Annotation Extension Relation:dependent on: Difference between revisions
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==Annotation Extension Usage Examples== | ==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.'' | |||
{| class="wikitable" border="1" | |||
|- | |||
! Gene Name (col 2) | |||
! GO ID (col 5) | |||
! Reference (col 6) | |||
! Evidence (col 7) | |||
! Annotation Extension (col 16) | |||
|- | |||
| Q9Y572 <span style="color:green">RIP3</span> | |||
|GO:0051092 <span style="color:green">positive regulation of NF-kappaB transcription factor activity</span> | |||
| PMID:21931591 | |||
| IDA | |||
| | |||
dependent_on(UniProtKB:Q13490 <span style="color:green">IAP2</span>) | |||
|} |
Revision as of 06:25, 31 July 2012
Definition
Child terms
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) |