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inhibition of Cdc20 promotes mitotic cell death more effectively than loss of APC/C activity through differential effects on Mcl-1 degradation, providing an improved strategy to kill cancer cells.
These findings present a novel degradation-independent function of Mcl-1 phosphorylation in anticancer therapy that could be useful for developing new Mcl-1-targeting agents to overcome therapeutic resistance
A great number of indirect and selective Mcl-1 inhibitors have been produced and some of these have shown efficacy in several clinical trials. Thus, therapeutic manipulation of Mcl-1 can be a useful strategy to combat cancer
this study is the first to identify hnRNP F/H and K as regulators of Mcl-1 alternative splicing.
Casp3 cleavage partially impaired the anti-apoptotic activity of Mcl-1 by reducing its mitochondrial localization and impeding its association with the permeability transition pore-forming protein Bak.
MLC1 p.Pro92Ser cause megalencephalic leukodystrophy with subcortical cysts and primary progressive multiple sclerosis.
MCL-1 protein expression is associated with poor outcome in breast cancer and support the therapeutic targeting of MCL-1 in this disease.
Bim phosphorylation can function as an additional regulator of Mcl-1 stability and a determinant of priming.
MCL-1 inhibitors are beneficial for targeted apoptosis of breast tumor ecosystems.
miR15a3p may suppress cell proliferation and migration and induce cell apoptosis in lens epithelial cells through inhibiting the expression of BCL2 and MCL1, which contributes to the onset of agerelated cataracts.
Activated TYK2 leads to STAT1 and STAT3 phosphorylation, activated expression of MCL1 and aberrant ALCL cell survival.
our results revealed the essential role of the MGMT-DUB3-MCL1 axis in the chemoresistance of ovarian cancer and identified that a combined treatment with HDACis and PaTrin-2 is an effective method for overcoming chemoresistance in ovarian cancer.
Mcl-1 gene was expressed in all seven lymphoma cell lines at different levels.
Our study suggested that LINC00152 was overexpressed in gastric cancer (GC) tissues, and it down-regulated miR-193a-3p to enhance MCL1 expression thereby promoting GC cells proliferation.
Lysosome-dependent Mcl-1 protein degradation leads to apoptosis of oral squamous cell carcinoma, thus Mcl-1 protein is an anti-apoptotic protein.
High MCL1 expression is associated with colorectal cancer.
HHT and bortezomib cooperate to kill DLBCL and MCL cells through a process involving MCL-1 down-regulation, NOXA up-regulation.
Mcl-1 and Survivin can be considered as promising molecular targets for the treatment of AML. The combination treatment with etoposide, and siRNA-mediated silencing of corresponding genes may be a novel strategy in chemoresistance AML treatment.
The inhibition of MCL-1, BCL-XL, and FGFR1 to maximize therapeutic response in FGFR1-expressing lung SqCC.
Findings suggested a tumor-suppressor role of the miR-29 family in control of MTX resistance and cell apoptosis through regulating COL3A1 or MCL1.
Bcl-xL could sequester Bak in response to the BH3 mimetic ABT-737, despite this molecule targeting Bcl-xL. These findings highlight the importance of Bak sequestration in resistance to anti-cancer treatments, including BH3 mimetics.
stimulation of T cells with IL-15, which depended on PI3K and JAK/STAT pathways; despite upregulating Bim, IL-15 inhibited spontaneous apoptosis; this was likely because of a concomitant upregulation of Mcl-1, which depended on the two same upstream pathways but was post-transcriptional
Targeting Mcl-1 enhances DNA replication stress sensitivity to cancer therapy.
study suggests that LMMHA induced significantly increased levels of inflammatory factors in bronchoalveolar lavage fluid and activation of the PI3K/Akt1 pathway, which up-regulates the expression of the anti-apoptotic protein Mcl-1 and inhibits the activation of caspase-3, thereby suppressing neutrophil apoptosis to trigger lung inflammation.
the MCL-1 BH3 interaction with VLCAD revealed a separable, gain-of-function role for MCL-1 in the regulation of lipid metabolism.
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.
miR-29b suppressed cellular proliferation and promoted apoptosis of pulmonary artery smooth muscle cells, possibly through the inhibition of Mcl-1 and CCND2.
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.
analysis of how a hydrophobic staple induces an unanticipated structural rearrangement in Mcl-1 upon binding
Mcl-1 is a disease-specific target of Cdk5, which associates with Cdk5 under basal conditions, but is not regulated by it.
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.
Even though the Mcl-1 protein in Mcl1-flox-del homozygous animals is normal, the males were still infertile.
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.
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.
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
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.
Our findings indicate that MCL-1 expression is an important biomarker of TEC survival
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.
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
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.
transgenic overexpression of bcl2-like Bcl-xL-like protein 1 or zfMcl-1a in zebrafish larvae interrupts regulation of the homeostatic balance between cell proliferation and programmed cell death during hepatogenesis and leads to liver hyperplasia
This gene encodes an anti-apoptotic protein, which is a member of the Bcl-2 family. Alternative splicing results in multiple transcript variants. The longest gene product (isoform 1) enhances cell survival by inhibiting apoptosis while the alternatively spliced shorter gene products (isoform 2 and isoform 3) promote apoptosis and are death-inducing.
bcl-2-like protein 3
, bcl-2-related protein EAT/mcl1
, induced myeloid leukemia cell differentiation protein Mcl-1
, myeloid cell leukemia ES
, induced myeloid leukemia cell differentiation protein Mcl-1 homolog
, myeloid cell leukemia protein 1
, BCL2 family apoptosis regulator
, LOW QUALITY PROTEIN: induced myeloid leukemia cell differentiation protein Mcl-1
, myeloid cell leukemia sequence 1 (BCL2-related)