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Human Polyclonal CHD7 Primary Antibody for 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
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 Antibodies) deregulation is an important driver of the neural crest-derived aspects of Chd7 dependent CHARGE syndrome.
knockdown of the jumonji (show JARID2 Antibodies) domain-containing histone demethylase (show MBD2 Antibodies) fbxl10 (show KDM2B Antibodies)/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 (show SH2B1 Antibodies)), and results in the loss of asymmetric expression of spaw in the lateral plate mesoderm, which is consistent with more general laterality defects.
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 (show KALRN Antibodies) 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 Antibodies) and CHD7 both bind with high affinity to short linker DNA, whereas CHD8 (show CHD8 Antibodies) requires longer DNA for binding; thus, CHD8 (show CHD8 Antibodies) slides nucleosomes into positions with more flanking linker DNA than CHD7; CHD6 (show CHD6 Antibodies) 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 Antibodies) 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 Antibodies)) osteogenic differentiation and provided a potential target for controlling MSC (show MSC Antibodies) osteogenesis.
we have identified mild cerebellar hypoplasia and distinct cerebellar foliation anomalies in Chd7 (show CHD3 Antibodies) gt/+ mice. Our findings imply a specific function for CHD7 (show CHD3 Antibodies) in controlling the spatiotemporal initiation of cerebellar fissures and show that normal fissure formation requires bi-allelic Chd7 (show CHD3 Antibodies) expression, consistent with the haploinsuffi- cient nature of CHARGE syndrome.
Chd7 (show CHD3 Antibodies) deficiency delays leukemia initiation induced by Cbfb (show CBFB Antibodies)-MYH11 (show MYH11 Antibodies).
CHD7 (show CHD3 Antibodies) is an important factor in the proliferation and stemness maintenance of neural stem/progenitor cells.
Chd7 (show CHD3 Antibodies) regulates the proliferation and identity of oligodendrocyte precursor cells after spinal cord injury.
CHD7 (show CHD3 Antibodies) is necessary for maintaining an open, accessible chromatin state at the Reln (show RELN Antibodies) locus. Taken together, this study shows that Reln (show RELN Antibodies) gene expression is regulated by chromatin remodeling, identifies CHD7 (show CHD3 Antibodies) as a previously unrecognized upstream regulator of Reln (show RELN Antibodies), and provides direct in vivo evidence that a mammalian CHD (show CHRD Antibodies) protein can control brain development
Chd7 (show CHD3 Antibodies) coordinates with Sox10 (show SOX10 Antibodies) 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 Antibodies) functions.
Chd7 (show CHD3 Antibodies) mutant mice are models for determining the molecular etiology of ocular defects in CHARGE syndrome.
This work reveals the importance of CHD7 (show CHD3 Antibodies) in the cardiogenic mesoderm for multiple processes during cardiovascular development.
Findings directly link CHD7 (show CHD3 Antibodies) to pathways involved in NSC quiescence and identify the first chromatin-remodeling factor (show ASH1L Antibodies) with a role in NSC quiescence and maintenance.
Conditional deletion of Chd7 (show CHD3 Antibodies) in ectodermal and endodermal derivatives or migrating neural crest cells results in varied and severe craniofacial defects.
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