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Syntaxin binding protein 5

Tomosyn, LGL3, Stxbp5, LLGL3, KIAA1006, tomosyn-1
Syntaxin 1 is a component of the 7S and 20S SNARE complexes which are involved in docking and fusion of synaptic vesicles with the presynaptic plasma membrane. This gene encodes a syntaxin 1 binding protein. In rat, a similar protein dissociates syntaxin 1 from the Munc18/n-Sec1/rbSec1 complex to form a 10S complex, an intermediate which can be converted to the 7S SNARE complex. Thus this protein is thought to be involved in neurotransmitter release by stimulating SNARE complex formation. Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: von Willebrand factor, Insulin, HAD, CAN, SNAP-25
Papers on Tomosyn
Genetics of Venous Thrombosis: update in 2015.
Trégouët et al., Marseille, France. In Thromb Haemost, Dec 2015
To date, 17 genes have been robustly demonstrated to harbour genetic variations associated with VT risk: ABO, F2, F5, F9, F11, FGG, GP6, KNG1, PROC, PROCR, PROS1, SERPINC1, SLC44A2, STXBP5, THBD, TSPAN15 and VWF.
Genome-wide association studies identify genetic loci for low von Willebrand factor levels.
O'Donnell et al., Rotterdam, Netherlands. In Eur J Hum Genet, Nov 2015
All loci were within or close to genes, including STXBP5 (Syntaxin Binding Protein 5) (6q24), STAB5 (stabilin-5) (12q23), ABO (9q34), VWF (12p13) and UFM1 (ubiquitin-fold modifier 1) (13q13).
Structural basis for recognition of the Sec4 Rab GTPase by its effector, the Lgl/tomosyn homologue, Sro7.
Brennwald et al., Chapel Hill, United States. In Mol Biol Cell, Oct 2015
Finally, analysis of the surface variation within the homologous interaction site on tomosyn-1 and Lgl-1 structural models suggests a possible conserved Rab GTPase effector function in tomosyn vertebrate homologues.
A Combined Optogenetic-Knockdown Strategy Reveals a Major Role of Tomosyn in Mossy Fiber Synaptic Plasticity.
Ashery et al., Tel Aviv-Yafo, Israel. In Cell Rep, Aug 2015
One such protein, tomosyn, is believed to reduce P(r) by interfering with the SNARE complex formation.
CLEC4M and STXBP5 gene variations contribute to von Willebrand factor level variation in von Willebrand disease.
WiN Study Group et al., Rotterdam, Netherlands. In J Thromb Haemost, Jun 2015
PATIENTS/METHODS: In 364 type 1 VWD and 240 type 2 VWD patients from the nationwide cross-sectional 'Willebrand in The Netherlands' (WiN) study, we studied the association between eight SNPs in STXBP5, SCARA5, ABO, VWF, STAB2, STX2, TC2N, and CLEC4M, and VWF antigen (VWF:Ag), VWF activity (VWF:Act), and bleeding phenotype as assessed with the Tosetto bleeding score.
Tomosyn is a novel Akt substrate mediating insulin-dependent GLUT4 exocytosis.
Hirata et al., Fukuoka, Japan. In Int J Biochem Cell Biol, May 2015
In the present study, we identified tomosyn at Ser-783 as a possible Akt-substrate motif and examined whether the phosphorylation at Ser-783 is involved in the regulation of GLUT4 expression.
Homozygous mutation of STXBP5L explains an autosomal recessive infantile-onset neurodegenerative disorder.
Gecz et al., Adelaide, Australia. In Hum Mol Genet, May 2015
We combined family-based whole-exome and whole-genome sequencing of parents and affected siblings and, after filtering of likely non-pathogenic variants, identified a unique missense variant in syntaxin-binding protein 5-like (STXBP5L c.3127G>A, p.Val1043Ile [CCDS43137.1]) in the IBD interval.
Homozygous deletions at 3p22, 5p14, 6q15, and 9p21 result in aberrant expression of tumor suppressor genes in gastric cancer.
Kim et al., South Korea. In Genes Chromosomes Cancer, Mar 2015
In addition, we observed that homozygous focal deletions generated truncated transcripts of TGFBR2, CTNNA1, and STXBP5.
Syntaxin-binding protein 5 exocytosis regulation: differential role in endothelial cells and platelets.
Lillicrap, In J Clin Invest, 2014
GWAS have consistently identified the gene encoding syntaxin-binding protein 5 (STXBP5) in this context.
The genetic basis of obesity-associated type 2 diabetes (diabesity) in polygenic mouse models.
Schürmann et al., Potsdam, Germany. In Mamm Genome, 2014
Outcross populations of these models have been employed in the genome-wide search for mouse diabetes genes, and have led to positional cloning of the strong candidates Pctp, Tbc1d1, Zfp69, and Ifi202b (NZO-derived obesity) and Sorcs1, Lisch-like, Tomosyn-2, App, Tsc2, and Ube2l6 (obesity caused by the ob or db mutation).
Syntaxin-binding protein STXBP5 inhibits endothelial exocytosis and promotes platelet secretion.
Lowenstein et al., In J Clin Invest, 2014
Recent genome-wide association studies (GWAS) have identified syntaxin-binding protein 5 (STXBP5) as a candidate gene linked to changes in vWF plasma levels, though the functional relationship between STXBP5 and vWF is unknown.
Platelet secretion and hemostasis require syntaxin-binding protein STXBP5.
Whiteheart et al., In J Clin Invest, 2014
Syntaxin-binding protein 5 (STXBP5; also known as tomosyn-1) was identified by mass spectrometry, and its expression in isolated platelets was confirmed by RT-PCR analysis.
The N- and C-terminal domains of tomosyn play distinct roles in soluble N-ethylmaleimide-sensitive factor attachment protein receptor binding and fusion regulation.
Shen et al., Boulder, United States. In J Biol Chem, 2014
Tomosyn negatively regulates SNARE-dependent exocytic pathways including insulin secretion, GLUT4 exocytosis, and neurotransmitter release.
Genetic variation associated with plasma von Willebrand factor levels and the risk of incident venous thrombosis.
Rosendaal et al., Seattle, United States. In Blood, 2011
Genetic variation in STXBP5 gene is associated with venous thrombosis.
Structural and functional analysis of tomosyn identifies domains important in exocytotic regulation.
Stuenkel et al., Ann Arbor, United States. In J Biol Chem, 2011
multiple domains outside the R-SNARE of tomosyn are critical to the efficacy of inhibition by tomosyn on exocytotic secretion
Effect of genetic variations in syntaxin-binding protein-5 and syntaxin-2 on von Willebrand factor concentration and cardiovascular risk.
de Maat et al., Rotterdam, Netherlands. In Circ Cardiovasc Genet, 2010
Genetic variability in STXBP5 and STX2 affects both VWF concentration and activity in young individuals with premature arterial thrombosis.
[Novel roles of tomosyn in regulated vesicle fusion].
Sakisaka, Kōbe, Japan. In Seikagaku, 2009
It regulates vesicle fusion. (review)
[Roles of tomosyn in regulated synaptic vesicle fusion].
Sakisaka et al., In Tanpakushitsu Kakusan Koso, 2009
regulates SNARE complex formation and synaptic vesicle fusion. (review)
Friends and foes in synaptic transmission: the role of tomosyn in vesicle priming.
Yizhar et al., Tel Aviv-Yafo, Israel. In Trends Neurosci, 2009
One of the prominent members of this diverse family is tomosyn.
Minireview: recent developments in the regulation of glucose transporter-4 traffic: new signals, locations, and partners.
Klip et al., Toronto, Canada. In Endocrinology, 2005
At the cell periphery, GLUT4-containing vesicles tether, dock, and fuse with the PM assisted by the exocyst complex followed by engagement of a soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex [with vesicle-associated membrane protein (VAMP)2 as the vesicular (v)-SNARE and soluble NSF-attachment protein (SNAP)23 and syntaxin4 as target (t)-SNAREs] regulated by the accessory proteins Munc18c, Synip and Tomosyn.
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