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    VPS4B vacuolar protein sorting 4 homolog B [ Homo sapiens (human) ]

    Gene ID: 9525, updated on 2-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    p-AKT/VPS4B regulates the small extracellular vesicle size in venous malformation endothelial cells.

    p-AKT/VPS4B regulates the small extracellular vesicle size in venous malformation endothelial cells.
    Lai WQ, Xia HF, Chen GH, Wang XL, Yang JG, Wu LZ, Zhao YF, Jia YL, Chen G.

    06/12/2024
    Analysis of individual HIV-1 budding event using fast AFM reveals a multiplexed role for VPS4.

    Analysis of individual HIV-1 budding event using fast AFM reveals a multiplexed role for VPS4.
    Harel S, Altaras Y, Nachmias D, Rotem-Dai N, Dvilansky I, Elia N, Rousso I., Free PMC Article

    11/12/2022
    Synthetic Lethal Interaction between the ESCRT Paralog Enzymes VPS4A and VPS4B in Cancers Harboring Loss of Chromosome 18q or 16q.

    Synthetic Lethal Interaction between the ESCRT Paralog Enzymes VPS4A and VPS4B in Cancers Harboring Loss of Chromosome 18q or 16q.
    Neggers JE, Paolella BR, Asfaw A, Rothberg MV, Skipper TA, Yang A, Kalekar RL, Krill-Burger JM, Dharia NV, Kugener G, Kalfon J, Yuan C, Dumont N, Gonzalez A, Abdusamad M, Li YY, Spurr LF, Wu WW, Durbin AD, Wolpin BM, Piccioni F, Root DE, Boehm JS, Cherniack AD, Tsherniak A, Hong AL, Hahn WC, Stegmaier K, Golub TR, Vazquez F, Aguirre AJ., Free PMC Article

    12/25/2021
    Synthetic lethality between VPS4A and VPS4B triggers an inflammatory response in colorectal cancer.

    Synthetic lethality between VPS4A and VPS4B triggers an inflammatory response in colorectal cancer.
    Szymańska E, Nowak P, Kolmus K, Cybulska M, Goryca K, Derezińska-Wołek E, Szumera-Ciećkiewicz A, Brewińska-Olchowik M, Grochowska A, Piwocka K, Prochorec-Sobieszek M, Mikula M, Miączyńska M., Free PMC Article

    07/31/2021
    VPS4B mutation impairs the osteogenic differentiation of dental follicle cells derived from a patient with dentin dysplasia type I.

    VPS4B mutation impairs the osteogenic differentiation of dental follicle cells derived from a patient with dentin dysplasia type I.
    Li Q, Lu F, Chen T, Zhang K, Lu Y, Li X, Wang Y, Liu L, Tian Q, Xiong F, Chen D., Free PMC Article

    09/19/2020
    VPS4B, via Wnt-beta-catenin signalling, acts as a regulator of the proliferation and differentiation of hDPSCs

    Vacuolar protein sorting 4B regulates the proliferation and odontoblastic differentiation of human dental pulp stem cells through the Wnt-β-catenin signalling pathway.
    Pan Y, Lu T, Peng L, Chen Z, Li M, Zhang K, Xiong F, Wu B.

    12/7/2019
    VPS4B might facilitate chondrocyte apoptosis in Osteoarthritis via p38 MAPK signaling pathway.

    Vacuolar Protein Sorting 4B (VPS4B) Regulates Apoptosis of Chondrocytes via p38 Mitogen-Activated Protein Kinases (MAPK) in Osteoarthritis.
    Xu L, Zhai L, Ge Q, Liu Z, Tao R.

    07/14/2018
    Knockdown of vps4b in zebrafish recapitulated the reduction of tooth size.

    A splicing mutation in VPS4B causes dentin dysplasia I.
    Yang Q, Chen D, Xiong F, Chen D, Liu C, Liu Y, Yu Q, Xiong J, Liu J, Li K, Zhao L, Ye Y, Zhou H, Hu L, Tian Z, Shang X, Zhang L, Wei X, Zhou W, Li D, Zhang W, Xu X.

    11/4/2017
    Our findings support a role for VPS4B in MM cell proliferation, adhesion, and drug resistance, and pave the way for a novel therapeutic approach targeting this molecule.

    Cell adhesion down-regulates the expression of vacuolar protein sorting 4B (VPS4B) and contributes to drug resistance in multiple myeloma cells.
    Tang J, Ji L, Wang Y, Huang Y, Yin H, He Y, Liu J, Miao X, Wu Y, Xu X, He S, Cheng C.

    02/27/2016
    Lack of ALG-2, ALIX or Vps4B each prevents shedding, and repair of the injured cell membrane

    Mechanism of Ca²⁺-triggered ESCRT assembly and regulation of cell membrane repair.
    Scheffer LL, Sreetama SC, Sharma N, Medikayala S, Brown KJ, Defour A, Jaiswal JK., Free PMC Article

    11/21/2015
    Crystal structures of three molecular complexes reveal that IST1 binds to the MIT domains of VPS4 and LIP5.

    Distinct mechanisms of recognizing endosomal sorting complex required for transport III (ESCRT-III) protein IST1 by different microtubule interacting and trafficking (MIT) domains.
    Guo EZ, Xu Z., Free PMC Article

    06/6/2015
    ESCRT-III protein CHMP5 inhibits LIP5-mediated VPS4 activation by inducing a moderate conformational change within LIP5.

    A novel mechanism of regulating the ATPase VPS4 by its cofactor LIP5 and the endosomal sorting complex required for transport (ESCRT)-III protein CHMP5.
    Vild CJ, Li Y, Guo EZ, Liu Y, Xu Z., Free PMC Article

    05/30/2015
    High Vacuolar protein sorting 4B results in more apoptosis of intestinal epithelial cells via p38 MAPK in Crohn's disease.

    Vacuolar protein sorting 4B regulates apoptosis of intestinal epithelial cells via p38 MAPK in Crohn's disease.
    Zhang D, Wang L, Yan L, Miao X, Gong C, Xiao M, Ni R, Tang Q.

    05/23/2015
    Taken together, it was concluded that VPS4B and its DN mutant VPS4B-K180Q have anti-HBV effect in vivo, which helps develop molecular therapeutic strategies for HBV infection.

    Inhibition of HBV replication by VPS4B and its dominant negative mutant VPS4B-K180Q in vivo.
    Xia J, Wang W, Li L, Liu Z, Liu M, Yang D.

    09/13/2014
    Protein kinase CK2 alpha is involved in the phosphorylation of the ESCRT-III subunits CHMP3 and CHMP2B, as well as of VPS4B/SKD1, an ATPase that mediates ESCRT-III disassembly.

    CK2 involvement in ESCRT-III complex phosphorylation.
    Salvi M, Raiborg C, Hanson PI, Campsteijn C, Stenmark H, Pinna LA.

    04/26/2014
    VPS4B may promote the progression of Carcinoma, Non-Small-Cell Lung (NSCLC) and be a biotarget for NSCLCs therapy.

    Vacuolar protein sorting 4B, an ATPase protein positively regulates the progression of NSCLC via promoting cell division.
    Liu Y, Lv L, Xue Q, Wan C, Ni T, Chen B, Liu Y, Zhou Y, Ni R, Mao G.

    02/15/2014
    An inverse correlation between VPS4B expression and EGFR abundance is observed in breast tumors, and high-grade or recurrent breast carcinomas exhibit lower VPS4B expression.

    Identification of an AAA ATPase VPS4B-dependent pathway that modulates epidermal growth factor receptor abundance and signaling during hypoxia.
    Lin HH, Li X, Chen JL, Sun X, Cooper FN, Chen YR, Zhang W, Chung Y, Li A, Cheng CT, Yang L, Deng X, Liu X, Yen Y, Johnson DL, Shih HM, Yang A, Ann DK., Free PMC Article

    04/14/2012
    It was found that neither siRNA knockdown of VPS4A and VPS4B expression nor the use of cell lines that inducibly express VPS4A or VPS4B dominant negative mutants, inhibited influenza virus budding.

    Influenza virus budding does not require a functional AAA+ ATPase, VPS4.
    Watanabe R, Lamb RA., Free PMC Article

    01/1/2011
    ESCRT-III/VPS4 proteins function at centrosomes to help regulate their maintenance or proliferation and then at midbodies during abscission, thereby helping ensure the ordered progression through the different stages of cell division.

    Human ESCRT-III and VPS4 proteins are required for centrosome and spindle maintenance.
    Morita E, Colf LA, Karren MA, Sandrin V, Rodesch CK, Sundquist WI., Free PMC Article

    09/6/2010
    Observational study of gene-disease association. (HuGE Navigator)

    Genetic analysis of diabetic nephropathy on chromosome 18 in African Americans: linkage analysis and dense SNP mapping.
    McDonough CW, Bostrom MA, Lu L, Hicks PJ, Langefeld CD, Divers J, Mychaleckyj JC, Freedman BI, Bowden DW., Free PMC Article

    09/20/2009
    Overall, we see no role for the ESCRT pathway in influenza virus budding and the significance of the M1-VPS28 interaction remains to be determined.

    Budding of filamentous and non-filamentous influenza A virus occurs via a VPS4 and VPS28-independent pathway.
    Bruce EA, Medcalf L, Crump CM, Noton SL, Stuart AD, Wise HM, Elton D, Bowers K, Digard P.

    01/21/2010
    ATP hydrolysis would eliminate this interaction and subsequent nucleotide release causes the domains to rotate, which together lead to the disassembly of the SKD1 oligomer

    Nucleotide-dependent conformational changes and assembly of the AAA ATPase SKD1/VPS4B.
    Inoue M, Kamikubo H, Kataoka M, Kato R, Yoshimori T, Wakatsuki S, Kawasaki M.

    01/21/2010
    studies reveal how the VPS4 ATPases recognize their CHMP substrates to facilitate the membrane fission events required for the release of viruses, endosomal vesicles and daughter cells

    ESCRT-III recognition by VPS4 ATPases.
    Stuchell-Brereton MD, Skalicky JJ, Kieffer C, Karren MA, Ghaffarian S, Sundquist WI.

    01/21/2010
    Upon coexpression of mutated CHMP3, CHMP4B, or CHMP4C forms, as well as of ATPase-defective Vps4A or Vps4B mutants, HBV assembly and egress were potently blocked.

    Hepatitis B virus maturation is sensitive to functional inhibition of ESCRT-III, Vps4, and gamma 2-adaptin.
    Lambert C, Döring T, Prange R., Free PMC Article

    01/21/2010
    Here, we report that dominant negative forms of Vps4A, Vps4B, and AIP1 inhibit HTLV-1 budding.

    Regulation of HTLV-1 Gag budding by Vps4A, Vps4B, and AIP1/Alix.
    Urata S, Yokosawa H, Yasuda J., Free PMC Article

    01/21/2010
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