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Syntaxin 16

Syntaxin 16, STX16
This gene encodes a protein that is a member of the syntaxin or t-SNARE (target-SNAP receptor) family. These proteins are found on cell membranes and serve as the targets for V-SNARES (vesicle-SNAP receptors) permitting specific synaptic vesicle docking and fusion. A microdeletion in the region of chromosome 20 where this gene is located has been associated with pseudohypoparathyroidism type Ib. Multiple transcript variants have been found for this gene. Read-through transcription also exists between this gene and the neighboring downstream aminopeptidase-like 1 (NPEPL1) gene. [provided by RefSeq, Mar 2011] (from NCBI)
Top mentioned proteins: Parathyroid Hormone, CAN, HAD, V1a, VAMP4
Papers using Syntaxin 16 antibodies
Cell biology of acid secretion by the parietal cell
Gleeson Paul A. et al., In Biology of the Cell, 2002
... A rabbit polyclonal antibody against syntaxin 16 was purchased from Synaptic Systems (Gottingen, Germany) ...
Papers on Syntaxin 16
Abnormal Methylation Status of the GNAS Exon 1A Region in Pseudohypohyperparathyroidism Combined With Turner Syndrome.
Ye et al., Hefei, China. In Am J Med Sci, Dec 2015
She had no family history of hypocalcemia and no STX16 gene deletions.
Analysis of Multiple Families with Single Individuals Affected by Pseudohypoparathyroidism Type Ib (PHP1B) Reveals Only One Novel Maternally Inherited GNAS Deletion.
Jüppner et al., Le Kremlin-Bicêtre, France. In J Bone Miner Res, Nov 2015
In the autosomal dominant disease variant, these methylation abnormalities are caused by deletions in STX16 or GNAS on the maternal allele.
Similar frequency of paternal uniparental disomy involving chromosome 20q (patUPD20q) in Japanese and Caucasian patients affected by sporadic pseudohypoparathyroidism type Ib (sporPHP1B).
Jüppner et al., Boston, United States. In Bone, Oct 2015
Familial forms of PHP1B are caused by maternally inherited microdeletions within STX16, the gene encoding syntaxin 16, or within GNAS, a complex genetic locus on chromosome 20q13.3
TSH elevations as the first laboratory evidence for pseudohypoparathyroidism type Ib (PHP-Ib).
Jüppner et al., Boston, United States. In J Bone Miner Res, May 2015
LOM at GNAS exon A/B alone led in the fourth patient to the identification of a maternally inherited 3-kb STX16 deletion, a well-established cause of autosomal dominant PHP-Ib.
Very small deletions within the NESP55 gene in pseudohypoparathyroidism type 1b.
Mackay et al., Southampton, United Kingdom. In Eur J Hum Genet, Apr 2015
PHP1b can be caused by loss of imprinting affecting GNAS A/B alone (associated with STX16 deletion), or the entire GNAS cluster (associated with deletions of NESP55 in a minority of cases).
Integrated genomic analyses identify frequent gene fusion events and VHL inactivation in gastrointestinal stromal tumors.
Sohn et al., Seoul, South Korea. In Oncotarget, Apr 2015
We additionally identified three recurrent read-through fusion transcripts: POLA2-CDC42EP2, C8orf42-FBXO25, and STX16-NPEPL1.
Loss of methylation at GNAS exon A/B is associated with increased intrauterine growth.
Jüppner et al., Caen, France. In J Clin Endocrinol Metab, Apr 2015
RESULTS: As newborns, AD-PHP1B patients were bigger than their healthy siblings and well above the reference average; increased sizes were particularly evident if the mothers were unaffected carriers of STX16 deletions.
Growth hormone deficiency in monozygotic twins with autosomal dominant pseudohypoparathyroidism type Ib.
Ogata et al., Tokyo, Japan. In Endocr J, 2014
To date, while GH deficiency (GHD) has been reported in multiple patients with PHP-Ia caused by mutations on the maternally expressed GNAS coding regions and in two patients with sporadic form of PHP-Ib accompanied by broad methylation defects of maternally derived GNAS differentially methylated regions (DMRs), it has not been identified in a patient with an autosomal dominant form of PHP-Ib (AD-PHP-Ib) accompanied by an STX16 microdeletion and an isolated loss of methylation (LOM) at exon A/B-DMR.
Different pattern of epigenetic changes of the GNAS gene locus in patients with pseudohypoparathyroidism type Ic confirm the heterogeneity of underlying pathomechanisms in this subgroup of pseudohypoparathyroidism and the demand for a new classification of GNAS-related disorders.
Thiele et al., Lübeck, Germany. In J Clin Endocrinol Metab, 2014
One patient had an exclusive loss of methylation of exon A/B associated with a STX16 deletion; four patients had an additional loss of methylation in XL and AS and a gain of methylation in NESP; and one patient presented with partial GNAS methylation changes concerning all differentially methylated regions.
A congenital neutrophil defect syndrome associated with mutations in VPS45.
Somech et al., Bethesda, United States. In N Engl J Med, 2013
The level of VPS45 protein was reduced, as were the VPS45 binding partners rabenosyn-5 and syntaxin-16.
Pseudohypoparathyroidism type 1b due to paternal uniparental disomy of chromosome 20q.
Suri et al., Nottingham, United Kingdom. In J Clin Endocrinol Metab, 2013
The molecular cause of autosomal dominant familial PHP1b has been well-defined with identification of microdeletions within the GNAS locus or the nearby STX16, but the molecular mechanism of the GNAS imprinting defects in sporadic PHP1b cases remains elusive.
GNAS -Related Loss-of-Function Disorders and the Role of Imprinting.
Silve et al., Le Kremlin-Bicêtre, France. In Horm Res Paediatr, 2012
Likewise, alterations in the methylation at promoters of GNAS transcripts, associated or not with deletions of imprinting control regions in the nearby STX16 gene or within GNAS, prompt resistance to parathormone when affecting the maternal allele.
GNAS epigenetic defects and pseudohypoparathyroidism: time for a new classification?
Spada et al., Milano, Italy. In Horm Metab Res, 2012
The familial form of the disease (AD-PHP-Ib) is typically associated with an isolated loss of imprinting at the exon A/B DMR due to microdeletions disrupting the upstream STX16 gene.
The cystic fibrosis transmembrane conductance regulator's expanding SNARE interactome.
Lee et al., Singapore, Singapore. In Traffic, 2011
Two SNAREs, STX6 and STX16 that function at the trans-Golgi network (TGN), have now been revealed as members of the CFTR SNARE interactome.
Syntaxin 16 binds to cystic fibrosis transmembrane conductance regulator and regulates its membrane trafficking in epithelial cells.
Lee et al., Seoul, South Korea. In J Biol Chem, 2010
Results suggest that STX16 mediates recycling of CFTR and constitutes an important component of CFTR trafficking machinery in intestinal epithelial cells.
Aurora B-mediated phosphorylation of RASSF1A maintains proper cytokinesis by recruiting Syntaxin16 to the midzone and midbody.
Lim et al., Taejŏn, South Korea. In Cancer Res, 2009
phosphorylation of RASSF1A by Aurora B is required for the recruitment of Syntaxin16
Syntaxin 16 is enriched in neuronal dendrites and may have a role in neurite outgrowth.
Tang et al., Singapore, Singapore. In Mol Membr Biol, 2008
Syntaxin 16 may thus play a role in neurite outgrowth and perhaps other specific dendritic anterograde/retrograde traffic.
The GNAS locus and pseudohypoparathyroidism.
Bastepe, Boston, United States. In Adv Exp Med Biol, 2007
A unique 3-kb microdeletion that disrupts the neighboring STX16 1ocus has been identified in this disorder and appears to be the cause of the loss of imprinting.
Lack of Gnas epigenetic changes and pseudohypoparathyroidism type Ib in mice with targeted disruption of syntaxin-16.
Jüppner et al., Boston, United States. In Endocrinology, 2007
Mice genetically altered to carry the equivalent of STX16del4-6 contributing to pseudohypoparathyroidism type 1b.
Syntaxin 16 and syntaxin 5 are required for efficient retrograde transport of several exogenous and endogenous cargo proteins.
Johannes et al., Paris, France. In J Cell Sci, 2007
function of syntaxin 16 was specifically required for, and restricted to, the retrograde pathway
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