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| | ==Cryo-EM structure of Seneca Valley Virus-Anthrax Toxin Receptor 1 complex== | | ==Cryo-EM structure of Seneca Valley Virus-Anthrax Toxin Receptor 1 complex== |
| - | <StructureSection load='6cx1' size='340' side='right' caption='[[6cx1]], [[Resolution|resolution]] 3.80Å' scene=''> | + | <SX load='6cx1' size='340' side='right' viewer='molstar' caption='[[6cx1]], [[Resolution|resolution]] 3.80Å' scene=''> |
| | == Structural highlights == | | == Structural highlights == |
| - | <table><tr><td colspan='2'>[[6cx1]] is a 5 chain structure with sequence from [http://en.wikipedia.org/wiki/ ] and [http://en.wikipedia.org/wiki/Senecavirus_a Senecavirus a]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6CX1 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6CX1 FirstGlance]. <br> | + | <table><tr><td colspan='2'>[[6cx1]] is a 5 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Senecavirus_A Senecavirus A]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6CX1 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6CX1 FirstGlance]. <br> |
| - | </td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6cx1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6cx1 OCA], [http://pdbe.org/6cx1 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6cx1 RCSB], [http://www.ebi.ac.uk/pdbsum/6cx1 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6cx1 ProSAT]</span></td></tr> | + | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution|Resolution]] 3.8Å</td></tr> |
| | + | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=6cx1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6cx1 OCA], [https://pdbe.org/6cx1 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6cx1 RCSB], [https://www.ebi.ac.uk/pdbsum/6cx1 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6cx1 ProSAT]</span></td></tr> |
| | </table> | | </table> |
| | == Disease == | | == Disease == |
| - | [[http://www.uniprot.org/uniprot/ANTR1_HUMAN ANTR1_HUMAN]] Defects in ANTXR1 are associated with susceptibility to hemangioma capillary infantile (HCI) [MIM:[http://omim.org/entry/602089 602089]]. HCI are benign, highly proliferative lesions involving aberrant localized growth of capillary endothelium. They are the most common tumor of infancy, occurring in up to 10% of all births. Hemangiomas tend to appear shortly after birth and show rapid neonatal growth for up to 12 months characterized by endothelial hypercellularity and increased numbers of mast cells. This phase is followed by slow involution at a rate of about 10% per year and replacement by fibrofatty stroma.<ref>PMID:18931684</ref> | + | [https://www.uniprot.org/uniprot/ANTR1_HUMAN ANTR1_HUMAN] Defects in ANTXR1 are associated with susceptibility to hemangioma capillary infantile (HCI) [MIM:[https://omim.org/entry/602089 602089]. HCI are benign, highly proliferative lesions involving aberrant localized growth of capillary endothelium. They are the most common tumor of infancy, occurring in up to 10% of all births. Hemangiomas tend to appear shortly after birth and show rapid neonatal growth for up to 12 months characterized by endothelial hypercellularity and increased numbers of mast cells. This phase is followed by slow involution at a rate of about 10% per year and replacement by fibrofatty stroma.<ref>PMID:18931684</ref> |
| | == Function == | | == Function == |
| - | [[http://www.uniprot.org/uniprot/ANTR1_HUMAN ANTR1_HUMAN]] Plays a role in cell attachment and migration. Interacts with extracellular matrix proteins and with the actin cytoskeleton. Mediates adhesion of cells to type 1 collagen and gelatin, reorganization of the actin cytoskeleton and promotes cell spreading. Plays a role in the angiogenic response of cultured umbilical vein endothelial cells.<ref>PMID:15777794</ref> <ref>PMID:16762926</ref> | + | [https://www.uniprot.org/uniprot/ANTR1_HUMAN ANTR1_HUMAN] Plays a role in cell attachment and migration. Interacts with extracellular matrix proteins and with the actin cytoskeleton. Mediates adhesion of cells to type 1 collagen and gelatin, reorganization of the actin cytoskeleton and promotes cell spreading. Plays a role in the angiogenic response of cultured umbilical vein endothelial cells.<ref>PMID:15777794</ref> <ref>PMID:16762926</ref> |
| | == References == | | == References == |
| | <references/> | | <references/> |
| | __TOC__ | | __TOC__ |
| - | </StructureSection> | + | </SX> |
| - | [[Category: Senecavirus a]] | + | [[Category: Homo sapiens]] |
| - | [[Category: Bostina, M]] | + | [[Category: Large Structures]] |
| - | [[Category: Burga, L]] | + | [[Category: Senecavirus A]] |
| - | [[Category: Easingwood, R]] | + | [[Category: Bostina M]] |
| - | [[Category: Jayawardena, N]]
| + | [[Category: Burga L]] |
| - | [[Category: Takizawa, Y]]
| + | [[Category: Easingwood R]] |
| - | [[Category: Wolf, M]]
| + | [[Category: Jayawardena N]] |
| - | [[Category: Anthrax toxin receptor]] | + | [[Category: Takizawa Y]] |
| - | [[Category: Picornavirus]] | + | [[Category: Wolf M]] |
| - | [[Category: Senecavirus]] | + | |
| - | [[Category: Virus]] | + | |
| - | [[Category: Virus-receptor complex]] | + | |
| Structural highlights
Disease
ANTR1_HUMAN Defects in ANTXR1 are associated with susceptibility to hemangioma capillary infantile (HCI) [MIM:602089. HCI are benign, highly proliferative lesions involving aberrant localized growth of capillary endothelium. They are the most common tumor of infancy, occurring in up to 10% of all births. Hemangiomas tend to appear shortly after birth and show rapid neonatal growth for up to 12 months characterized by endothelial hypercellularity and increased numbers of mast cells. This phase is followed by slow involution at a rate of about 10% per year and replacement by fibrofatty stroma.[1]
Function
ANTR1_HUMAN Plays a role in cell attachment and migration. Interacts with extracellular matrix proteins and with the actin cytoskeleton. Mediates adhesion of cells to type 1 collagen and gelatin, reorganization of the actin cytoskeleton and promotes cell spreading. Plays a role in the angiogenic response of cultured umbilical vein endothelial cells.[2] [3]
References
- ↑ Jinnin M, Medici D, Park L, Limaye N, Liu Y, Boscolo E, Bischoff J, Vikkula M, Boye E, Olsen BR. Suppressed NFAT-dependent VEGFR1 expression and constitutive VEGFR2 signaling in infantile hemangioma. Nat Med. 2008 Nov;14(11):1236-46. doi: 10.1038/nm.1877. Epub 2008 Oct 19. PMID:18931684 doi:10.1038/nm.1877
- ↑ Hotchkiss KA, Basile CM, Spring SC, Bonuccelli G, Lisanti MP, Terman BI. TEM8 expression stimulates endothelial cell adhesion and migration by regulating cell-matrix interactions on collagen. Exp Cell Res. 2005 Apr 15;305(1):133-44. PMID:15777794 doi:10.1016/j.yexcr.2004.12.025
- ↑ Werner E, Kowalczyk AP, Faundez V. Anthrax toxin receptor 1/tumor endothelium marker 8 mediates cell spreading by coupling extracellular ligands to the actin cytoskeleton. J Biol Chem. 2006 Aug 11;281(32):23227-36. Epub 2006 Jun 8. PMID:16762926 doi:10.1074/jbc.M603676200
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