RIPK3 Proteine (RIPK3)

Human Receptor-Interacting serine-threonine Kinase 3 (RIPK3) Interaktionspartner

1. The major function of RIP1 (zeige UQCRFS1 Proteine) kinase activity in TNF (zeige TNF Proteine)-induced necroptosis is to autophosphorylate serine 161. This specific phosphorylation then enables RIP1 (zeige UQCRFS1 Proteine) to recruit RIP3 and form a functional necrosome, a central controller of necroptosis.

2. RIPK3-dependent cell death and inflammasome activation in FLT3 (zeige FLT3 Proteine)-internal-tandem-duplication-expressing leukemia-initiating cells

3. The necroptosis-inducing kinase RIPK3 reduces adipose tissue inflammation and glucose intolerance.

4. We showed that RIP3 spontaneously drives a necroptosis-induced inflammation in established intestinal cell lines and in ileal/colonic samples from IBD patients.

5. These data demonstrate that caspase-8 (zeige CASP8 Proteine) functions in synovial antigen-presenting cells to regulate the response to inflammatory stimuli by controlling RIPK3 action, and this delicate balance maintains homeostasis within the joint.

6. The induced expression of RIP3 by UHRF1 (zeige UHRF1 Proteine) RNAi depends on the presence of Sp1 (zeige PSG1 Proteine). Remarkably, the ectopic expression of RIP3 in RIP3-null cancer cells results in a decrease in tumor growth in mice. Therefore, our findings offer insights into RIP3 expression control in cancer cells and suggest an inhibitory effect of RIP3 on tumorigenesis.

7. 2-hydroxyglutarate bound to DNMT1 (zeige DNMT1 Proteine) and stimulated its association with the RIP3 promoter, inducing hypermethylation that reduces RIP3 protein and consequently impaired RIP3-dependent necroptosis.

8. the in vivo effects were diametrically reversed with RIP3 deletion or RIP1 (zeige UQCRFS1 Proteine) blockade, resulting in marked tumor protection. The dichotomy between the in vivo and in vitro results suggests that the microenvironmental milieu resulting from RIP1 (zeige UQCRFS1 Proteine)/RIP3 signaling is likely responsible for its protumorigenic effects

9. Shikonin induces glioma cell necroptosis in vitro by reactive oxygen species overproduction and promoting RIP1 (zeige UQCRFS1 Proteine)/RIP3 necrosome formation.

10. In critically ill trauma patients, plasma levels of the necroptosis mediator RIP3 at 48 h were associated with AKI stage and RBC (zeige CACNA1C Proteine) transfusions.

Mouse (Murine) Receptor-Interacting serine-threonine Kinase 3 (RIPK3) Interaktionspartner

1. Aldehyde dehydrogenase 2 deficiency negates chronic low-to-moderate alcohol consumption-induced cardioprotecion possibly via ROS-dependent apoptosis and RIP1/RIP3/MLKL-mediated necroptosis.

2. The major function of RIP1 (zeige RALBP1 Proteine) kinase activity in TNF (zeige TNF Proteine)-induced necroptosis is to autophosphorylate serine 161. This specific phosphorylation then enables RIP1 (zeige RALBP1 Proteine) to recruit RIP3 and form a functional necrosome, a central controller of necroptosis.

3. Deficiency in RIPK3 attenuated serum and lung cytokines, lung injury and neutrophil infiltration and lung and gut (zeige GUSB Proteine) apoptosis. These data suggest that RIPK3, in part, is responsible for the systemic inflammatory response in neonatal sepsis.

4. Our results demonstrated that Ripk3 was strongly upregulated in murine hearts subjected to IR injury and cardiomyocytes treated with LPS (zeige TLR4 Proteine) and H2O2..the present study helps to elucidate how necroptosis is mediated by ER stress, via the calcium overload /XO/ROS (zeige ROS1 Proteine)/mPTP (zeige PTPN2 Proteine) opening axis

5. RIP3-ablation attenuated oxidative stress, inflammation and apoptosis in astrocytes, which was dependent on AMPKalpha (zeige GRK4 Proteine) activation.

6. The necroptosis-inducing kinase RIPK3 reduces adipose tissue inflammation and glucose intolerance.

7. RIP3-mediated signaling is not a critical driver of acute radiation syndrome

8. RIPK3 promotes adenovirus type 5 oncolytic activity.

9. p55TNFR-IKK2 (zeige IKBKB Proteine)-Ripk3 signalling orchestrates arthritogenic and death responses in synovial fibroblasts

10. in Mycobacterium tuberculosis-infected macrophages, mitochondria are an essential platform for induction of necrosis by activating RIPK3 function and preventing caspase 8 (zeige CASP8 Proteine)-activation.