7pnp: Difference between revisions
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==Human Angiogenin mutant-S28A== | ==Human Angiogenin mutant-S28A== | ||
<StructureSection load='7pnp' size='340' side='right'caption='[[7pnp]]' scene=''> | <StructureSection load='7pnp' size='340' side='right'caption='[[7pnp]], [[Resolution|resolution]] 1.80Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7PNP OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7PNP FirstGlance]. <br> | <table><tr><td colspan='2'>[[7pnp]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7PNP OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7PNP FirstGlance]. <br> | ||
</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=7pnp FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7pnp OCA], [https://pdbe.org/7pnp PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7pnp RCSB], [https://www.ebi.ac.uk/pdbsum/7pnp PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7pnp ProSAT]</span></td></tr> | </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=7pnp FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7pnp OCA], [https://pdbe.org/7pnp PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7pnp RCSB], [https://www.ebi.ac.uk/pdbsum/7pnp PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7pnp ProSAT]</span></td></tr> | ||
</table> | </table> | ||
== Disease == | |||
[https://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN] Defects in ANG are the cause of susceptibility to amyotrophic lateral sclerosis type 9 (ALS9) [MIM:[https://omim.org/entry/611895 611895]. ALS is a degenerative disorder of motor neurons in the cortex, brain stem and spinal cord. ALS is characterized by muscular weakness and atrophy.<ref>PMID:17886298</ref> <ref>PMID:15557516</ref> <ref>PMID:16501576</ref> <ref>PMID:17900154</ref> <ref>PMID:18087731</ref> <ref>PMID:17703939</ref> | |||
== Function == | |||
[https://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN] May function as a tRNA-specific ribonuclease that abolishes protein synthesis by specifically hydrolyzing cellular tRNAs. Binds to actin on the surface of endothelial cells; once bound, angiogenin is endocytosed and translocated to the nucleus. Angiogenin induces vascularization of normal and malignant tissues. Angiogenic activity is regulated by interaction with RNH1 in vivo.<ref>PMID:1400510</ref> <ref>PMID:19354288</ref> | |||
== References == | |||
<references/> | |||
__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
[[Category: Homo sapiens]] | |||
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
[[Category: Leonidas DD]] | [[Category: Leonidas DD]] | ||
[[Category: Papaioannou OSE]] | [[Category: Papaioannou OSE]] |
Revision as of 08:49, 31 May 2023
Human Angiogenin mutant-S28AHuman Angiogenin mutant-S28A
Structural highlights
DiseaseANGI_HUMAN Defects in ANG are the cause of susceptibility to amyotrophic lateral sclerosis type 9 (ALS9) [MIM:611895. ALS is a degenerative disorder of motor neurons in the cortex, brain stem and spinal cord. ALS is characterized by muscular weakness and atrophy.[1] [2] [3] [4] [5] [6] FunctionANGI_HUMAN May function as a tRNA-specific ribonuclease that abolishes protein synthesis by specifically hydrolyzing cellular tRNAs. Binds to actin on the surface of endothelial cells; once bound, angiogenin is endocytosed and translocated to the nucleus. Angiogenin induces vascularization of normal and malignant tissues. Angiogenic activity is regulated by interaction with RNH1 in vivo.[7] [8] References
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