulate chromatin were mutated in CpG island methylator phenotype 1 colorectal carcinoma; the highest rates of mutation were observed in CHD7 and CHD8.
results from de novo events and a large parallel case-control study provide strong evidence in favour of CHD8 and KATNAL2 as genuine autism risk factors
we identify a crucial developmental role for Chd8 in regulating axon guidance gene expression in the early postnatal period and, for the first time, associate Chd8 haploinsufficiency with functional over-connectivity of specific brain areas
Our results suggest that a CHD8 mutation leads to sexually dimorphic changes ranging from transcription to behavior in mice
Chd8 deficiency results in reduced axon and dendritic growth, disruption of axon projections to the contralateral cortex, and delayed neuronal migration.
CHD7 and CHD8 bind in Oligodendrocyte precursor cells to a majority of ASD risk-associated genes, suggesting an implication of oligodendrocyte lineage cells in ASD neurological defects.
Genome-wide gene expression patterns in Arid1b hKO mice were similar to those in Autism spectrum disorder (ASD)patients and Chd8-haploinsufficient mice, an ASD model, and to developmental changes in gene expression in fast-spiking cells in the mouse brain. Our results suggest that Arid1b haploinsufficiency causes ASD-like phenotypes in mice.
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.
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 and histone H1, with formation of the trimeric complex on chromatin being required for inhibition of beta-catenin-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 to regulate expression of Birc5 and CARD10.
These observations reveal a mode of p53 regulation mediated by CHD8, which may set a threshold for induction of apoptosis during early embryogenesis by counteracting p53 function through recruitment of histone H1.
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