2016年7月20日 · RIPK1 and RIPK3 are homologous kinases, previously linked to activation of necroptotic death. In this study, we have described roles for these kinases as master regulators of pro-inflammatory gene expression induced by lipopolysaccharide, independent of their well-documented cell death functions.

2015年2月18日 · Here we show that following LPS treatment, or LPS-induced necroptosis, the TLR adaptor protein TRIF and inhibitor of apoptosis proteins (IAPs: X-linked IAP, cellular IAP1 and IAP2) regulate RIPK3...

RIPK3能够与RIPK1结合形成“坏死性小体”这一结构能够导致下游MLKL的激活，后者是细胞裂解与坏死的关键调节因子。 与RIPK1、RIPK3引发的细胞死亡信号通路不同，目前有一些研究也表明两类激酶能够直接促进炎症信号的激活。 在巨噬细胞中，天然免疫受体TLR3与TLR4激活后，如果有Z-vad（caspase激酶抑制剂）的存在，那么RIPK1、RIPK3以及MLKL的活性将得到释放。 对于天然免疫信号来说，TLR4受到LPS刺激引起的炎性基因的表达是重要的组成部分。 而由 …

2020年3月9日 · In this study, we found that blockage of both necroptosis and pyroptosis (double deletion of Ripk3 / Gsdmd or Mlkl / Gsdmd) resulted in accumulative protection against septic shock, systemic...

2016年7月19日 · RIPK1 and RIPK3 are homologous kinases, previously linked to activation of necroptotic death. In this study, we have described roles for these kinases as master regulators of pro-inflammatory gene expression induced by lipopolysaccharide, independent of their well-documented cell death functions.

2019年1月15日 · Importantly, the described RIPK3 antiviral pathway is specific to neurotropic flavivirus infections, and the authors show that RIPK3 does not function to control itaconate production in either bone-marrow-derived macrophages (BMDM) or microglial cells, both targets of ZIKV replication.

2019年8月27日 · Here, we report that cells undergoing necroptosis in response to direct RIPK3 activation or viral infection continue de novo synthesis of cytokines and chemokines for several hours after they have lost plasma membrane integrity and irreversibly committed to cell death.

2017年4月6日 · Using a mouse model of West Nile virus (WNV) encephalitis, we show that RIPK3 restricts WNV pathogenesis independently of cell death. Ripk3−/− mice exhibited enhanced mortality compared to wild-type (WT) controls, while mice lacking the necroptotic effector MLKL, or both MLKL and caspase-8, were unaffected.

2019年7月9日 · RIPK1, RIPK3, ZBP1 and TRIF, the four mammalian proteins harboring RIP homotypic interaction motif (RHIM) domains, are key components of inflammatory signaling and programmed cell death. RHIM-domain protein activation is mediated by their oligomerization; however, mechanisms that promote a return to homeostasis remain unknown.

Receptor interacting protein kinase 3 (RIP3 or RIPK3) has emerged as a central player in necroptosis and a potential target to control inflammatory disease. Here, three selective small molecule compounds are shown to inhibit RIP3 kinase-dependent necroptosis, although their therapeutic value is undermined by a surprising, concentration ...