4ahi: Difference between revisions

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-{{STRUCTURE_4ahi|  PDB=4ahi  |  SCENE=  }}
+==K40I - Angiogenin mutants and amyotrophic lateral sclerosis - a biochemical and biological analysis==
-===K40I - Angiogenin mutants and amyotrophic lateral sclerosis - a biochemical and biological analysis===
+<StructureSection load='4ahi' size='340' side='right' caption='[[4ahi]], [[Resolution|resolution]] 2.80&Aring;' scene=''>
-{{ABSTRACT_PUBMED_23047679}}
+== Structural highlights ==
+<table><tr><td colspan='2'>[[4ahi]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4AHI OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4AHI FirstGlance]. <br>
+</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1hby|1hby]], [[1h53|1h53]], [[2ang|2ang]], [[1un3|1un3]], [[1a4y|1a4y]], [[1b1j|1b1j]], [[1un4|1un4]], [[1un5|1un5]], [[1h0d|1h0d]], [[1k59|1k59]], [[1b1e|1b1e]], [[1k5b|1k5b]], [[1k58|1k58]], [[1ang|1ang]], [[1k5a|1k5a]], [[1awz|1awz]], [[1b1i|1b1i]], [[1h52|1h52]], [[4ahf|4ahf]], [[4ahe|4ahe]], [[4ahd|4ahd]], [[4ahh|4ahh]], [[4ahj|4ahj]], [[4ahk|4ahk]], [[4ahl|4ahl]], [[4ahm|4ahm]], [[4ahg|4ahg]]</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=4ahi FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4ahi OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4ahi RCSB], [http://www.ebi.ac.uk/pdbsum/4ahi PDBsum]</span></td></tr>
+</table>
+== Disease ==
+[[http://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] Defects in ANG are the cause of susceptibility to amyotrophic lateral sclerosis type 9 (ALS9) [MIM:[http://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 ==
+[[http://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>
+<div style="background-color:#fffaf0;">
+== Publication Abstract from PubMed ==
+Mutations in angiogenin (ANG), a member of the ribonuclease A superfamily, are associated with amyotrophic lateral sclerosis (ALS; sporadic and familial) and Parkinson's disease. We have previously shown that ANG is expressed in neurons during neuro-ectodermal differentiation, and that it has both neurotrophic and neuroprotective functions. Here we report the atomic resolution structure of native ANG and 11 ANG-ALS variants. We correlate the structural changes to the effects on neuronal survival and the ability to induce stress granules in neuronal cell lines. ANG-ALS variants that affect the structure of the catalytic site and either decrease or increase the RNase activity affect neuronal survival. Neuronal cell lines expressing the ANG-ALS variants also lack the ability to form stress granules. Our structure-function studies on these ANG-ALS variants are the first to provide insights into the cellular and molecular mechanisms underlying their role in ALS.
-==Disease==
+Structural and molecular insights into the mechanism of action of human angiogenin-ALS variants in neurons.,Thiyagarajan N, Ferguson R, Subramanian V, Acharya KR Nat Commun. 2012 Oct 9;3:1121. doi: 10.1038/ncomms2126. PMID:23047679<ref>PMID:23047679</ref>
-[[http://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] Defects in ANG are the cause of susceptibility to amyotrophic lateral sclerosis type 9 (ALS9) [MIM:[http://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==
+From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
-[[http://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>
+</div>
+== References ==
-==About this Structure==
+<references/>
-[[4ahi]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4AHI OCA].
+__TOC__
+</StructureSection>
-==Reference==
-<references group="xtra"/><references/>
 [[Category: Homo sapiens]]
-[[Category: Acharya, K R.]]
+[[Category: Acharya, K R]]
-[[Category: Ferguson, R.]]
+[[Category: Ferguson, R]]
-[[Category: Pham, T.]]
+[[Category: Pham, T]]
-[[Category: Saha, S.]]
+[[Category: Saha, S]]
-[[Category: Subramanian, V.]]
+[[Category: Subramanian, V]]
-[[Category: Thiyagarajan, N.]]
+[[Category: Thiyagarajan, N]]
 [[Category: Amyotrophic]]
 [[Category: Hydrolase]]
 [[Category: Lateral sclerosis]]
 [[Category: Neovascularisation]]