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present observation and published data suggest that phenotype present in patients with duplication of 14q11.2 region, encompassing the SUPT16H (show 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 (show BRD4 ELISA Kits) and NSD3 (show WHSC1L1 ELISA Kits).
Taken together our data demonstrate that CHD8 is involved in late stages of progesterone receptor (show 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 (show CTCFL ELISA Kits)/CTCF (show CTCF ELISA Kits) ratio indicate frequent disruption of CTCF (show CTCF ELISA Kits) and its effector genes in PCa (show FLVCR1 ELISA Kits).
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
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 ELISA Kits) and histone H1 (show H1F0 ELISA Kits), with formation of the trimeric complex on chromatin being required for inhibition of beta-catenin (show 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 (show CTCF ELISA Kits) to regulate expression of Birc5 (show BIRC5 ELISA Kits) and CARD10 (show CARD10 ELISA Kits).
These observations reveal a mode of p53 (show TP53 ELISA Kits) regulation mediated by CHD8, which may set a threshold for induction of apoptosis during early embryogenesis by counteracting p53 (show TP53 ELISA Kits) function through recruitment of histone H1 (show H1F0 ELISA Kits).
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