Recombinant cynomolgus monkey RIP protein (Active)

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

RIP also known as Receptor-Interacting Protein or RIPK1 is a serine/threonine-protein kinase with a mass of approximately 74 kDa. It plays an important role in cell death and survival signaling pathways. RIP is expressed ubiquitously across various tissues indicating its importance in many cellular functions. The protein contains a kinase domain an intermediate domain for protein-protein interactions and a death domain which facilitates its involvement in apoptotic signaling processes.

Biological function summary

Receptor-Interacting Protein Kinase 1 (RIPK1) participates in regulating both necroptosis and apoptosis distinguishing itself as an important mediator in cell death mechanisms. As part of the necrosome complex which includes RIPK3 and MLKL RIPK1 functions in necroptosis—a programmed form of necrosis. This characteristic involvement shows its dual role in maintaining cell fate decisions making it an integral part of immune response and inflammation control.

Pathways

RIPK1 strongly associates with the TNF signaling pathway and NF-kB pathway. Its interaction with TNF receptor 1 (TNFR1) and consequent involvement with TRADD and TRAF2 mediates the signal transduction necessary for the activation of NF-kB leading to transcription of genes involved in survival and inflammation. This connection illustrates its capability to switch between promoting cell survival through NF-kB and facilitating cell death via necroptosis or apoptosis depending on cellular context and cues.

RIPK1 plays a significant role in conditions such as inflammatory diseases and neurodegenerative disorders. Its overactivation results in excessive cell death implicated in inflammatory conditions; necrostatin a necroptosis inhibitor targets RIPK1 to potentially mitigate this damage. Furthermore RIPK1's dysregulation links to Alzheimer's disease where it can interact with components like RIPK3 to exacerbate neurodegenerative processes. This relationship underlines the potential of targeting RIPK1 therapeutically to manage inflammation and neurodegeneration.