U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination
    • Showing Current items.

    DOCK4 dedicator of cytokinesis 4 [ Homo sapiens (human) ]

    Gene ID: 9732, updated on 6-May-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Heterozygous loss-of-function variants in DOCK4 cause neurodevelopmental delay and microcephaly.

    Heterozygous loss-of-function variants in DOCK4 cause neurodevelopmental delay and microcephaly.
    Herbst C, Bothe V, Wegler M, Axer-Schaefer S, Audebert-Bellanger S, Gecz J, Cogne B, Feldman HB, Horn AHC, Hurst ACE, Kelly MA, Kruer MC, Kurolap A, Laquerriere A, Li M, Mark PR, Morawski M, Nizon M, Pastinen T, Polster T, Saugier-Veber P, SeSong J, Sticht H, Stieler JT, Thifffault I, van Eyk CL, Marcorelles P, Vezain-Mouchard M, Abou Jamra R, Oppermann H., Free PMC Article

    05/3/2024
    Integration analysis of lncRNA and mRNA expression data identifies DOCK4 as a potential biomarker for elderly osteoporosis.

    Integration analysis of lncRNA and mRNA expression data identifies DOCK4 as a potential biomarker for elderly osteoporosis.
    Wu C, Wang C, Xiao B, Li S, Sheng Y, Wang Q, Tao J, Zhang Y, Jiang X., Free PMC Article

    03/7/2024
    Genetic variations in DOCK4 contribute to schizophrenia susceptibility in a Chinese cohort: A genetic neuroimaging study.

    Genetic variations in DOCK4 contribute to schizophrenia susceptibility in a Chinese cohort: A genetic neuroimaging study.
    Xu X, He B, Zeng J, Yin J, Wang X, Luo X, Liang C, Luo S, Yan H, Xiong S, Tan Z, Lv D, Dai Z, Lin Z, Lin J, Ye X, Chen R, Li Y, Wang Y, Chen W, Luo Z, Li K, Ma G.

    03/7/2023
    DOCK4 regulates ghrelin production in gastric X/A-like cells.

    DOCK4 regulates ghrelin production in gastric X/A-like cells.
    Huang Y, Yang Y, Zhao Y, Guo D, Chen L, Shi L, Xu G.

    06/25/2022
    DOCK4 stimulates MUC2 production through its effect on goblet cell differentiation.

    DOCK4 stimulates MUC2 production through its effect on goblet cell differentiation.
    Qin T, Yang J, Huang D, Zhang Z, Huang Y, Chen H, Xu G.

    11/13/2021
    Up-regulated cytotrophoblast DOCK4 contributes to over-invasion in placenta accreta spectrum.

    Up-regulated cytotrophoblast DOCK4 contributes to over-invasion in placenta accreta spectrum.
    McNally L, Zhou Y, Robinson JF, Zhao G, Chen LM, Chen H, Kim MY, Kapidzic M, Gormley M, Hannibal R, Fisher SJ., Free PMC Article

    09/12/2020
    SR-B1 drives endothelial cell LDL transcytosis via DOCK4 to promote atherosclerosis

    SR-B1 drives endothelial cell LDL transcytosis via DOCK4 to promote atherosclerosis.
    Huang L, Chambliss KL, Gao X, Yuhanna IS, Behling-Kelly E, Bergaya S, Ahmed M, Michaely P, Luby-Phelps K, Darehshouri A, Xu L, Fisher EA, Ge WP, Mineo C, Shaul PW., Free PMC Article

    02/8/2020
    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 promotes loss of proliferation in glioblastoma progenitor cells through nuclear beta-catenin accumulation and subsequent miR-302-367 cluster expression.
    Debruyne DN, Turchi L, Burel-Vandenbos F, Fareh M, Almairac F, Virolle V, Figarella-Branger D, Baeza-Kallee N, Lagadec P, Kubiniek V, Paquis P, Fontaine D, Junier MP, Chneiweiss H, Virolle T.

    10/13/2018
    DOCK4 signalling is necessary for lateral filopodial protrusions and tubule remodelling prior to vascular lumen formation

    A Rac/Cdc42 exchange factor complex promotes formation of lateral filopodia and blood vessel lumen morphogenesis.
    Abraham S, Scarcia M, Bagshaw RD, McMahon K, Grant G, Harvey T, Yeo M, Esteves FOG, Thygesen HH, Jones PF, Speirs V, Hanby AM, Selby PJ, Lorger M, Dear TN, Pawson T, Marshall CJ, Mavria G., Free PMC Article

    04/23/2016
    These data identify DOCK4 as a putative 7q gene whose reduced expression can lead to erythroid dysplasia

    Reduced DOCK4 expression leads to erythroid dysplasia in myelodysplastic syndromes.
    Sundaravel S, Duggan R, Bhagat T, Ebenezer DL, Liu H, Yu Y, Bartenstein M, Unnikrishnan M, Karmakar S, Liu TC, Torregroza I, Quenon T, Anastasi J, McGraw KL, Pellagatti A, Boultwood J, Yajnik V, Artz A, Le Beau MM, Steidl U, List AF, Evans T, Verma A, Wickrema A., Free PMC Article

    03/5/2016
    activator DOCK4 as a key component of the TGF-beta/Smad pathway that promotes lung ADC cell extravasation and metastasis.

    TGF-β/Smad signaling through DOCK4 facilitates lung adenocarcinoma metastasis.
    Yu JR, Tai Y, Jin Y, Hammell MC, Wilkinson JE, Roe JS, Vakoc CR, Van Aelst L., Free PMC Article

    03/21/2015
    The study found significant associations between autism and a SNP of the DOCK4 gene.

    Family-based association study of ZNF533, DOCK4 and IMMP2L gene polymorphisms linked to autism in a northeastern Chinese Han population.
    Liang S, Wang XL, Zou MY, Wang H, Zhou X, Sun CH, Xia W, Wu LJ, Fujisawa TX, Tomoda A., Free PMC Article

    12/20/2014
    The Atypical guanine nucleotide exchange factor Dock4 regulates neurite differentiation through modulation of Rac1 GTPase and actin dynamics.

    The atypical guanine nucleotide exchange factor Dock4 regulates neurite differentiation through modulation of Rac1 GTPase and actin dynamics.
    Xiao Y, Peng Y, Wan J, Tang G, Chen Y, Tang J, Ye WC, Ip NY, Shi L., Free PMC Article

    09/14/2013
    This study revealed ROCK4 as novel schizophrenia candidate genes in the Jewish population.

    DOCK4 and CEACAM21 as novel schizophrenia candidate genes in the Jewish population.
    Alkelai A, Lupoli S, Greenbaum L, Kohn Y, Kanyas-Sarner K, Ben-Asher E, Lancet D, Macciardi F, Lerer B.

    09/8/2012
    novel epigenetic alterations in myelodysplastic leukocytes and implicate DOCK4 as a pathogenic gene located on the 7q chromosomal region.

    Aberrant epigenetic and genetic marks are seen in myelodysplastic leukocytes and reveal Dock4 as a candidate pathogenic gene on chromosome 7q.
    Zhou L, Opalinska J, Sohal D, Yu Y, Mo Y, Bhagat T, Abdel-Wahab O, Fazzari M, Figueroa M, Alencar C, Zhang J, Kambhampati S, Parmar S, Nischal S, Hueck C, Suzuki M, Freidman E, Pellagatti A, Boultwood J, Steidl U, Sauthararajah Y, Yajnik V, McMahon C, Gore SD, Platanias LC, Levine R, Melnick A, Wickrema A, Greally JM, Verma A., Free PMC Article

    01/28/2012
    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

    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.
    Maestrini E, Pagnamenta AT, Lamb JA, Bacchelli E, Sykes NH, Sousa I, Toma C, Barnby G, Butler H, Winchester L, Scerri TS, Minopoli F, Reichert J, Cai G, Buxbaum JD, Korvatska O, Schellenberg GD, Dawson G, de Bildt A, Minderaa RB, Mulder EJ, Morris AP, Bailey AJ, Monaco AP, IMGSAC, Maestrini E, Pagnamenta AT, Lamb JA, Bacchelli E, Sykes NH, Sousa I, Toma C, Barnby G, Butler H, Winchester L, Scerri TS, Minopoli F, Reichert J, Cai G, Buxbaum JD, Korvatska O, Schellenberg GD, Dawson G, de Bildt A, Minderaa RB, Mulder EJ, Morris AP, Bailey AJ, Monaco AP, IMGSAC., Free PMC Articles: PMC2934739, PMC2934739

    01/1/2011
    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.

    Characterization of a family with rare deletions in CNTNAP5 and DOCK4 suggests novel risk loci for autism and dyslexia.
    Pagnamenta AT, Bacchelli E, de Jonge MV, Mirza G, Scerri TS, Minopoli F, Chiocchetti A, Ludwig KU, Hoffmann P, Paracchini S, Lowy E, Harold DH, Chapman JA, Klauck SM, Poustka F, Houben RH, Staal WG, Ophoff RA, O'Donovan MC, Williams J, Nöthen MM, Schulte-Körne G, Deloukas P, Ragoussis J, Bailey AJ, Maestrini E, Monaco AP, International Molecular Genetic Study Of Autism Consortium, Pagnamenta AT, Bacchelli E, de Jonge MV, Mirza G, Scerri TS, Minopoli F, Chiocchetti A, Ludwig KU, Hoffmann P, Paracchini S, Lowy E, Harold DH, Chapman JA, Klauck SM, Poustka F, Houben RH, Staal WG, Ophoff RA, O'Donovan MC, Williams J, Nöthen MM, Schulte-Körne G, Deloukas P, Ragoussis J, Bailey AJ, Maestrini E, Monaco AP, International Molecular Genetic Study Of Autism Consortium., Free PMC Articles: PMC2941017, PMC2941017

    11/27/2010
    Clinical trial of gene-disease association and gene-environment interaction. (HuGE Navigator)

    Personalized smoking cessation: interactions between nicotine dose, dependence and quit-success genotype score.
    Rose JE, Behm FM, Drgon T, Johnson C, Uhl GR., Free PMC Article

    06/30/2010
    Cell migration is regulated by platelet-derived growth factor receptor endocytosis, which involves DOCK4.

    Cell migration is regulated by platelet-derived growth factor receptor endocytosis.
    Kawada K, Upadhyay G, Ferandon S, Janarthanan S, Hall M, Vilardaga JP, Yajnik V., Free PMC Article

    08/28/2009
    Observational study of gene-disease association. (HuGE Navigator)See all PubMed (3) articles

    Characterization of a family with rare deletions in CNTNAP5 and DOCK4 suggests novel risk loci for autism and dyslexia.
    Pagnamenta AT, Bacchelli E, de Jonge MV, Mirza G, Scerri TS, Minopoli F, Chiocchetti A, Ludwig KU, Hoffmann P, Paracchini S, Lowy E, Harold DH, Chapman JA, Klauck SM, Poustka F, Houben RH, Staal WG, Ophoff RA, O'Donovan MC, Williams J, Nöthen MM, Schulte-Körne G, Deloukas P, Ragoussis J, Bailey AJ, Maestrini E, Monaco AP, International Molecular Genetic Study Of Autism Consortium, Pagnamenta AT, Bacchelli E, de Jonge MV, Mirza G, Scerri TS, Minopoli F, Chiocchetti A, Ludwig KU, Hoffmann P, Paracchini S, Lowy E, Harold DH, Chapman JA, Klauck SM, Poustka F, Houben RH, Staal WG, Ophoff RA, O'Donovan MC, Williams J, Nöthen MM, Schulte-Körne G, Deloukas P, Ragoussis J, Bailey AJ, Maestrini E, Monaco AP, International Molecular Genetic Study Of Autism Consortium.

    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.
    Maestrini E, Pagnamenta AT, Lamb JA, Bacchelli E, Sykes NH, Sousa I, Toma C, Barnby G, Butler H, Winchester L, Scerri TS, Minopoli F, Reichert J, Cai G, Buxbaum JD, Korvatska O, Schellenberg GD, Dawson G, de Bildt A, Minderaa RB, Mulder EJ, Morris AP, Bailey AJ, Monaco AP, IMGSAC, Maestrini E, Pagnamenta AT, Lamb JA, Bacchelli E, Sykes NH, Sousa I, Toma C, Barnby G, Butler H, Winchester L, Scerri TS, Minopoli F, Reichert J, Cai G, Buxbaum JD, Korvatska O, Schellenberg GD, Dawson G, de Bildt A, Minderaa RB, Mulder EJ, Morris AP, Bailey AJ, Monaco AP, IMGSAC.

    Analysis of DNA copy number alterations in ovarian serous tumors identifies new molecular genetic changes in low-grade and high-grade carcinomas.
    Kuo KT, Guan B, Feng Y, Mao TL, Chen X, Jinawath N, Wang Y, Kurman RJ, Shih IeM, Wang TL.

    05/6/2009
    DOCK4 interacts with the beta-catenin degradation complex, consisting of the proteins adenomatosis polyposis coli, Axin and glycogen synthase kinase 3beta.

    Molecular association between beta-catenin degradation complex and Rac guanine exchange factor DOCK4 is essential for Wnt/beta-catenin signaling.
    Upadhyay G, Goessling W, North TE, Xavier R, Zon LI, Yajnik V., Free PMC Article

    01/21/2010
    DOCK4 may be regulated by PIP(3) to exert its function

    Identification of DOCK4 and its splicing variant as PIP3 binding proteins.
    Kanai A, Ihara S, Ohdaira T, Shinohara-Kanda A, Iwamatsu A, Fukui Y.

    01/21/2010
    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 is regulated by RhoG and promotes Rac-dependent cell migration.
    Hiramoto K, Negishi M, Katoh H.

    01/21/2010
    firstprevious page of 1 nextlast