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http://www.nanopub.org/nschema#hasProvenance
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http://www.tkuhn.ch/bel2nanopub/RARFCDrn9hkz-c_wquCf3gsrfVJSQj_S6wg_35YjXPf4s
http://www.nanopub.org/nschema#hasPublicationInfo
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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.tkuhn.ch/bel2nanopub/RARFCDrn9hkz-c_wquCf3gsrfVJSQj_S6wg_35YjXPf4s#_1
http://www.selventa.com/vocabulary/variantOf
http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=990
http://www.tkuhn.ch/bel2nanopub/RARFCDrn9hkz-c_wquCf3gsrfVJSQj_S6wg_35YjXPf4s#_1
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://www.ebi.ac.uk/ontology-lookup/?termId=MOD:00000
http://www.tkuhn.ch/bel2nanopub/RARFCDrn9hkz-c_wquCf3gsrfVJSQj_S6wg_35YjXPf4s#_1
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://www.ebi.ac.uk/ontology-lookup/?termId=MOD:00696
http://www.tkuhn.ch/bel2nanopub/RARFCDrn9hkz-c_wquCf3gsrfVJSQj_S6wg_35YjXPf4s#_2
http://purl.obolibrary.org/obo/BFO_0000066
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http://www.w3.org/1999/02/22-rdf-syntax-ns#object
http://purl.bioontology.org/ontology/MSH/D017209
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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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p(HGNC:BCL2,pmod(P,T,69)) -| bp(MESHPP:Apoptosis)
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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1.4
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Single-site phosphorylation at serine 70 (S70) is required for Bcl2's antiapoptotic function, and multisite phosphorylation at threonine 69 (T69), S70, and S87 has been reported to inactivate Bcl2. To address this apparent conflict and identify the regulatory role for Bcl2 phosphorylation in cell death and cell cycle control, a series of serine/threonine (S/T) --> glutamate/alanine (E/A) mutants including T69E/A, S70E/A, S87E/A, T69E/S70A/S87A (EAA), T69A/S70E/S87A (AEA), T69A/S70A/S87E (AAE), T69E/S70E/S87E (EEE), and T69A/S70A/S87A (AAA) was created to mimic or abrogate, respectively, either single-site or multisite phosphorylation. The survival and cell cycle status of cells expressing the phosphomimetic or nonphosphorylatable Bcl2 mutants were compared. Surprisingly, all of the E but not the A Bcl2 mutants potently enhance cell survival after stress and retard G(1)/S cell cycle transition. The EEE Bcl2 mutant is the most potent, indicating a possible cumulative advantage for multisite phosphorylation of Bcl2 in survival and retardation of G(1)/S transition functions.
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http://www.w3.org/ns/prov#wasQuotedFrom
http://www.ncbi.nlm.nih.gov/pubmed/14660795
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http://www.w3.org/2000/01/rdf-schema#label
Selventa
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http://www.w3.org/ns/prov#hadPrimarySource
http://www.ncbi.nlm.nih.gov/pubmed/14660795
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http://www.w3.org/ns/prov#wasDerivedFrom
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http://www.tkuhn.ch/bel2nanopub/RARFCDrn9hkz-c_wquCf3gsrfVJSQj_S6wg_35YjXPf4s#pubinfo
http://www.tkuhn.ch/bel2nanopub/RARFCDrn9hkz-c_wquCf3gsrfVJSQj_S6wg_35YjXPf4s
http://purl.org/dc/terms/created
2014-07-03T14:30:18.888+02:00
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http://orcid.org/0000-0001-6818-334X
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