STX16_HUMAN » Syntaxin-16

STX16_HUMAN » Syntaxin-16
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Topology in Golgi apparatus membrane
TopologyGolgi lumenal side
cytoplasmic side
STX16_HUMAN » Syntaxin-16 » Syn16;
Hydrophobic Thickness 34.8 ± 1.1 Å
Tilt Angle 0 ± 13°
ΔGtransfer -32.4 kcal/mol
ΔGfold -28.6 kcal/mol
Links UniProtKB, Pfam, Interpro, iHOP, STRING, HGNC
Topology In
TM Segments 301-323 (292-324)
Pathways

Neuronal System (Reactome)

SNARE interactions in vesicular transport (KEGG)

PDB none
OPM none
Complexes none
Interactions

STX4, Complex: STX4:STX16

STX6, Complex: STX6:STX16, PubMed

STX6, Complex: VTI1B:STX6:STX16:VTI1A:VAMP4

VAMP3, Complex: VAMP3:STX16, PubMed

VAMP4, Complex: VAMP4:STX16, PubMed

VAMP5, Complex: STX16:VAMP5

VTI1A, Complex: STX16:VTI1A, PubMed

Domains

AA: 77-265, PDBID: 1BR0, Subunit A, Seq Identity:16%, Syntaxin

AA: 266-318, PDBID: 2NPS, Subunit B, Seq Identity:41%, SNARE domain

UniProt annotation for STX16_HUMAN » Syntaxin-16
FUNCTION: SNARE involved in vesicular transport from the late endosomes to the trans-Golgi network.

SUBUNIT: Interacts with GCC2.

TISSUE SPECIFICITY: Ubiquitous.

DISEASE: Pseudohypoparathyroidism 1B (PHP1B) OMIM: A disorder characterized by end-organ resistance to parathyroid hormone, hypocalcemia and hyperphosphatemia. Patients affected with PHP1B lack developmental defects characteristic of Albright hereditary osteodystrophy, and typically show no other endocrine abnormalities besides resistance to PTH. Note=The gene represented in this entry is involved in disease pathogenesis. Microdeletions involving STX16 can cause loss of methylation at exon A/B of GNAS, resulting in PHP1B.

UniProt features for STX16_HUMAN » Syntaxin-16
CHAIN 1 325 Syntaxin-16.
DOMAIN 230 292 t-SNARE coiled-coil homology.
Amino Acid Sequence for STX16_HUMAN » Syntaxin-16
MATRRLTDAF LLLRNNSIQN RQLLAEQVSS HITSSPLHSR SIAAELDELA DDRMALVSGI SLDPEAAIGV TKRPPPKWVD GVDEIQYDVG RIKQKMKELA SLHDKHLNRP TLDDSSEEEH AIEITTQEIT QLFHRCQRAV QALPSRARAC SEQEGRLLGN VVASLAQALQ ELSTSFRHAQ SGYLKRMKNR EERSQHFFDT SVPLMDDGDD NTLYHRGFTE DQLVLVEQNT LMVEEREREI RQIVQSISDL NEIFRDLGAM IVEQGTVLDR IDYNVEQSCI KTEDGLKQLH KAEQYQKKNR KMLVILILFV IIIVLIVVLV GVKSR