Annotation Extension Relation:dependent on: Difference between revisions

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===Range===
===Range===


ENTITY_UNION:0000007 ! chemical, gene product, complex, cellular component, modification or sequence feature
[[ENTITY_UNION:0000007]] ! chemical, gene product, complex, cellular component, modification or sequence feature


==Annotation Extension Usage Examples==
==Annotation Extension Usage Examples==

Revision as of 09:45, 1 August 2012

Definition

Child terms

localization_dependent_on

requires_localization

requires_modification

requires_regulator

requires_sequence_feature

requires_substance

requires_target_sequence_feature

Scope of use

Domain

BFO:0000001 ! entity (Biological Process, Molecular Function, Cellular Component)

Range

ENTITY_UNION:0000007 ! chemical, gene product, complex, cellular component, modification or sequence feature

Annotation Extension Usage Examples

IAP2-dependent regulation of NF-kB activity:

Statement from paper:

To test whether RIP3 and RIP4 have to be ubiquitinated by cIAP1/2 in order to mediate NF-kB activation, we compared RIP-mediated NF-kB luciferase reporter activity when ectopically expressed in HEK293T cells in the presence or absence of the IAP inhibitor BV6, a treatment that induces rapid auto-ubiquitination and degradation of endogenous cIAP1/2[41]. As shown in Figure 4A, BV6 treatment greatly impaired TNF and RIP1–RIP4-induced NF-kB activation but had no impact on TAK1-mediated NF-kB induction (Figure 4A). Those results, which indicate that cIAP1/2 act upstream of TAK1, are consistent with a role for cIAP1/2 as E3 ligases regulating RIP1–4-mediated activation of NF-kB.


Gene Name (col 2) GO ID (col 5) Reference (col 6) Evidence (col 7) Annotation Extension (col 16)
Q9Y572 RIP3 GO:0051092 positive regulation of NF-kappaB transcription factor activity PMID:21931591 IDA

dependent_on(UniProtKB:Q13490 IAP2)


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