1ang: Difference between revisions
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{{STRUCTURE_1ang| PDB=1ang | SCENE= }} | {{STRUCTURE_1ang| PDB=1ang | SCENE= }} | ||
===CRYSTAL STRUCTURE OF HUMAN ANGIOGENIN REVEALS THE STRUCTURAL BASIS FOR ITS FUNCTIONAL DIVERGENCE FROM RIBONUCLEASE=== | |||
{{ABSTRACT_PUBMED_8159679}} | |||
== | ==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> | |||
==About this Structure== | ==About this Structure== | ||
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==Reference== | ==Reference== | ||
<ref group="xtra">PMID:008159679</ref><ref group="xtra">PMID:009000628</ref><references group="xtra"/> | <ref group="xtra">PMID:008159679</ref><ref group="xtra">PMID:009000628</ref><references group="xtra"/><references/> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Acharya, K R.]] | [[Category: Acharya, K R.]] | ||
