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Human MCL-1 Protein expressed in Escherichia coli (E. coli) - ABIN1098214
Bae, Leo, Hsu, Hsueh: MCL-1S, a splicing variant of the antiapoptotic BCL-2 family member MCL-1, encodes a proapoptotic protein possessing only the BH3 domain. in The Journal of biological chemistry 2000
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miR (show MLXIP Proteins)-32/MCL-1 pathway members were identified as key early genetic events driving melanoma progression.
GSK3B-MCL1 signaling to regulate axonal autophagy might be important for the successful completion of Wallerian degeneration.
Specific downregulation of Mcl-1 significantly increases apoptosis of peritoneal macrophages and that the MAPK (show MAPK1 Proteins) signaling pathway is the primary mediator of Mcl-1 expression.
MCL1 plays a pivotal role in Leydig-cell steroidogenesis, and might provide novel insights into metabolic regulation in this cell
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 (show RAB1A Proteins) Proteins c-myc (show MYC Proteins) overexpressing B cell progenitors.
MCL-1 loss in early B-lymphoid progenitors delayed MYC (show MYC Proteins)-driven lymphomagenesis.
High Mcl-1 levels enhanced mTOR (show FRAP1 Proteins) phosphorylation and augmented the differentiation of terminal effector cells and effector memory CD8 (show CD8A Proteins) T cells.
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.
Data demonstrate that soluble factors from MM cells are able to generate MDSC through Mcl-1 upregulation.
a mechanism of inverse coregulation between BECN1 (show BECN1 Proteins) and MCL1 significantly contributes to their opposing roles in tumorigenesis
Therefore, the present data support a model whereby MCL-1 depletion increases 53BP1 and RIF1 colocalization at DNA double-strand break.
in addition to MCL-1, BCL-XL (show BCL2L1 Proteins) is heterogeneously expressed in HMCLs and patient samples. The expression profile of BCL-XL (show BCL2L1 Proteins) relative to BCL-2 (show BCL2 Proteins) and MCL-1 may be an important predictor of response to venetoclax sensitivity as a monotherapy and in combination with bortezomib.
chidamide promotes Mcl-1 degradation through the ubiquitin-proteasome pathway, suppressing the maintenance of mitochondrial aerobic respiration by Mcl-1, and resulting in inhibition of pancreatic cancer cell proliferation.
Bufalin induced cell apoptosis in H1975 cells may be through downregulation of Mcl-1. Proteasomal degradation of Mcl-1 via GSK-3beta activation was involved in bufalin-induced apoptosis.
BRAF (show BRAF Proteins)(V600E)-mediated MEK (show MAP2K1 Proteins)/ERK (show EPHB2 Proteins) activation can upregulate MCL-1 by phosphorylation/stabilization to confer apoptosis resistance that can be reversed by MCL-1 antagonism combined with cobimetinib, suggesting a novel therapeutic strategy against BRAF (show BRAF Proteins)(V600E)-mutant CRCs
sorafenib overcomes TRAIL resistance in renal cell carcinoma (show MOK Proteins) by a mechanism that does not rely on Mcl-1 down-regulation but involves ROS (show ROS1 Proteins) accumulation and increased activation of caspase-8 (show CASP8 Proteins)
These results suggest that mitochondrial Mcl-1 is an essential signaling mediator regulating the activation of autophagy and apoptosis during T. gondii infection.
MCL1 has a role in lung cancer cell survival via chaperone-mediated autophagy
this study reveals a vital role of MCL1 in retinoic acid -mediated survival of normal B cells
knockdown of MCL-1 in MRT cell lines induced apoptosis and increased DOX sensitivity in malignant rhabdoid tumor cells
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-related protein EAT/mcl1
, induced myeloid leukemia cell differentiation protein Mcl-1 homolog
, bcl-2-like protein 3
, induced myeloid leukemia cell differentiation protein Mcl-1
, myeloid cell leukemia ES
, myeloid cell leukemia protein 1