1hes: Difference between revisions
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{{STRUCTURE_1hes| PDB=1hes | SCENE= }} | {{STRUCTURE_1hes| PDB=1hes | SCENE= }} | ||
===MU2 ADAPTIN SUBUNIT (AP50) OF AP2 ADAPTOR (SECOND DOMAIN), COMPLEXED WITH P-SELECTIN INTERNALIZATION PEPTIDE SHLGTYGVFTNAA=== | |||
{{ABSTRACT_PUBMED_11247301}} | |||
=== | ==Disease== | ||
[[http://www.uniprot.org/uniprot/LYAM3_HUMAN LYAM3_HUMAN]] Defects in SELP may be a cause of susceptibility to ischemic stroke (ISCHSTR) [MIM:[http://omim.org/entry/601367 601367]]; also known as cerebrovascular accident or cerebral infarction. A stroke is an acute neurologic event leading to death of neural tissue of the brain and resulting in loss of motor, sensory and/or cognitive function. Ischemic strokes, resulting from vascular occlusion, is considered to be a highly complex disease consisting of a group of heterogeneous disorders with multiple genetic and environmental risk factors.<ref>PMID:14681304</ref> | |||
==Function== | |||
[[http://www.uniprot.org/uniprot/LYAM3_HUMAN LYAM3_HUMAN]] Ca(2+)-dependent receptor for myeloid cells that binds to carbohydrates on neutrophils and monocytes. Mediates the interaction of activated endothelial cells or platelets with leukocytes. The ligand recognized is sialyl-Lewis X. Mediates rapid rolling of leukocyte rolling over vascular surfaces during the initial steps in inflammation through interaction with PSGL1.<ref>PMID:7585950</ref> | |||
==About this Structure== | ==About this Structure== | ||
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==Reference== | ==Reference== | ||
<ref group="xtra">PMID:011247301</ref><references group="xtra"/> | <ref group="xtra">PMID:011247301</ref><references group="xtra"/><references/> | ||
[[Category: Rattus norvegicus]] | [[Category: Rattus norvegicus]] | ||
[[Category: Evans, P R.]] | [[Category: Evans, P R.]] | ||
Revision as of 04:53, 25 March 2013
MU2 ADAPTIN SUBUNIT (AP50) OF AP2 ADAPTOR (SECOND DOMAIN), COMPLEXED WITH P-SELECTIN INTERNALIZATION PEPTIDE SHLGTYGVFTNAAMU2 ADAPTIN SUBUNIT (AP50) OF AP2 ADAPTOR (SECOND DOMAIN), COMPLEXED WITH P-SELECTIN INTERNALIZATION PEPTIDE SHLGTYGVFTNAA
Template:ABSTRACT PUBMED 11247301
DiseaseDisease
[LYAM3_HUMAN] Defects in SELP may be a cause of susceptibility to ischemic stroke (ISCHSTR) [MIM:601367]; also known as cerebrovascular accident or cerebral infarction. A stroke is an acute neurologic event leading to death of neural tissue of the brain and resulting in loss of motor, sensory and/or cognitive function. Ischemic strokes, resulting from vascular occlusion, is considered to be a highly complex disease consisting of a group of heterogeneous disorders with multiple genetic and environmental risk factors.[1]
FunctionFunction
[LYAM3_HUMAN] Ca(2+)-dependent receptor for myeloid cells that binds to carbohydrates on neutrophils and monocytes. Mediates the interaction of activated endothelial cells or platelets with leukocytes. The ligand recognized is sialyl-Lewis X. Mediates rapid rolling of leukocyte rolling over vascular surfaces during the initial steps in inflammation through interaction with PSGL1.[2]
About this StructureAbout this Structure
1hes is a 2 chain structure with sequence from Rattus norvegicus. Full crystallographic information is available from OCA.
ReferenceReference
- ↑ Zee RY, Cook NR, Cheng S, Reynolds R, Erlich HA, Lindpaintner K, Ridker PM. Polymorphism in the P-selectin and interleukin-4 genes as determinants of stroke: a population-based, prospective genetic analysis. Hum Mol Genet. 2004 Feb 15;13(4):389-96. Epub 2003 Dec 17. PMID:14681304 doi:10.1093/hmg/ddh039
- ↑ Pouyani T, Seed B. PSGL-1 recognition of P-selectin is controlled by a tyrosine sulfation consensus at the PSGL-1 amino terminus. Cell. 1995 Oct 20;83(2):333-43. PMID:7585950