Identifiers
receptor interacting serine/threonine kinase 1
HUGO:RIPK1 hgnc_id:HGNC:10019 HGNC:10019 ENTREZ:8737 UNIPROT:Q13546
receptor (TNFRSF)-interacting serine-threonine kinase 1
HUGO:RIPK1 HGNC:10019 ENTREZ:8737 UNIPROT:Q13546
HUGO:RIPK1
Maps_Modules
HMC:TUMOR_PROMOTING_INFLAMMATION
HMC:ACTIVATING_INVASION_AND_METASTASIS
Cancer Associated Fibroblasts / INFLAMMATORY_SIGNALING_PATHWAYS
HMC:RESISTING_CELL_DEATH
HMC:DEREGULATING_CELLULAR_ENERGETICS
Regulated Cell Death / APOPTOSIS
Regulated Cell Death / CASPASES
Regulated Cell Death / DEATH_RECEPTOR_PATHWAYS
Regulated Cell Death / FAS_RESPONSE
Regulated Cell Death / GLUTAMINE_METABOLISM
Regulated Cell Death / NECROPTOSIS
Regulated Cell Death / TNF_RESPONSE
Regulated Cell Death / TRAIL_RESPONSE
Regulated Cell Death / ER_STRESS
HMC:AVOIDING_IMMUNE_DESTRUCTION
Innate Immunity / IMMUNOSTIMULATORY_CYTOKINE_PATHWAYS
Innate Immunity / IMMUNOSTIMULATORY_CORE_PATHWAYS
HMC:EVADING_GROWTH_SUPPRESSORS
Survival / MAPK
References
PMID:21232017; PMID:18641653
TNF induces TRADD-dependent and RIPK1-dependent recruitment of TRAF2 to TNFR1.
TRADD is essential for TNFR1 signaling in MEFs
PMID:26587781
PMID:19632174
RIP kinases at the crossroads of cell death and survival
PMID:19524513
PMID:28574505
PMID:23010170
PMID:26653790
erastin-induced cell death proceeds normally on knockdown of RIPK1/RIPK3
PMID:21232017, PMID:21133840, PMID:18641653
TNF treatment is thought to result in the formation of a TRADD-RIP-TRAF2 complex at the membrane.
PMID:11274345
References
in_re884( Innate Immunity ):
PMID:14660645, PMID:18264787, PMID:11460167
Activated TAK1 phosphorylates IKK-beta proteins
leading to activation of NF-??B downstream of HMGB1.
PMID:21232017, PMID:21133840, PMID:17301840
PMID:24958845, PMID:24699077
The LUBAC complex ubiquitinates NEMO, a subunit of the IKK complex downstream of TNF and upregulates IkBa degradetion.
PMID:11280761
VEGF signaling blocs TNF-?? induced activation of I??B kinase (IKK complex).This decreased IKK activation correlated with the inhibition of I??B?? phosphorylation and degradation of I??B?? and I??B?? in HPCs, and this inhibition is inhdependent or FLT1 and KDR