Recombinant Mouse Mixed lineage kinase domain-like protein (Mlkl)

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. PMID:27840306
2. M. tuberculosis and TNFalpha synergise to induce necroptosis in murine fibroblasts via RIPK1-dependent mechanisms and characterized by phosphorylation of Ser345 of the MLKL necroptosis death effector. PMID:28892415
3. hydrostatic pressure (EHP)-induced RGC-5 cell necroptosis was mediated by MLKL PMID:28981598
4. Biological events and molecular signaling following MLKL activation during necroptosis have been reported. PMID:28854080
5. The authors report here that male reproductive organs of both Ripk3- 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. PMID:28807105
6. Data indicate that mixed-lineage kinase domain-like protein (MLKL) oligomerization, membrane translocation, and cell death occur simultaneously with NLR family pyrin domain containing 3 (NLRP3) activation in bone marrow-derived macrophages. PMID:28096356
7. Pull down experiments with biotinylated Sorafenib show that it binds independently RIPK1, RIPK3 and MLKL. Moreover, it inhibits RIPK1 and RIPK3 kinase activity. In vivo Sorafenib protects against TNF-induced systemic inflammatory response syndrome (SIRS) and renal ischemia-reperfusion injury (IRI). PMID:28661484
8. Knock-out mice deficient in MLKL or RIP3 had increased survival and reduced pulmonary injury during Serratia marcescens pneumonia. PMID:28387756
9. Our findings reveal that MLKL and FADD play critical roles in preventing lymphoproliferative disease and activating the NLRP3 inflammasome PMID:27498868
10. RIPK3 and/or MLKL may exert functions independently of necroptosis. PMID:27523270
11. Data suggest that necroptotic cells externalize phosphatidylserine (PS) after translocation of phosphorylated Mlkl to cell membrane; necroptotic cells with exposed PS release extracellular vesicles containing Mlkl; inhibition of Mlkl after PS exposure can reverse process of necroptosis and restore cell viability. PMID:28650960
12. results reveal a pathway for MLKL-dependent programmed necrosis that is executed in the absence of RIPK3 and potentially drives the pathogenesis of severe liver diseases. PMID:27756058
13. Mice deficient in RIPK3 or doubly deficient in MLKL and FADD, but not MLKL alone, are more susceptible to influenza A virus than their wild-type counterparts, revealing an important role for RIPK3-mediated apoptosis in antiviral immunity. PMID:27321907
14. MLKL octamer formation depends on alpha-helices 4 and 5. PMID:27920255
15. The findings reported here indicate that palmitate induces RIP1/RIP3-dependent necrosis via MLKL-mediated pore formation of RAW 264.7 cells in the plasma membrane, which could provide a new mechanism to explain the link between elevated levels of free fatty acids (FFAs), palmitate in particular, and macrophage death. PMID:27856241
16. The results indicate that RIP1 and MLKL contribute to necroptotic cell death after HCoV-OC43 infection to limit viral replication. PMID:27795420
17. In AML, Mlkl expression is reduced. This leads to reduced activation of the inflammasome and reduced myeloid differentiation. PMID:27411587
18. we demonstrate that the phosphorylation of Ser345 is not required for the interaction between RIPK3 and MLKL in the necrosome, but is essential for MLKL translocation, accumulation in the plasma membrane, and consequent necroptosis. PMID:26024392
19. deficiency of RIPK3 or MLKL prevents oxalate crystal-induced acute kidney injury. PMID:26817517
20. RIPK3 can promote NLRP3 inflammasome and IL-1beta inflammatory responses independent of MLKL and necroptotic cell death PMID:25693118
21. Cisplatin stimulates RIP1/RP3/MLKL-dependent necrotic cell death in renal tubules, which finally causes renal dysfunction PMID:25788533
22. These data reveal a potential role for RIPK3 as a suppressor of MLKL activation and indicate that phosphorylation can fine-tune the ability of MLKL to induce necroptosis. PMID:26283547
23. MLKL acctivation unleashes the four-helix bundle domain to induce membrane localization and necroptotic cell death PMID:25288762
24. Ectopic expression of ICP6, but not RHIM mutant ICP6, directly activated RIP3/MLKL-mediated necrosis. PMID:25316792
25. Knockdown of RIPK3 or MLKL blocks TNF-induced necroptosis. PMID:24434512
26. [review] Although studies have demonstrated that mixed lineage kinase domain-like (MLKL) protein is the only substrate of RIP3 kinase that is essential for necroptotic death, the molecular determinants acting downstream of MLKL remain ambiguous. PMID:24556404
27. Data suggest that nucleotide- (ATP-) binding residues of human MLKL have divergently evolved from mouse Mlkl and conventional protein kinases; studies include small-angle X-ray scattering, thermal shift of nucleotide binding, and sequence alignment. PMID:24219132
28. Neither Mlkl nor Rip3 deficiency provided protection against polymicrobial sepsis-induced animal death in the study of septic shock induced by CLP. PMID:23835476
29. Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL. PMID:24019532
30. crystal structure determined; structure-guided mutation of the MLKL pseudoactive site resulted in constitutive, RIPK3-independent necroptosis, demonstrating that modification of MLKL is essential for propagation of the necroptosis pathway downstream of RIPK3 PMID:24012422
31. the importance of the RIP3-MLKL interaction in the formation of functional necrosomes and suggest that translocation of necrosomes to mitochondria-associated membranes is essential for necroptosis signaling. PMID:23612963
32. Findings implicate MLKL as a key mediator of necrosis signaling downstream of the kinase RIP3. PMID:22265413

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UNIGENE: Mm.207971

KEGG: mmu:74568

STRING: 10090.ENSMUSP00000113718