4oav: Difference between revisions
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' | {{STRUCTURE_4oav| PDB=4oav | SCENE= }} | ||
===Complete human RNase L in complex with 2-5A (5'-ppp heptamer), AMPPCP and RNA substrate.=== | |||
{{ABSTRACT_PUBMED_24578532}} | |||
==Disease== | |||
[[http://www.uniprot.org/uniprot/RN5A_HUMAN RN5A_HUMAN]] Defects in RNASEL are a cause of susceptibility to prostate cancer hereditary type 1 (HPC1) [MIM:[http://omim.org/entry/601518 601518]]. It is a condition associated with familial predisposition to cancer of the prostate. Most prostate cancers are adenocarcinomas that develop in the acini of the prostatic ducts. Other rare histopathologic types of prostate cancer that occur in approximately 5% of patients include small cell carcinoma, mucinous carcinoma, prostatic ductal carcinoma, transitional cell carcinoma, squamous cell carcinoma, basal cell carcinoma, adenoid cystic carcinoma (basaloid), signet-ring cell carcinoma and neuroendocrine carcinoma. | |||
==Function== | |||
[[http://www.uniprot.org/uniprot/RN5A_HUMAN RN5A_HUMAN]] Endoribonuclease that functions in the interferon (IFN) antiviral response. In INF treated and virus infected cells, RNASEL probably mediates its antiviral effects through a combination of direct cleavage of single-stranded viral RNAs, inhibition of protein synthesis through the degradation of rRNA, induction of apoptosis, and induction of other antiviral genes. RNASEL mediated apoptosis is the result of a JNK-dependent stress-response pathway leading to cytochrome c release from mitochondria and caspase-dependent apoptosis. Therefore, activation of RNASEL could lead to elimination of virus infected cells under some circumstances. Might play a central role in the regulation of mRNA turnover.<ref>PMID:11585831</ref> | |||
==About this Structure== | |||
[[4oav]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4OAV OCA]. | |||
==Reference== | |||
<ref group="xtra">PMID:024578532</ref><references group="xtra"/><references/> | |||
[[Category: Chitrakar, A.]] | |||
[[Category: Donovan, J.]] | |||
[[Category: Han, Y.]] | |||
[[Category: Korennykh, A.]] | |||
[[Category: Rath, S.]] | |||
[[Category: Whitney, G.]] | |||
[[Category: 2s']] | |||
[[Category: 2-5a]] | |||
[[Category: 5'-linked oligoadenylate]] | |||
[[Category: 5'-oligoadenylate]] | |||
[[Category: Antiviral response]] | |||
[[Category: Dsrna]] | |||
[[Category: Dsrna response]] | |||
[[Category: Hpc1]] | |||
[[Category: Hydrolase-rna complex]] | |||
[[Category: Innate immune response]] | |||
[[Category: Interferon]] | |||
[[Category: Ire1]] | |||
[[Category: Ken-domain containing]] | |||
[[Category: Kinase]] | |||
[[Category: Pseudokinase]] | |||
[[Category: Regulated rna decay]] | |||
[[Category: Ridd]] | |||
[[Category: Rna]] | |||
[[Category: Rna decay]] | |||
[[Category: Rnase]] | |||
[[Category: Rnase l protein kinase]] | |||
Revision as of 16:40, 12 March 2014
Complete human RNase L in complex with 2-5A (5'-ppp heptamer), AMPPCP and RNA substrate.Complete human RNase L in complex with 2-5A (5'-ppp heptamer), AMPPCP and RNA substrate.
Template:ABSTRACT PUBMED 24578532
DiseaseDisease
[RN5A_HUMAN] Defects in RNASEL are a cause of susceptibility to prostate cancer hereditary type 1 (HPC1) [MIM:601518]. It is a condition associated with familial predisposition to cancer of the prostate. Most prostate cancers are adenocarcinomas that develop in the acini of the prostatic ducts. Other rare histopathologic types of prostate cancer that occur in approximately 5% of patients include small cell carcinoma, mucinous carcinoma, prostatic ductal carcinoma, transitional cell carcinoma, squamous cell carcinoma, basal cell carcinoma, adenoid cystic carcinoma (basaloid), signet-ring cell carcinoma and neuroendocrine carcinoma.
FunctionFunction
[RN5A_HUMAN] Endoribonuclease that functions in the interferon (IFN) antiviral response. In INF treated and virus infected cells, RNASEL probably mediates its antiviral effects through a combination of direct cleavage of single-stranded viral RNAs, inhibition of protein synthesis through the degradation of rRNA, induction of apoptosis, and induction of other antiviral genes. RNASEL mediated apoptosis is the result of a JNK-dependent stress-response pathway leading to cytochrome c release from mitochondria and caspase-dependent apoptosis. Therefore, activation of RNASEL could lead to elimination of virus infected cells under some circumstances. Might play a central role in the regulation of mRNA turnover.[1]
About this StructureAbout this Structure
4oav is a 4 chain structure. Full crystallographic information is available from OCA.
ReferenceReference
- ↑ Han Y, Donovan J, Rath S, Whitney G, Chitrakar A, Korennykh A. Structure of Human RNase L Reveals the Basis for Regulated RNA Decay in the IFN Response. Science. 2014 Feb 27. PMID:24578532 doi:http://dx.doi.org/10.1126/science.1249845
- ↑ Le Roy F, Bisbal C, Silhol M, Martinand C, Lebleu B, Salehzada T. The 2-5A/RNase L/RNase L inhibitor (RLI) [correction of (RNI)] pathway regulates mitochondrial mRNAs stability in interferon alpha-treated H9 cells. J Biol Chem. 2001 Dec 21;276(51):48473-82. Epub 2001 Oct 3. PMID:11585831 doi:10.1074/jbc.M107482200
Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)
OCA- Chitrakar, A.
- Donovan, J.
- Han, Y.
- Korennykh, A.
- Rath, S.
- Whitney, G.
- 2s'
- 2-5a
- 5'-linked oligoadenylate
- 5'-oligoadenylate
- Antiviral response
- Dsrna
- Dsrna response
- Hpc1
- Hydrolase-rna complex
- Innate immune response
- Interferon
- Ire1
- Ken-domain containing
- Kinase
- Pseudokinase
- Regulated rna decay
- Ridd
- Rna
- Rna decay
- Rnase
- Rnase l protein kinase