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Vacuolar protein sorting 33 homolog B

VPS33B
Vesicle mediated protein sorting plays an important role in segregation of intracellular molecules into distinct organelles. Genetic studies in yeast have identified more than 40 vacuolar protein sorting (VPS) genes involved in vesicle transport to vacuoles. This gene is a member of the Sec-1 domain family, and encodes the human ortholog of rat Vps33b which is homologous to the yeast class C Vps33 protein. The mammalian class C Vps proteins are predominantly associated with late endosomes/lysosomes, and like their yeast counterparts, may mediate vesicle trafficking steps in the endosome/lysosome pathway. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HAD, CAN, AGE, Rab7, ACID
Papers on VPS33B
Characterization of the Mammalian CORVET and HOPS Complexes and Their Modular Restructuring for Endosome Specificity.
New
Neefjes et al., Utrecht, Netherlands. In J Biol Chem, Jan 2016
Here, we provide a detailed analysis of interactions within the mammalian CORVET and HOPS as well as an additional endosomal-targeting complex (VIPAS39-VPS33B) that does not exist in yeast.
Characterization of a Novel Integrin Binding Protein, VPS33B, Which Is Important for Platelet Activation and In Vivo Thrombosis and Hemostasis.
New
Li et al., Suzhou, China. In Circulation, Jan 2016
METHODS AND RESULTS: Here, we show that VPS33B, a member of the Sec1/Munc18 family, binds directly to the integrin β subunit.
The Role of Platelets and ε-Aminocaproic Acid in Arthrogryposis, Renal Dysfunction, and Cholestasis (ARC) Syndrome Associated Hemorrhage.
New
Shavit et al., In Pediatr Blood Cancer, Nov 2015
We report a patient with ARC syndrome and compound heterozygous mutations in VPS33B (vacuolar protein sorting 33B) who presented with significant bleeding requiring numerous admissions and transfusions.
VPS33B regulates protein sorting into and maturation of α-granule progenitor organelles in mouse megakaryocytes.
New
Gissen et al., Birmingham, United Kingdom. In Blood, Aug 2015
Arthrogryposis, renal dysfunction, and cholestasis (ARC) syndrome is caused by deficiencies in the trafficking proteins VPS33B or VIPAR, and is associated with a bleeding diathesis and a marked reduction in platelet α-granules.
Identification of novel mutations in the VPS33B gene involved in arthrogryposis, renal dysfunction, and cholestasis syndrome.
New
Park et al., Seoul, South Korea. In Clin Genet, Jul 2015
Arthrogryposis, renal dysfunction, and cholestasis (ARC) syndrome is an autosomal recessive disorder caused by mutations in the VPS33B and VIPAS39.
Recruitment of VPS33A to HOPS by VPS16 Is Required for Lysosome Fusion with Endosomes and Autophagosomes.
New
Luzio et al., Cambridge, United Kingdom. In Traffic, Jul 2015
There was no effect of depleting either VIPAR or VPS33B, paralogs of VPS16 and VPS33A, on fusion of lysosomes with either endosomes or autophagosomes and immunoprecipitation showed that they form a complex distinct from HOPS.
New potential eukaryotic substrates of the mycobacterial protein tyrosine phosphatase PtpA: hints of a bacterial modulation of macrophage bioenergetics state.
Villarino et al., Montevideo, Uruguay. In Sci Rep, 2014
So far only two unrelated macrophage components (VPS33B, GSK3α) have been identified as PtpA substrates.
Arthrogryposis-renal dysfunction-cholestasis (ARC) syndrome: from molecular genetics to clinical features.
Review
Zhang et al., Shanghai, China. In Ital J Pediatr, 2013
UNLABELLED: Arthrogryposis-renal dysfunction-cholestasis (ARC) syndrome is a rare but fatal autosomal recessive multisystem disorder caused by mutations in the VPS33B or VIPAR gene.
Glomerular involvement in the arthrogryposis, renal dysfunction and cholestasis syndrome.
Coward et al., Bristol, United Kingdom. In Clin Kidney J, 2013
BACKGROUND: Arthrogryposis, renal dysfunction and cholestasis (ARC) syndrome is a multisystem autosomal-recessive disorder caused by defects in the VPS33B and VIPAR genes, involved in localization of apical membrane proteins.
Inhibitory effect of SPE-39 due to tyrosine phosphorylation and ubiquitination on the function of Vps33B in the EGF-stimulated cells.
GeneRIF
Konishi et al., Shōbara, Japan. In Febs Lett, 2012
SPE-39 due to tyrosine phosphorylation and ubiquitination on the function of Vps33B in the EGF-stimulated cells
Advances in our understanding of the molecular basis of disorders of platelet function.
Review
Nurden et al., Pessac, France. In J Thromb Haemost, 2011
Defects of α-granule biosynthesis also involve germline VPS33B mutations in the ARC (arthrogryposis, renal dysfunction and cholestasis) syndrome.
Mutations in VIPAR cause an arthrogryposis, renal dysfunction and cholestasis syndrome phenotype with defects in epithelial polarization.
Impact
Gissen et al., Birmingham, United Kingdom. In Nat Genet, 2010
Mutations in VPS33B account for most cases of ARC.
Arc syndrome without arthrogryposis, with hip dislocation and renal glomerulocystic appearance: a case report.
Review
Sayli et al., Ankara, Turkey. In Eur J Pediatr, 2009
INTRODUCTION: Arthrogryposis-renal dysfunction-cholestasis (ARC) syndrome is a rare multisystem disorder first described in 1979 and recently ascribed to mutation in VPS33B whose product acts in intracellular trafficking.
Clinical characteristics and VPS33B mutations in patients with ARC syndrome.
GeneRIF
Yoo et al., Seoul, South Korea. In J Pediatr Gastroenterol Nutr, 2009
We assessed the clinical characteristics and investigated the VPS33B mutations in Korean patients with ARC (arthrogryposis, renal dysfunction, and cholestasis) syndrome.
Mycobacterium tuberculosis virulence is mediated by PtpA dephosphorylation of human vacuolar protein sorting 33B.
GeneRIF
Av-Gay et al., Vancouver, Canada. In Cell Host Microbe, 2008
Genetic deletion of ptpA attenuates Mycobacterium tuberculosis growth in human macrophages and identify VPS33B, a regulator of membrane fusion, as a PtpA substrate.
Defective lamellar granule secretion in arthrogryposis, renal dysfunction, and cholestasis syndrome caused by a mutation in VPS33B.
GeneRIF
Sprecher et al., Haifa, Israel. In Arch Dermatol, 2008
The present observations indicate that VPS33B deficiency results in abnormal secretion of lamellar granules, which underlies ichthyosis in ARC syndrome.
Requirement of VPS33B, a member of the Sec1/Munc18 protein family, in megakaryocyte and platelet alpha-granule biogenesis.
GeneRIF
Kahr et al., Toronto, Canada. In Blood, 2006
VPS33B is involved in intracellular vesicle trafficking
Ichthyosis associated with ARC syndrome: ARC syndrome is one of the differential diagnoses of ichthyosis.
Review
Koh et al., Ulsan, South Korea. In Pediatr Dermatol, 2005
Novel identification of the mutation in VPS33B in this syndrome, which involves intracellular protein trafficking by regulation of vesicle-to-target sensory nerve action potential receptor (SNARE) family, might explain the consistent combination of membrane fusion defects.
Mutations in VPS33B, encoding a regulator of SNARE-dependent membrane fusion, cause arthrogryposis-renal dysfunction-cholestasis (ARC) syndrome.
Impact
GeneRIF
Maher et al., Birmingham, United Kingdom. In Nat Genet, 2004
encodes a homolog of the class C yeast vacuolar protein sorting gene, that contains a Sec1-like domain important in the regulation of vesicle-to-target SNARE complex formation and subsequent membrane fusion
Molecular basis of intrahepatic cholestasis.
Review
Bull et al., San Francisco, United States. In Ann Med, 2003
Alagille syndrome patients carry mutations in JAG1, and mutations in VPS33B have been identified in patients with arthrogryposis, renal dysfunction and cholestasis syndrome (ARC).
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