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CASP1 — RIPK2

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: RIPK2 — CASP1 (physical association, affinity chromatography technology) Thome et al., Curr Biol 1998*
• IRef Hprd Interaction: CASP1 — RIPK2 (in vivo) Thome et al., Curr Biol 1998*
• IRef Intact Interaction: CASP1 — RIPK2 (physical association, coimmunoprecipitation) Thome et al., Curr Biol 1998*
• IRef Ophid Interaction: CASP1 — RIPK2 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005
• IRef Ophid Interaction: CASP1 — RIPK2 (aggregation, confirmational text mining) Thome et al., Curr Biol 1998*

Text-mined interactions from Literome

Lee et al., J Biol Chem 2001 : COP binds to both RIP2 and the caspase-1 prodomain and inhibits RIP2 induced caspase-1 oligomerization
Sarkar et al., J Immunol 2006 : This RIP2 induced NF-kappaB activity and caspase-1 binding was inhibited in a dose dependent fashion by ASC
da Silva Correia et al., Cell Death Differ 2007 (Breast Neoplasms) : In contrast, several lines of evidence show that Nod1 dependent JNK activation and IL-8 production did not require the presence of caspase 8 but required activation of TAK1 as well as RIP2
Gentle et al., J Biol Chem 2011 : After receptor ligation, RIPK1 not only modulates activation of both canonical and NIK dependent NF-?B, but also regulates caspase-8 activation and cell death
Oh et al., J Pharmacol Exp Ther 2011 (Inflammation...) : In activated human mast cells, the receptor interacting protein 2 (RIP2) , I?B kinase ( IKK ) -ß, nuclear factor-?B ( NF-?B ) /RelA, and caspase-1 activation were increased, but increased RIP2, IKK-ß, NF-?B/RelA, and caspase-1 activation were inhibited by the treatment of IPT
Duprez et al., Immunity 2011 (Cecal Diseases...) : An additional switch decides, depending on the cellular context, between caspase dependent apoptosis and RIP kinase ( RIPK ) -mediated necrosis, also termed necroptosis