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RIPK1-DD has a role in mediating RIPK1 dimerization and activation of its kinase activity during necroptosis and RIPK1-dependent apoptosis
We further identified this underlying mechanism also involved a PPARgamma (zeige PPARG Proteine)-induced ANXA1 (zeige ANXA1 Proteine)-dependent autoubiquitination of cIAP1 (zeige BIRC2 Proteine), the direct E3 ligase of RIP1 (zeige UQCRFS1 Proteine), shifting cIAP1 (zeige BIRC2 Proteine) toward proteosomal degradation..our study provides first insight for the suitability of using drug-induced expression of ANXA1 (zeige ANXA1 Proteine) as a new player in RIP1 (zeige UQCRFS1 Proteine)-induced death machinery in triple-negative breast cancer
data suggest that artesunate could induce RIP1-dependent cell death in human renal carcinoma.
RIP1 (zeige UQCRFS1 Proteine) has a role in CD40 (zeige CD40 Proteine)-mediated activation of caspase-8 (zeige CASP8 Proteine), which in turn leads to induction of apoptosis
High RIPK1 expression is associated with Alzheimer's disease.
These data represent the first report of decreased RIPK1 expression in neutrophils of Systemic Lupus Erythematosus patients and imply that RIPK1 may be involved in neutrophil death and neutrophil extracellular traps formation.
Data indicate that receptor (TNFRSF)-interacting serine-threonine kinase 1 (RIPK1) polymorphism is a prognostic biomarker for tumor development and survival of hepatocellular carcinoma (HCC (zeige FAM126A Proteine)) patients after hepatectomy.
we found that ORF3 protein downregulates TLR3 (zeige TLR3 Proteine)-mediated NF-kappaB (zeige NFKB1 Proteine) signaling via TRADD (zeige TRADD Proteine) and RIP1 (zeige UQCRFS1 Proteine). Our findings provide a new perspective on the cellular response in HEV infection and expand our understanding of the molecular mechanisms of Hepatitis E virus (HEV) pathogenesis in innate immunity.
Existence of a kinase-independent role of nuclear RIPK1 in the regulation of PARP1 (zeige PARP1 Proteine).
Study identify and quantify over 8,000 phosphorylated peptides, among which are numerous known sites in the TNF (zeige TNF Proteine)-RSC, NFkappaB (zeige NFKB1 Proteine), and MAP kinase (zeige MAPK1 Proteine) signaling systems. Functional analysis of S320 phosphorylation in RIPK1 demonstrates a role for this event in suppressing its kinase activity, association with CASPASE-8 (zeige CASP8 Proteine) and FADD (zeige FADD Proteine) proteins, and subsequent necrotic cell death during inflammatory TNFalpha (zeige TNF Proteine) stimulation.
two different modes of necroptosis induction by TNFalpha (zeige TNF Proteine) exist which are differentially regulated by iuRIPK1 formation. Overall, this work reveals a distinct mechanism of RIPK1 activation that mediates the signaling mechanism of RDA as well as a type of necroptosis.
We show that inflammation and autoimmunity are prevented upon expression of kinase inactive RIPK1 or deletion of RIPK3 (zeige RIPK3 Proteine) or MLKL. We provide evidence that the inflammation is not driven by microbial ligands, but depends on the release of danger-associated molecular patterns and MyD88 (zeige MYD88 Proteine)-dependent signaling.
RIPK1 kinase activity mediates TWEAK (zeige TNFSF12 Proteine)-induced apoptosis.
The authors report here that male reproductive organs of both Ripk3 (zeige RIPK3 Proteine)- and Mlkl-knockout mice retain 'youthful' morphology and function into advanced age, while those of age-matched wild-type mice deteriorate. Feeding of wild-type mice with an RIPK1 inhibitor prior to the normal onset of age-related changes in their reproductive organs blocked the appearance of signs of aging.
Pull down experiments with biotinylated Sorafenib show that it binds independently RIPK1, RIPK3 (zeige RIPK3 Proteine) and MLKL. Moreover, it inhibits RIPK1 and RIPK3 (zeige RIPK3 Proteine) kinase activity. In vivo Sorafenib protects against TNF (zeige TNF Proteine)-induced systemic inflammatory response syndrome (SIRS) and renal ischemia-reperfusion injury (IRI).
The study provides genetic evidence that different RIP1 kinase inactive mutations have distinct impacts on the embryogenesis of Fadd-deficient mice.
Excessive death of hepatocytes is a characteristic of liver injury. A new programmed cell death pathway has been described involving upstream death ligands such as TNF (zeige TNF Proteine) and downstream kinases such as RIPK1.
TNFalpha (zeige TNF Proteine)-induced phosphorylation of RIPK1 in the intermediate domain by TAK1 (zeige NR2C2 Proteine) plays a key role in regulating the decision between three distinct mechanisms of cell death: necroptosis, RIPK1-independent and dependent apoptosis.
Interaction of xFADD and xRIP1 induced synergistic activation of JNK (zeige MAPK8 Proteine) and NF-kappaB (zeige NFKB1 Proteine).
Serine-threonine kinase which transduces inflammatory and cell-death signals (necroptosis) following death receptors ligation, activation of pathogen recognition receptors (PRRs), and DNA damage. Upon activation of TNFR1 by the TNF-alpha family cytokines, TRADD and TRAF2 are recruited to the receptor. Ubiquitination by TRAF2 via 'Lys-63'-link chains acts as a critical enhancer of communication with downstream signal transducers in the mitogen-activated protein kinase pathway and the NF-kappa-B pathway, which in turn mediate downstream events including the activation of genes encoding inflammatory molecules. Polyubiquitinated protein binds to IKBKG/NEMO, the regulatory subunit of the IKK complex, a critical event for NF-kappa-B activation. Interaction with other cellular RHIM-containing adapters initiates gene activation and cell death. RIPK1 and RIPK3 association, in particular, forms a necroptosis-inducing complex.
, cell death protein RIP
, receptor interacting protein
, receptor-interacting protein 1
, receptor-interacting serine/threonine-protein kinase 1
, serine/threonine-protein kinase RIP
, receptor (TNFRSF)-interacting serine-threonine kinase 1
, receptor interacting serine/threonine kinase 1 L homeolog
, receptor-interacting protein 1 beta