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Updated: Mar 10, 2026

Generation of a RIP1 Knockout U937 Cell Line Using the CRISPR-Cas9 System
Published on: April 11, 2025
Mechanisms of RIPK3-induced inflammation
Inbar Shlomovitz1, Sefi Zargrian1, Motti Gerlic1
1Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Abstract:
Receptor-interacting protein kinase 3 (RIP3/RIPK3) is a multifunctional regulator of cell death and inflammation. It controls signalling downstream of the tumor necrosis factor (TNF) receptor family, DNA-dependent activator of IFN-regulatory factors (DAI) and toll-like receptors (TLRs). Today, it is also widely recognized as a component of caspase-independent cell death known as necroptosis, and cytokine production via activation of the inflammasome. Its role in inflammasome activation, in particular, make the interpretation of its role in vivo more complex. In this review, we focus on divergent roles for RIPK3 in cell death and inflammation.
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