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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.


VAPB, ALS8, VAMP-associated protein
The protein encoded by this gene is a type IV membrane protein found in plasma and intracellular vesicle membranes. The encoded protein is found as a homodimer and as a heterodimer with VAPA. This protein also can interact with VAMP1 and VAMP2 and may be involved in vesicle trafficking. [provided by RefSeq, Jul 2008] (from NCBI)
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Top mentioned proteins: Als, CAN, MSP, SOD, V1a
Papers using VAPB antibodies
Phosphorylation of kinesin light chain-1 at serine-460 modulates binding and trafficking of calsyntenin-1
Miller Christopher C.J. et al., In Human Molecular Genetics, 2010
... Amyotrophic lateral sclerosis mutant VAPB transgenic mice develop TDP-43 pathology ...
Papers on VAPB
VAP (VAMP-Associated Proteins) as Receptors that couple Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Proteostasis with Lipid Homeostasis.
Aridor et al., Pittsburgh, United States. In J Biol Chem, Feb 2016
VAPB inhibited the degradation of ΔF508-CFTR.
A systematic screening to identify de novo mutations causing sporadic early-onset Parkinson's disease.
Bras et al., Kiel, Germany. In Hum Mol Genet, Jan 2016
Of the genes identified to carry de novo mutations, PTEN, VAPB and ASNA1 are supported by various sources of data to be involved in PD.
C-Terminal Auto-Regulatory Motif of Hepatitis C Virus NS5B Interacts with Human VAPB-MSP to Form a Dynamic Replication Complex.
Song et al., Singapore, Singapore. In Plos One, Dec 2015
Previous functional studies have already established that the human ER-anchored VAPB protein acts as a host factor to form a complex with HCV NS5A and NS5B, which may be established as a drug target.
Vapb/Amyotrophic lateral sclerosis 8 knock-in mice display slowly progressive motor behavior defects accompanying ER stress and autophagic response.
Tsuda et al., Montréal, Canada. In Hum Mol Genet, Dec 2015
Although transgenic mice overexpressing the mutant vesicle-associated membrane protein-associated protein B (VAPB) protein with neuron-specific promoters have provided some insight into the toxic properties of the mutant proteins, their role in pathogenesis remains unclear.
Atypical familial amyotrophic lateral sclerosis with initial symptoms of pain or tremor in a Chinese family harboring VAPB-P56S mutation.
Shen et al., Beijing, China. In J Neurol, Dec 2015
Mutations associated with ALS have been identified in more than 20 genes, but ALS type 8 (ALS8), which is caused by mutations in vesicle-associated membrane protein-associated protein B (VAPB), is rare.
The BioPlex Network: A Systematic Exploration of the Human Interactome.
Gygi et al., Boston, United States. In Cell, Aug 2015
For example, mutations in the membrane protein VAPB implicated in familial amyotrophic lateral sclerosis perturb a defined community of interactors.
[Association between VAPB mutations and familial amyotrophic lateral sclerosis in Chinese patients].
Fan et al., Beijing, China. In Zhonghua Yi Xue Za Zhi, Jul 2015
CONCLUSION: VAPB mutations are not a common cause and ALS8 is rare in Chinese FALS.
Autophagy and Neurodegeneration: Insights from a Cultured Cell Model of ALS.
Borgese et al., Milano, Italy. In Cells, 2014
In this review, we focus on the main molecular features of autophagy to provide a framework for discussion of our recent findings about the role in disease pathogenesis of the ALS-linked form of the VAPB gene product, a mutant protein that drives the generation of unusual cytoplasmic inclusions.
Golgi Fragmentation in ALS Motor Neurons. New Mechanisms Targeting Microtubules, Tethers, and Transport Vesicles.
Rabouille et al., Marseille, France. In Front Neurosci, 2014
Here, we present the different mechanisms that may underlie Golgi fragmentation in animal and cellular models of ALS linked to mutations in SOD1, TARDBP (TDP-43), VAPB, and C9Orf72 and we propose a novel one based on findings in progressive motor neuronopathy (pmn) mice.
Amyotrophic lateral sclerosis-associated mutant VAPBP56S perturbs calcium homeostasis to disrupt axonal transport of mitochondria.
Miller et al., London, United Kingdom. In Hum Mol Genet, 2012
ALS mutant VAPBP56S perturbs anterograde mitochondrial axonal transport by disrupting Ca(2+) homeostasis and effecting the Miro1/kinesin-1 interaction with tubulin.
VAPB interacts with the mitochondrial protein PTPIP51 to regulate calcium homeostasis.
Miller et al., London, United Kingdom. In Hum Mol Genet, 2012
Loss of either VAPB or PTPIP51 perturbs uptake of Calcium by mitochondria and results in amyotrophic lateral sclerosis.
VapB as a regulator of osteoclastogenesis via modulation of PLCγ2-Ca(2+)-NFAT signaling.
Lee et al., Iksan, South Korea. In Febs Lett, 2012
VapB positively regulates RANKL-mediated osteoclastogenesis via PLCgamma2-Ca(2+)-NFAT signaling
Endoplasmic reticulum stress and the ER mitochondrial calcium cycle in amyotrophic lateral sclerosis.
Grosskreutz et al., Jena, Germany. In Amyotroph Lateral Scler, 2012
TDP-43 and VAPB seem to be involved in UPR signalling as well.
Molecular pathology and genetic advances in amyotrophic lateral sclerosis: an emerging molecular pathway and the significance of glial pathology.
Shaw et al., Sheffield, United Kingdom. In Acta Neuropathol, 2011
Of potentially even greater importance it emerges that TDP-43 accumulation and inclusion formation characterises not only most sALS cases but also those that arise from mutations in several genes including TARDBP (predominantly ALS cases) itself, C9ORF72 (ALS and FTD cases), progranulin (predominantly FTD phenotypes), VAPB (predominantly ALS cases) and in some ALS cases with rare genetic variants of uncertain pathogenicity (CHMP2B).
Stress signaling from the endoplasmic reticulum: A central player in the pathogenesis of amyotrophic lateral sclerosis.
Atkin et al., Australia. In Iubmb Life, 2011
Furthermore, mutations to vesicle-associated membrane protein-associated protein B (VAPB), an ER transmembrane protein involved in ER stress regulation, also cause some cases of familial ALS.
Accumulation of wildtype and ALS-linked mutated VAPB impairs activity of the proteasome.
Raoul et al., Marseille, France. In Plos One, 2010
endoplasmic reticulum stress and corruption of the proteasome function might contribute to the aberrant protein homeostasis associated with hVAPB
Structural, stability, dynamic and binding properties of the ALS-causing T46I mutant of the hVAPB MSP domain as revealed by NMR and MD simulations.
Song et al., Singapore, Singapore. In Plos One, 2010
T46I mutant of the hVAPB MSP domain is associated with amyotrophic lateral sclerosis.
From ER to Eph receptors: new roles for VAP fragments.
Cox et al., Bar Harbor, United States. In Cell, 2008
Dominantly inherited mutations in an endoplasmic reticulum protein called VAPB have been found in a subset of patients with a rare familial form of amyotrophic lateral sclerosis (ALS).
The amyotrophic lateral sclerosis 8 protein VAPB is cleaved, secreted, and acts as a ligand for Eph receptors.
Bellen et al., Houston, United States. In Cell, 2008
Study shows that the MSP domains of VAP protein, VAPB are cleaved and secreted ligands for Eph receptors
A VAMP-binding protein from Aplysia required for neurotransmitter release.
Bartsch et al., New York City, United States. In Science, 1995
A 33-kilodalton membrane protein, termed VAP-33 (VAMP-associated protein of 33 kilodaltons), was identified whose corresponding messenger RNA was detected only in the central nervous system and the gill of Aplysia.
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