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DOCK4 is a member of the dedicator of cytokinesis (DOCK) family and encodes a protein with a DHR-1 (CZH-1) domain, a DHR-2 (CZH-2) domain and an SH3 domain. Additionally we are shipping DOCK4 Kits (7) and and many more products for this protein.
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Human Monoclonal DOCK4 Primary Antibody for IF, IHC (p) - ABIN564203
Eiring, Neviani, Santhanam, Oaks, Chang, Notari, Willis, Gambacorti-Passerini, Volinia, Marcucci, Caligiuri, Leone, Perrotti: Identification of novel posttranscriptional targets of the BCR/ABL oncoprotein by ribonomics: requirement of E2F3 for BCR/ABL leukemogenesis. in Blood 2008
DOCK4 over expression suppresses selfrenewal and tumorigenicity of glioblastoma (GBM) stem-like cells. Accordingly in the frame of GBM median of survival, increased level of DOCK4 predicts improved patient survival.
DOCK4 signalling is necessary for lateral filopodial protrusions and tubule remodelling prior to vascular lumen formation
These data identify DOCK4 as a putative 7q gene whose reduced expression can lead to erythroid dysplasia
activator DOCK4 as a key component of the TGF-beta/Smad pathway that promotes lung ADC cell extravasation and metastasis.
The study found significant associations between autism and a SNP of the DOCK4 gene.
The Atypical guanine nucleotide exchange factor Dock4 regulates neurite differentiation through modulation of Rac1 GTPase and actin dynamics.
This study revealed ROCK4 as novel schizophrenia candidate genes in the Jewish population.
novel epigenetic alterations in myelodysplastic leukocytes and implicate DOCK4 as a pathogenic gene located on the 7q chromosomal region.
Evidence for the involvement of DOCK4 in autism susceptibility was supported by independent replication of association at rs2217262 and the finding of a deletion segregating in a sib-pair family
Data suggest that exonic deletions of DOCK4 may act as a risk factor for reading impairment. Genomic disruption of both DOCK4 and CNTNAP5 genes may have an additive effect and may result in a more severe autism spectrum phenotype.
Taken together, these results suggest that Dock4 plays an important role in the regulation of cell migration through activation of Rac1, and that RhoG is a key upstream regulator for Dock4.
DOCK4 may be regulated by PIP(3) to exert its function
DOCK4 interacts with the beta-catenin degradation complex, consisting of the proteins adenomatosis polyposis coli, Axin and glycogen synthase kinase 3beta.
Cell migration is regulated by platelet-derived growth factor receptor endocytosis, which involves DOCK4.
This gene is a member of the dedicator of cytokinesis (DOCK) family and encodes a protein with a DHR-1 (CZH-1) domain, a DHR-2 (CZH-2) domain and an SH3 domain. This membrane-associated, cytoplasmic protein functions as a guanine nucleotide exchange factor and is involved in regulation of adherens junctions between cells. Mutations in this gene have been associated with ovarian, prostate, glioma, and colorectal cancers. Alternatively spliced variants which encode different protein isoforms have been described, but only one has been fully characterized.
dedicator of cytokinesis 4
, dedicator of cytokinesis protein 4-like
, dedicator of cytokinesis protein 4