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evolutionarily conserved role for CHD7 in orchestrating neural crest gene expression programs
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 (show SOX10 ELISA Kits) deregulation is an important driver of the neural crest-derived aspects of Chd7 dependent CHARGE syndrome.
knockdown of the jumonji (show JARID2 ELISA Kits) domain-containing histone demethylase (show MBD2 ELISA Kits) fbxl10 (show KDM2B ELISA Kits)/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.
Data suggest protein levels of kalirin (show KALRN ELISA Kits) and CHD7 in circulating extracellular vesicles (EVs) as endothelial dysfunction markers to monitor vascular condition in hypertensive patients with albuminuria.
Data suggest that CHD6 (show CHD6 ELISA Kits) and CHD7 both bind with high affinity to short linker DNA, whereas CHD8 (show CHD8 ELISA Kits) requires longer DNA for binding; thus, CHD8 (show CHD8 ELISA Kits) slides nucleosomes into positions with more flanking linker DNA than CHD7; CHD6 (show CHD6 ELISA Kits) disrupts nucleosomes in a distinct non-sliding manner.
Our findings provide evidence that CHARGE and Kabuki syndromes result from dysregulatrion of CHD7 and KMT2D (show MLL2 ELISA Kits) 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 (show MSC ELISA Kits)) osteogenic differentiation and provided a potential target for controlling MSC (show MSC ELISA Kits) 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 (show Vcan ELISA Kits), 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).
Chd7 (show CHD3 ELISA Kits) regulates the proliferation and identity of oligodendrocyte precursor cells after spinal cord injury.
CHD7 (show CHD3 ELISA Kits) is necessary for maintaining an open, accessible chromatin state at the Reln (show RELN ELISA Kits) locus. Taken together, this study shows that Reln (show RELN ELISA Kits) gene expression is regulated by chromatin remodeling, identifies CHD7 (show CHD3 ELISA Kits) as a previously unrecognized upstream regulator of Reln (show RELN ELISA Kits), and provides direct in vivo evidence that a mammalian CHD (show CHRD ELISA Kits) protein can control brain development
Chd7 (show CHD3 ELISA Kits) coordinates with Sox10 (show SOX10 ELISA Kits) 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 (show CHD3 ELISA Kits) functions.
Chd7 (show CHD3 ELISA Kits) mutant mice are models for determining the molecular etiology of ocular defects in CHARGE syndrome.
This work reveals the importance of CHD7 (show CHD3 ELISA Kits) in the cardiogenic mesoderm for multiple processes during cardiovascular development.
Findings directly link CHD7 (show CHD3 ELISA Kits) to pathways involved in NSC quiescence and identify the first chromatin-remodeling factor (show ASH1L ELISA Kits) with a role in NSC quiescence and maintenance.
Conditional deletion of Chd7 (show CHD3 ELISA Kits) in ectodermal and endodermal derivatives or migrating neural crest cells results in varied and severe craniofacial defects.
CHD7 (show CHD3 ELISA Kits) gene mutation is associated with CHARGE syndrome.
Findings demonstrate critical, cooperative roles for Retinoic Acid (RA) and CHD7 (show CHD3 ELISA Kits) in subventricular zone neural stem cell function and inner ear development, suggesting that altered RA signaling may be an effective method for treating Chd7 (show CHD3 ELISA Kits) deficiency.
Chd7 (show CHD3 ELISA Kits) may have critical selector gene functions during inner ear morphogenesis.
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