RIPK2

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RIPK2

A gene on chromosome 8q21 that encodes a serine/threonine/tyrosine kinase which is intimately involved in modulating innate and adaptive immune responses. Upon stimulation by bacterial peptidoglycans, NOD1 and NOD2 are activated, oligomerise, and recruit RIPK2 through CARD-CARD domains. Once recruited, RIPK2 autophosphorylates and undergoes “Lys-63”-linked polyubiquitination by E3 ubiquitin ligases BIRC2 and BIRC3. The polyubiquitinated protein then recruits MAP3K7/TAK1 to IKBKG/NEMO, induces “Lys-63”-linked polyubiquitination of IKBKG/NEMO and activates IKBKB/IKKB.

In turn, NF-kappaB is released from NF-kappaB inhibitors and translocates to the nucleus, where it activates transcription of myriad genes involved in immune response, growth control or anti-apoptosis. It also plays a role during engagement of the T-cell receptor in promoting BCL10 phosphorylation and subsequent NF-kappaB activation.
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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.
NOD1 activation resulting from LRR sensing of NOD1 ligand is initiated by a NOD1 conformational change that allows a homotypic interaction between NOD1 CARD domains and NOD1 auto-oligomerization; this, in turn, is followed by recruitment of RIP2, its initial down-stream signaling molecule.
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.
As shown in Figure 4, after LPS stimulation, the expression of NOD1, RIP2, and NF-[kappa]B was dramatically higher compared with the control group, while the expression of IKBa was lower.
As shown in Figure 5, the expression of NF-[kappa]B and RIP2 was significantly reduced by CBT and ML130 alone to a similar extent (P > 0.05).
tuberculosis-derived MDP via NOD2 and downstream activation of RIP2, TBK1, and IRF5 [101].
novicida induces type I IFN production in a manner independent of TLRs, NOD1/2, RIP2, ASC, Ipaf, IPS-1, RIG-I, and MDA5 but dependent on IRF3 [126].
Supports TCP, IP, IPX, SPX, SAP, RIP, RIP2, ICMP, UDP, ARP, and more.
Shamshiev et al., "The kinase-activity of Rip2 determines its stability and consequently Nod1--and Nod2-mediated immune responses," Journal of Biological Chemistry, vol.
Anti-RIP1 (0.2 [micro]g/mL; H-207, Santa Cruz Biotechnology, Santa Cruz, CA, USA) is a rabbit polyclonal antibody that does not cross react with RIP2 or RIP3.