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Human Polyclonal CHD7 Primary Antibody für ICC, IF - ABIN4297899
Colbert, Petrova, Fisher, Pantazides, Madden, Hardy, Warren, Pan, Nagaraju, Liu, Saka, Hall, Shelton, Gandhi, Pauly, Kowalski, Kooby, El-Rayes, Staley, Adsay, Curran, Landry, Maithel, Yu: CHD7 expression predicts survival outcomes in patients with resected pancreatic cancer. in Cancer research 2014
Show all 2 Pubmed References
Human Polyclonal CHD7 Primary Antibody für ELISA - ABIN547991
Gao, Gordon, Zhang, Browne, Helms, Gillum, Weber, Devroy, Swaney, Dobbs, Morcuende, Sheffield, Lovett, Bowcock, Herring, Wise: CHD7 gene polymorphisms are associated with susceptibility to idiopathic scoliosis. in American journal of human genetics 2007
evolutionarily conserved role for CHD7 in orchestrating neural crest gene expression programs
chd7 was critical for thymic development and T-lymphopenia in CHARGE syndrome may be mainly attributed to the defects of thymic organogenesis.
The conserved genetics and transparency of the zebrafish have provided new insights into the consequences of chd7 gene dysfunction on the GI system and cranial nerve patterning. These findings highlight the opportunity of the zebrafish to serve as a preclinical model for studying compounds that may improve GI motility in individuals with CHARGE syndrome.
Our zebrafish CHARGE model thus reveals important regulatory roles for Chd7 at multiple points of neural crest development viz., migration, fate choice and differentiation and we suggest that sox10 deregulation is an important driver of the neural crest-derived aspects of Chd7 dependent CHARGE syndrome.
knockdown of the jumonji domain-containing histone demethylase fbxl10/kdm2bb, a repressor of ribosomal RNA genes, rescues cell proliferation and cartilage defects in chd7 morphant embryos and can lead to complete rescue of the CHARGE syndrome phenotype.
Chd7 is required for the organization of the neural retina in zebrafish.
Data show that Chd7 deficiency leads to asymmetric segmentation of the presomitic mesoderm (PSM), and results in the loss of asymmetric expression of spaw in the lateral plate mesoderm, which is consistent with more general laterality defects.
Chd7 is enriched at the Sema3a promoter in neural crest cells, and loss of function of Chd7 inhibits Sema3a expression in CHARGE syndrome.
Pathogenic variants in CHD7 were present in 15 of 28 individuals (53.6%), whereas 4 (14.3%) individuals had pathogenic variants in other genes (RERE, KMT2D, EP300, or PUF60). A variant of uncertain clinical significance in KDM6A was identified in one (3.5%) individual.
Seventeen heterozygous CHD7 Rare Sequence Variants (RSV), including 2 protein-truncating variants and 15 missense variants, were identified in 18 of the 116 CHH probands. The allele frequency of CHD7 RSVs was significantly higher in CHH probands relative to CoLaus controls (7.8%, 18/232, vs. 0.1%, 1/810; P = 1.6 x 10-11).
These data suggest that CHD7 drives differentiation, and there is a lower limit for CHD7 to initiate differentiation and an upper limit for CHD7 if maintained in undifferentiated state, and such upper limit varies depending on culture condition.
Focus on the endocrine phenotypes associated with CHD7 mutational spectrum in humans (review).
results suggest CHD7, through its interactions with superenhancer elements, acts as a regulatory hub in the orchestration of the spatiotemporal dynamics of transcription factors to regulate neuroepithelial and CNS lineage identities.
These results demonstrate the oncogenic potential of CHD7 and its association with poor prognostic parameters in human cancer.
CHD7 mutation is associated with small Cell Lung Cancer.
CHD7 is an important factor in the proliferation and stemness maintenance of neural stem/progenitor cells.
Data suggest protein levels of kalirin and CHD7 in circulating extracellular vesicles (EVs) as endothelial dysfunction markers to monitor vascular condition in hypertensive patients with albuminuria.
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.
Our findings provide evidence that CHARGE and Kabuki syndromes result from dysregulatrion of CHD7 and KMT2D genes involved embryonal development that are expressed in a tissue-specific manner.
De novo missense variant in CHD7 identified in a family presenting with musculoskeletal abnormalities as the main manifestation of CHD7-related disease, representing a new phenotype.
This study established a new epigenetic regulation of mesenchymal stem cell (MSC) osteogenic differentiation and provided a potential target for controlling MSC osteogenesis.
the case of a girl with a novel heterozygous deletion in exon 15 of the CHD7 gene and combined agenesis of uterus and ovaries, besides gonadotropin deficiency, thus expanding the geno-phenotype of CHARGE syndrome.
We report here another sporadic case with mild CHARGE syndrome, with heart defect, sensorineural deafness and hypoplastic semi-circular canals. It should be emphasized that patients should not be rejected for CHD7 analysis if they do not fulfill criteria for atypical or typical CHARGE as there is a high intra- and inter-familial variability
Pathogenic CHD7 variants are associated with CHARGE syndrome.
Two mutations of CHD7 were identified including a novel splice-site mutation (c.2443-2A>G) and a previously known frameshift mutation (c.2504_2508delATCTT).
Data show that chromodomain helicase DNA-binding protein 7 (Chd7) is required for the maintenance of open chromatin and thus activation of genes essential for granule neuron differentiation.
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.
Findings extend current knowledge of the role of BMI1 and CHD7 in medulloblastoma pathogenesis, and they raise the possibility that pharmacological targeting of BMI1 or ERK may be particularly indicated in a subgroup of MB with low expression levels of CHD7.
we have identified mild cerebellar hypoplasia and distinct cerebellar foliation anomalies in Chd7 gt/+ mice. Our findings imply a specific function for CHD7 in controlling the spatiotemporal initiation of cerebellar fissures and show that normal fissure formation requires bi-allelic Chd7 expression, consistent with the haploinsuffi- cient nature of CHARGE syndrome.
Chd7 deficiency delays leukemia initiation induced by Cbfb-MYH11.
Chd7 regulates the proliferation and identity of oligodendrocyte precursor cells after spinal cord injury.
CHD7 is necessary for maintaining an open, accessible chromatin state at the Reln locus. Taken together, this study shows that Reln gene expression is regulated by chromatin remodeling, identifies CHD7 as a previously unrecognized upstream regulator of Reln, and provides direct in vivo evidence that a mammalian CHD protein can control brain development
Chd7 coordinates with Sox10 to regulate the initiation of myelinogenesis and acts as a molecular nexus of regulatory networks that account for the development of a seemingly diverse array of lineages, including oligodendrocytes and osteoblasts, pointing to previously uncharacterized Chd7 functions.
Chd7 mutant mice are models for determining the molecular etiology of ocular defects in CHARGE syndrome.
This work reveals the importance of CHD7 in the cardiogenic mesoderm for multiple processes during cardiovascular development.
Findings directly link CHD7 to pathways involved in NSC quiescence and identify the first chromatin-remodeling factor with a role in NSC quiescence and maintenance.
Conditional deletion of Chd7 in ectodermal and endodermal derivatives or migrating neural crest cells results in varied and severe craniofacial defects.
CHD7 gene mutation is associated with CHARGE syndrome.
Findings demonstrate critical, cooperative roles for Retinoic Acid (RA) and CHD7 in subventricular zone neural stem cell function and inner ear development, suggesting that altered RA signaling may be an effective method for treating Chd7 deficiency.
Chd7 may have critical selector gene functions during inner ear morphogenesis.
CHD7 may directly regulate Bmp4 expression by binding with an enhancer element downstream of the Bmp4 locus.
Otitis media in Chd7Ome/+ mice is characterized by Eustachian tube dysfunction, epithelial hyperplasia, middle ear effusion and associated hearing loss.
Chd7(Gt)(/+) mouse model of CHARGE syndrome demonstrates combined conductive and sensorineural hearing loss, correlating with changes in both middle and inner ears.
characterize gene regulation by Sox2 in neural stem cells. We
This gene encodes a protein that contains several helicase family domains. Mutations in this gene have been found in some patients with the CHARGE syndrome.
chromodomain helicase DNA binding protein 7
, chromodomain-helicase-DNA-binding protein 7-like
, ATP-dependent helicase CHD7
, chromodomain helicase DNA binding protein 7 isoform CRA_e
, chromodomain-helicase-DNA-binding protein 7
, chromodomain helicase DNA-binding protein 7