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Gene Review

STX16  -  syntaxin 16

Homo sapiens

Synonyms: SYN16, Syn16, Syntaxin-16, hsyn16
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Disease relevance of STX16


High impact information on STX16

  • The deleted region, which is flanked by two direct repeats, includes three exons of STX16, the gene encoding syntaxin-16, for which no evidence of imprinting could be found [2].
  • In the presence of either of the two microdeletions, parathyroid hormone resistance appears to develop over time, as documented in an affected individual who was diagnosed at birth with the 4.4-kb deletion of STX16 and who had normal serum parathyroid hormone levels until the age of 21 mo [1].
  • The kinetic characterization of inhibition by anti-Golgin-97 antibody in comparison with anti-Syntaxin 16 antibody established that Golgin-97 acts before Syntaxin 16 in endosome-to-TGN transport [3].
  • The kinetics of inhibition exhibited by syntaxin 16 and syntaxin 5 antibodies is similar [4].
  • Therefore, in spite of its co-localization and possible interaction with syntaxin 16, syntaxin 10 is not part of the syntaxin 16-based SNARE complex involved in endosome-TGN transport, and may have a hitherto unrecognized function in the TGN-endosome boundary [5].

Biological context of STX16

  • The novel 4.4-kb microdeletion overlaps with the previously identified deletion by 1,286 bp and, similar to the latter deletion, removes several exons of STX16 (encoding syntaxin-16) [1].
  • Affected individuals from this kindred share an epigenetic defect that is indistinguishable from that observed in patients with AD-PHP-Ib who carry the 3-kb microdeletion in the STX16 region (i.e., an isolated loss of methylation at GNAS exon A/B) [1].
  • Two frequent tetra-nucleotide repeat polymorphisms between VAPB and STX16 on chromosome 20q13 [6].

Anatomical context of STX16


Other interactions of STX16

  • Third, E. chaffeensis also inhibited the gene transcription of RAB5A, SNAP23, and STX16, which are involved in membrane trafficking [9].

Analytical, diagnostic and therapeutic context of STX16


  1. A novel STX16 deletion in autosomal dominant pseudohypoparathyroidism type Ib redefines the boundaries of a cis-acting imprinting control element of GNAS. Linglart, A., Gensure, R.C., Olney, R.C., Jüppner, H., Bastepe, M. Am. J. Hum. Genet. (2005) [Pubmed]
  2. Autosomal dominant pseudohypoparathyroidism type Ib is associated with a heterozygous microdeletion that likely disrupts a putative imprinting control element of GNAS. Bastepe, M., Fröhlich, L.F., Hendy, G.N., Indridason, O.S., Josse, R.G., Koshiyama, H., Körkkö, J., Nakamoto, J.M., Rosenbloom, A.L., Slyper, A.H., Sugimoto, T., Tsatsoulis, A., Crawford, J.D., Jüppner, H. J. Clin. Invest. (2003) [Pubmed]
  3. Autoantigen Golgin-97, an effector of Arl1 GTPase, participates in traffic from the endosome to the trans-golgi network. Lu, L., Tai, G., Hong, W. Mol. Biol. Cell (2004) [Pubmed]
  4. Participation of the syntaxin 5/Ykt6/GS28/GS15 SNARE complex in transport from the early/recycling endosome to the trans-Golgi network. Tai, G., Lu, L., Wang, T.L., Tang, B.L., Goud, B., Johannes, L., Hong, W. Mol. Biol. Cell (2004) [Pubmed]
  5. Trans-Golgi network syntaxin 10 functions distinctly from syntaxins 6 and 16. Wang, Y., Tai, G., Lu, L., Johannes, L., Hong, W., Luen Tang, B. Mol. Membr. Biol. (2005) [Pubmed]
  6. Two frequent tetra-nucleotide repeat polymorphisms between VAPB and STX16 on chromosome 20q13. Bastepe, M., Pincus, J.E., Jüppner, H. Mol. Cell. Probes (1999) [Pubmed]
  7. Molecular cloning and localization of human syntaxin 16, a member of the syntaxin family of SNARE proteins. Tang, B.L., Low, D.Y., Lee, S.S., Tan, A.E., Hong, W. Biochem. Biophys. Res. Commun. (1998) [Pubmed]
  8. The SNAREs vti1a and vti1b have distinct localization and SNARE complex partners. Kreykenbohm, V., Wenzel, D., Antonin, W., Atlachkine, V., von Mollard, G.F. Eur. J. Cell Biol. (2002) [Pubmed]
  9. Survival strategy of obligately intracellular Ehrlichia chaffeensis: novel modulation of immune response and host cell cycles. Zhang, J.Z., Sinha, M., Luxon, B.A., Yu, X.J. Infect. Immun. (2004) [Pubmed]
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