2eel
From Proteopedia
(Difference between revisions)
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- | + | ==Solution structure of the CIDE-N domain of human cell death activator CIDE-A== | |
- | + | <StructureSection load='2eel' size='340' side='right' caption='[[2eel]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''> | |
- | + | == Structural highlights == | |
- | ==Disease== | + | <table><tr><td colspan='2'>[[2eel]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2EEL OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2EEL FirstGlance]. <br> |
- | [[http://www.uniprot.org/uniprot/CIDEA_HUMAN CIDEA_HUMAN]] Note=In omental and subcutaneous adipose tissue of obese patients matched for BMI, expression levels correlate with insulin sensitivity. Expression is increased 5-6 fold in the group of patients with high insulin sensitivity, compared to the insulin-resistant group. This observation is consistent with the idea that triglyceride storage in adipocytes plays an important role in sequestering triglycerides and fatty acids away from the circulation and peripheral tissues, thus enhancing insulin sensitivity in liver and muscle.<ref>PMID:18509062</ref> | + | </td></tr><tr><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">CIDEA ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr> |
- | + | <tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2eel FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2eel OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2eel RCSB], [http://www.ebi.ac.uk/pdbsum/2eel PDBsum], [http://www.topsan.org/Proteins/RSGI/2eel TOPSAN]</span></td></tr> | |
- | ==Function== | + | <table> |
- | [[http://www.uniprot.org/uniprot/CIDEA_HUMAN CIDEA_HUMAN]] Acts as a CEBPB coactivator in mammary epithelial cells to control the expression of a subset of CEBPB downstream target genes, including ID2, IGF1, PRLR, SOCS1, SOCS3, XDH, but not casein. By interacting with CEBPB, strengthens the association of CEBPB with the XDH promoter, increases histone acetylation and dissociates HDAC1 from the promoter (By similarity). Binds to lipid droplets and regulates their enlargement, thereby restricting lipolysis and favoring storage. At focal contact sites between lipid droplets, promotes directional net neutral lipid transfer from the smaller to larger lipid droplets. The transfer direction may be driven by the internal pressure difference between the contacting lipid droplet pair and occurs at a lower rate than that promoted by CIDEC. When overexpressed, induces apoptosis. The physiological significance of its role in apoptosis is unclear.<ref>PMID:19843876</ref> | + | == Disease == |
- | + | [[http://www.uniprot.org/uniprot/CIDEA_HUMAN CIDEA_HUMAN]] Note=In omental and subcutaneous adipose tissue of obese patients matched for BMI, expression levels correlate with insulin sensitivity. Expression is increased 5-6 fold in the group of patients with high insulin sensitivity, compared to the insulin-resistant group. This observation is consistent with the idea that triglyceride storage in adipocytes plays an important role in sequestering triglycerides and fatty acids away from the circulation and peripheral tissues, thus enhancing insulin sensitivity in liver and muscle.<ref>PMID:18509062</ref> | |
- | == | + | == Function == |
- | [[ | + | [[http://www.uniprot.org/uniprot/CIDEA_HUMAN CIDEA_HUMAN]] Acts as a CEBPB coactivator in mammary epithelial cells to control the expression of a subset of CEBPB downstream target genes, including ID2, IGF1, PRLR, SOCS1, SOCS3, XDH, but not casein. By interacting with CEBPB, strengthens the association of CEBPB with the XDH promoter, increases histone acetylation and dissociates HDAC1 from the promoter (By similarity). Binds to lipid droplets and regulates their enlargement, thereby restricting lipolysis and favoring storage. At focal contact sites between lipid droplets, promotes directional net neutral lipid transfer from the smaller to larger lipid droplets. The transfer direction may be driven by the internal pressure difference between the contacting lipid droplet pair and occurs at a lower rate than that promoted by CIDEC. When overexpressed, induces apoptosis. The physiological significance of its role in apoptosis is unclear.<ref>PMID:19843876</ref> |
- | + | == Evolutionary Conservation == | |
- | == | + | [[Image:Consurf_key_small.gif|200px|right]] |
- | <references | + | Check<jmol> |
+ | <jmolCheckbox> | ||
+ | <scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/ee/2eel_consurf.spt"</scriptWhenChecked> | ||
+ | <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked> | ||
+ | <text>to colour the structure by Evolutionary Conservation</text> | ||
+ | </jmolCheckbox> | ||
+ | </jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/chain_selection.php?pdb_ID=2ata ConSurf]. | ||
+ | <div style="clear:both"></div> | ||
+ | == References == | ||
+ | <references/> | ||
+ | __TOC__ | ||
+ | </StructureSection> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Hayashi, F.]] | [[Category: Hayashi, F.]] |
Revision as of 00:33, 30 September 2014
Solution structure of the CIDE-N domain of human cell death activator CIDE-A
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Categories: Homo sapiens | Hayashi, F. | Nagashima, T. | Qin, X R. | RSGI, RIKEN Structural Genomics/Proteomics Initiative. | Yokoyama, S. | Apoptosis | Cell death activator cide-a | Cell death-inducing dffa-like effector some | Cide-n domain | National project on protein structural and functional analyse | Nppsfa | Riken structural genomics/proteomics initiative | Rsgi | Structural genomic