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RIP2Receptor Interacting Protein-2 (immunology)
RIP2Routing Information Protocol version 2
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18,19) This is most likely due to the fact that NOD1 signaling (as well as NOD2 signaling) engages a down-stream activation pathway that is somewhat independent of and additive to the pathway ordinarily utilized by TLR signaling, such as RIP2 signaling.
3-6) Such RIP2 recruitment is an obligate step in NOD1 (as well as NOD2) signaling since cells from mice deficient in RIP2 are unable to mediate NOD1 (or NOD2) activation of proinflammatory cytokine responses.
Following its activation by NOD1, RIP2 in a ubiquitinated form (see below) complexes with TAK1-binding protein 2 (TAB2) and TAB3 and then recruits TGF-[beta]-activated kinase 1 (TAK1) to form an activator of the I[kappa]B kinase (IKK) complex; this, in turn, leads to the phosphorylation/degradation of I[kappa]B[alpha] and nuclear translocation of nuclear factor-kappa B (NF-[kappa]B) subunits that promote transcription of NF-[kappa]B target genes through binding to multiple promoter sites.
NJJ suppresses the expressions of RIP2 and caspase-1 in the activated HMC-1 cells
PMACI increased the expressions of RIP2 and caspase-1; whereas NJJ suppressed the expressions of RIP2 and caspase-1 increased in the activated HMC-1 cells (Fig.
The protein kinase RIP2 is a member of the CARD protein family (caspase activation and recruitment domain) and has been shown to be an activator of NF-[kappa]B (Yin et al.
The researchers discovered that the medications target RIP2 as efficiently as they target the EGF-Receptor.