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SHANK3 (zeige SHANK3 ELISA Kits), CHD8, and ADNP (zeige ADNP ELISA Kits) had distinctly higher scores than all other genes in the dataset describing the genes associated with autism spectrum disorders.
Data suggest that CHD6 (zeige CHD6 ELISA Kits) and CHD7 (zeige CHD7 ELISA Kits) 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 (zeige CHD7 ELISA Kits); CHD6 (zeige CHD6 ELISA Kits) 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 (zeige SUPT16H ELISA Kits) 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 (zeige BRD4 ELISA Kits) and NSD3 (zeige WHSC1L1 ELISA Kits).
Taken together our data demonstrate that CHD8 is involved in late stages of progesterone receptor (zeige PGR ELISA Kits) 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 (zeige CTCFL ELISA Kits)/CTCF (zeige CTCF ELISA Kits) ratio indicate frequent disruption of CTCF (zeige CTCF ELISA Kits) and its effector genes in PCa (zeige FLVCR1 ELISA Kits).
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 (zeige GUSB ELISA Kits).
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 (zeige CTNNB1 ELISA Kits) and histone H1 (zeige H1F0 ELISA Kits), with formation of the trimeric complex on chromatin being required for inhibition of beta-catenin (zeige CTNNB1 ELISA Kits)-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 (zeige CTCF ELISA Kits) to regulate expression of Birc5 (zeige BIRC5 ELISA Kits) and CARD10 (zeige CARD10 ELISA Kits).
These observations reveal a mode of p53 (zeige TP53 ELISA Kits) regulation mediated by CHD8, which may set a threshold for induction of apoptosis during early embryogenesis by counteracting p53 (zeige TP53 ELISA Kits) function through recruitment of histone H1 (zeige H1F0 ELISA Kits).
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