Recombinant Mouse Induced myeloid leukemia cell differentiation protein Mcl-1 homolog (Mcl1)

1. These results indicate that the outer membrane protein MCL1 is degraded by the VCP-UBXD1 complex and that the process is promoted by the presence of mutant Huntingtin. PMID:27913212
2. miR-29b suppressed cellular proliferation and promoted apoptosis of pulmonary artery smooth muscle cells, possibly through the inhibition of Mcl-1 and CCND2. PMID:29662889
3. Authors treated Mcl-1(+/-) heterozygous mice, which have a ~50% reduction in MCL-1 protein in their cells, with a broad range of chemotherapeutic drugs. Monitoring of treated mice revealed that a wide range of chemotherapeutic drugs had no significant effect on the general well-being of Mcl-1(+/-) mice with no overt damage to a broad range of tissues. PMID:28800129
4. analysis of how a hydrophobic staple induces an unanticipated structural rearrangement in Mcl-1 upon binding PMID:29339518
5. Mcl-1 is a disease-specific target of Cdk5, which associates with Cdk5 under basal conditions, but is not regulated by it. PMID:28751497
6. These findings elucidate a crucial molecular pathway of B cell selection in the earliest phases of activation by identifying a novel link between B cell receptor affinity and BAFF-R signaling towards Mcl-1. PMID:27762293
7. Even though the Mcl-1 protein in Mcl1-flox-del homozygous animals is normal, the males were still infertile. PMID:27906183
8. The findings support a model in which survival is determined by quantitative participation of multiple anti-apoptotic proteins, BCL2, Mcl1, and BCL2A1, rather than by a single anti-apoptotic protein. PMID:28362427
9. This dynamic change in B cell survival mechanisms is unique to Epstein-Barr virus-infected cells and relies on regulation of MCL-1 mitochondrial localization and BFL-1 transcription by the viral EBNA3A protein. PMID:28425914
10. Overexpression of Mcl-1 via the hemopoietic cell specific vavP-Mcl-1 transgene markedly exacerbates and accelerates the lpr phenotype. The progressive splenomegaly and lymphadenopathy displayed by lpr mice was far more severe in Mcl-1tg/lpr littermates PMID:27813531
11. Endothelial cell -specific deletion of Mcl1 resulted in a dose-dependent increase in endothelial cell apoptosis in the angiogenic vasculature and a corresponding decline in vessel density. PMID:26943318
12. Our findings indicate that MCL-1 expression is an important biomarker of TEC survival PMID:28972012
13. These results identify MCL-1 as a critical prosurvival protein for preventing beta-cell death and clarify the mechanisms behind its downregulation by proinflammatory cytokines. PMID:28667119
14. These data show that Mcl-1 is dispensable for the regulation of apoptosis during infection with different large DNA viruses.Bcl-XL, on the other hand, can be important to maintain survival of virus-infected cells PMID:27537523
15. BCL-XL expression promotes survival of immature B cells, expression of BCL-2 is important for survival of mature B cells and long-lived plasma cells (PC), and expression of MCL-1 is important for survival throughout B-cell development. PMID:27560714
16. miR-32/MCL-1 pathway members were identified as key early genetic events driving melanoma progression. PMID:27846237
17. GSK3B-MCL1 signaling to regulate axonal autophagy might be important for the successful completion of Wallerian degeneration. PMID:28053206
18. Specific downregulation of Mcl-1 significantly increases apoptosis of peritoneal macrophages and that the MAPK signaling pathway is the primary mediator of Mcl-1 expression. PMID:26876933
19. MCL1 plays a pivotal role in Leydig-cell steroidogenesis, and might provide novel insights into metabolic regulation in this cell PMID:26995740
20. Although loss of one Mcl-1 allele did not noticeably impair the survival of normal B lymphoid cells, it markedly diminished the survival of Proto-Oncogene Proteins c-myc overexpressing B cell progenitors. PMID:26947081
21. MCL-1 loss in early B-lymphoid progenitors delayed MYC-driven lymphomagenesis. PMID:26962682
22. High Mcl-1 levels enhanced mTOR phosphorylation and augmented the differentiation of terminal effector cells and effector memory CD8 T cells. PMID:26855329
23. Data suggest Leishmania donovani exploits host anti-apoptotic protein MCL-1 to prevent apoptosis of host macrophages upon treatment with antiparasitic agents; thus, L. donovani protects its host, a factor in progression of visceral leishmaniasis. PMID:26670606
24. Data demonstrate that soluble factors from MM cells are able to generate MDSC through Mcl-1 upregulation. PMID:25871384
25. a mechanism of inverse coregulation between BECN1 and MCL1 significantly contributes to their opposing roles in tumorigenesis PMID:25837021
26. There is a non-redundant pathway linking IL-15 to Mcl1 in the maintenance of NK cells and innate immune responses in vivo. PMID:25119382
27. Authors recognize MCL-1 as the essential survival factor required for conservation of the postnatal PMF pool, growing follicle survival and effective oocyte mitochondrial function. PMID:25950485
28. Tax interacted with and activated TRAF6, and triggered its mitochondrial localization, where it conjugated four carboxyl-terminal lysine residues of MCL-1 with lysine 63-linked polyubiquitin chains PMID:25340740
29. deletion of Mir155 prevents Fas-induced hepatocyte apoptosis and liver injury through the up-regulation of Mcl1. PMID:25794705
30. Inverse co-regulation of Beclin 1 and Mcl-1 represents a mechanism of functional counteraction in cancer. PMID:25472497
31. miR-29a is involved in the pathogenesis of ulcerative colitis by regulating intestinal epithelial apoptosis via Mcl-1. PMID:25674218
32. MCL1, but not that of BAK, forms stable heterodimeric complexes with cBID in a manner adjustable by membrane cardiolipin content and curvature degree. PMID:25987560
33. MCL1 has lipid-dependent bimodal membrane activity. PMID:25314294
34. These results demonstrate that antagonism between PUMA and MCL-1 constitutes the major axis of control of hematopoietic stem cell survival. PMID:25847014
35. Cafestol overcomes ABT-737 resistance in Mcl-1-overexpressed renal carcinoma Caki cells through downregulation of Mcl-1 expression and upregulation of Bim expression. PMID:25375379
36. These data demonstrate that Mcl-1 is essential for mammopoiesis and identify EGF as a critical trigger of Mcl-1 translation to ensure survival of milk-producing alveolar cells. PMID:25730472
37. conditional gene deletion and loss of the granulocytic subset does not alter tumor growth or incidence in vivo PMID:25500368
38. analysis of the role of BCL-XL or MCL-1 in the development and sustained growth of thymic lymphoma elicited by loss of p53 reveals that only MCL-1 is critical PMID:25368374
39. Downregulation of Mcl-1 has anti-inflammatory pro-resolution effects and enhances bacterial clearance from the lung. PMID:24280938
40. Pro-apoptotic Bim and anti-apoptotic Mcl-1. PMID:24825007
41. Mcl-1 positively regulates cell viability and negatively regulates the bone-resorbing activity of osteoclasts both in vitro and in vivo. PMID:24096094
42. Noxa is targeted to the mitochondrial membrane where it neutralises Mcl-1 via its C-terminal BH3-domain. PMID:23733106
43. Data indicate that Mcl-1 deficient embryonic fibroblasts (MEFs) reliant only on Bcl-XL for survival, and Bax/Bak deficient MEFs support a mechanism-based induction of apoptosis. PMID:23767404
44. mouse Mcl1 is a prosurvival Bcl2 relative that blunts stress-induced apoptosis, causes male sterility, and promotes tumorigenesis PMID:24363325
45. Notch1 inhibits apoptosis of stimulated macrophages by directly controlling the mcl1 promoter. PMID:23872918
46. Mcl-1 is critical for promoting effector T-cell responses, but does so by combating pro-apoptotic molecules beyond Bim. PMID:23558951
47. Loss of parkin function through biallelic mutation of PARK2 may lead to death of dopaminergic neurons through unregulated SCF(Fbw7beta)-mediated ubiquitylation-dependent proteolysis of Mcl-1. PMID:23858059
48. data support the metabolic control of Mcl-1 expression as a key event in the effects of caloric restriction in sensitizing lymphoma cells to apoptosis PMID:23966420
49. Antiapoptotic Mcl-1 is critical for the survival and niche-filling capacity of Foxp3 regulatory T cells. PMID:23852275
50. In the absence of p27(Kip1), Mcl1 failed to induce neural progenitor cell (NPC) cell cycle exit, demonstrating that p27(Kip1) is required for Mcl1-mediated NPC terminal mitosis. PMID:23824576

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UNIGENE: Mm.1639

KEGG: mmu:17210

STRING: 10090.ENSMUSP00000044048