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Dedicator of cytokinesis 4

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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Akt, CAN, DOCK180, GEF, Rac1
Papers on DOCK4
Reduced DOCK4 expression leads to erythroid dysplasia in myelodysplastic syndromes.
Wickrema et al., Oxford, United Kingdom. In Proc Natl Acad Sci U S A, Dec 2015
Dedicator of cytokinesis 4 (DOCK4) is a GTPase exchange factor, and its gene maps to the commonly deleted 7q region.
Kaempferol inhibits vascular smooth muscle cell migration by modulating BMP-mediated miR-21 expression.
Kang et al., Inch'ŏn, South Korea. In Mol Cell Biochem, Sep 2015
Kaempferol activates the BMP signaling pathway, induces miR-21 expression and downregulates DOCK4, 5, and 7, leading to inhibition of cell migration.
The Roles of Genes in the Neuronal Migration and Neurite Outgrowth Network in Developmental Dyslexia: Single- and Multiple-Risk Genetic Variants.
Song et al., Wuhan, China. In Mol Neurobiol, Aug 2015
We first observed that KIAA0319L rs28366021, KIAA0319 rs4504469, and DOCK4 rs2074130 were significantly associated with DD risk after false discovery rate (FDR) adjustment for multiple comparisons (odds ratio (OR) = 0.672, 95 % confidence interval (CI) = 0.505-0.894,
Mutation specific functions of EGFR result in a mutation-specific downstream pathway activation.
French et al., Rotterdam, Netherlands. In Eur J Cancer, May 2015
Differential binding was confirmed using a proximity ligation assay and/or Western Blot for the dedicator of cytokinesis 4 (DOCK4), UDP-glucose glycoprotein glucosyltransferase 1 (UGGT1), MYC binding protein 2 (MYCBP2) and Smoothelin (SMTN).
TGF-β/Smad signaling through DOCK4 facilitates lung adenocarcinoma metastasis.
Van Aelst et al., New York City, United States. In Genes Dev, Mar 2015
Here, we report that in lung ADC cells, TGF-β potently induces expression of DOCK4, but not other DOCK family members, via the Smad pathway and that DOCK4 induction mediates TGF-β's prometastatic effects by enhancing tumor cell extravasation.
A Rac/Cdc42 exchange factor complex promotes formation of lateral filopodia and blood vessel lumen morphogenesis.
Mavria et al., Toronto, Canada. In Nat Commun, 2014
Here, using an organotypic system that recapitulates distinct stages of VEGF-dependent angiogenesis, we show that lumen formation requires early cytoskeletal remodelling and lateral cell-cell contacts, mediated through the RAC1 guanine nucleotide exchange factor (GEF) DOCK4 (dedicator of cytokinesis 4).
[Significance of chromosome 7 abnormalities in myeloid malignancies].
Chang et al., Shanghai, China. In Zhongguo Shi Yan Xue Ye Xue Za Zhi, 2014
Genes (EZH2, MLL5, DOCK4, SAMD9L/SAMD9) located in commonly deleted segments of 7q have been cloned and characterized along with the advance of molecular biology.This review summaries the current advancement about myeloid malignancies associated with monosomy7/del(7q).
Homozygous microdeletion of exon 5 in ZNF277 in a girl with specific language impairment.
Newbury et al., Bologna, Italy. In Eur J Hum Genet, 2014
Moreover, ZNF277 is adjacent to the DOCK4 and IMMP2L genes, which have been implicated in ASD.
Dock4 forms a complex with SH3YL1 and regulates cancer cell migration.
Katoh et al., Kyoto, Japan. In Cell Signal, 2014
Dock4 is a member of the Dock180 family of proteins that mediates cancer cell migration through activation of Rac.
Family-based association study of ZNF533, DOCK4 and IMMP2L gene polymorphisms linked to autism in a northeastern Chinese Han population.
Tomoda et al., Harbin, China. In J Zhejiang Univ Sci B, 2014
OBJECTIVE: A study in a Caucasian population has identified two single-nucleotide polymorphisms (SNPs) in ZNF533, one in DOCK4, and two in IMMP2L, which were all significantly associated with autism.
DOCK4 and CEACAM21 as novel schizophrenia candidate genes in the Jewish population.
Lerer et al., Jerusalem, Israel. In Int J Neuropsychopharmacol, 2012
This study revealed ROCK4 as novel schizophrenia candidate genes in the Jewish population.
Aberrant epigenetic and genetic marks are seen in myelodysplastic leukocytes and reveal Dock4 as a candidate pathogenic gene on chromosome 7q.
Verma et al., New York City, United States. In J Biol Chem, 2011
novel epigenetic alterations in myelodysplastic leukocytes and implicate DOCK4 as a pathogenic gene located on the 7q chromosomal region.
A theoretical molecular network for dyslexia: integrating available genetic findings.
Franke et al., Nijmegen, Netherlands. In Mol Psychiatry, 2011
We found that 10 of the 14 dyslexia candidate genes (ROBO1, KIAA0319, KIAA0319L, S100B, DOCK4, FMR1, DIP2A, GTF2I, DYX1C1 and DCDC2) fit into a theoretical molecular network involved in neuronal migration and neurite outgrowth.
Identification of a New Series of STAT3 Inhibitors by Virtual Screening.
Asai et al., Shizuoka, Japan. In Acs Med Chem Lett, 2010
We identified a N-[2-(1,3,4-oxadiazolyl)]-4-quinolinecarboxamide derivative, STX-0119, as a novel STAT3 dimerization inhibitor by a virtual screen using a customized version of the DOCK4 program with the crystal structure of STAT3.
High-density SNP association study and copy number variation analysis of the AUTS1 and AUTS5 loci implicate the IMMP2L-DOCK4 gene region in autism susceptibility.
IMGSAC et al., Bologna, Italy. In Mol Psychiatry, 2010
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
Characterization of a family with rare deletions in CNTNAP5 and DOCK4 suggests novel risk loci for autism and dyslexia.
International Molecular Genetic Study Of Autism Consortium et al., Oxford, United Kingdom. In Biol Psychiatry, 2010
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.
Cell migration is regulated by platelet-derived growth factor receptor endocytosis.
Yajnik et al., Boston, United States. In Mol Cell Biol, 2009
Cell migration is regulated by platelet-derived growth factor receptor endocytosis, which involves DOCK4.
Cell-cell junction formation: the role of Rap1 and Rap1 guanine nucleotide exchange factors.
Bos et al., Utrecht, Netherlands. In Biochim Biophys Acta, 2009
These multi-domain proteins, which include C3G, Epacs, PDZ-GEFs, RapGRPs and DOCK4, are regulated by various different stimuli and may function at different levels in junction formation.
Potential disease targets for drugs that disrupt protein-- protein interactions of Grb2 and Crk family adaptors.
Lewitzky et al., Oxford, United Kingdom. In Curr Pharm Des, 2005
Examples include newly found DOCK family proteins (DOCK3, DOCK4, and DOCK5) which are known or suspected effectors of Crk proteins and the interaction of Grb2 with the cell cycle regulator p27Kip1.
DOCK4, a GTPase activator, is disrupted during tumorigenesis.
Haber et al., United States. In Cell, 2003
We describe a deletion targeting DOCK4, a member of the CDM gene family encoding regulators of small GTPases.
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