Product Pathways - Apoptosis
Mcl-1 (D2W9E) Rabbit mAb (Alexa Fluor® 647 Conjugate) #78471
|78471S||100 µl ( 50 tests )||￥4,060.00 现货查询||购买询价|
|78471||carrier free & custom formulation / quantity||email request|
Species cross-reactivity is determined by western blot.
Applications Key: F=Flow Cytometry,
Specificity / Sensitivity
Mcl-1 (D2W9E) Rabbit mAb (Alexa Fluor® 647 Conjugate) recognizes endogenous levels of total Mcl-1 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro60 of mouse Mcl-1 protein.
This Cell Signaling Technology antibody is conjugated to Alexa Fluor® 647 fluorescent dye and tested in-house for direct flow cytometric analysis in human cells. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated Mcl-1 (D2W9E) Rabbit mAb #94296.
Flow cytometric analysis of L-929 cells using Mcl-1 (D2W9E) Rabbit mAb (Alexa Fluor® 647 Conjugate) (blue) compared to concentration matched Rabbit (DA1E) mAb IgG XP® Isotype Control (Alexa Fluor® 647 Conjugate) #2985 (red).
Mcl-1 is an anti-apoptotic member of the Bcl-2 family originally isolated from the ML-1 human myeloid leukemia cell line during phorbol ester-induced differentiation along the monocyte/macrophage pathway (1). Similar to other Bcl-2 family members, Mcl-1 localizes to the mitochondria (2), interacts with and antagonizes pro-apoptotic Bcl-2 family members (3), and inhibits apoptosis induced by a number of cytotoxic stimuli (4). Mcl-1 differs from its other family members in its regulation at both the transcriptional and post-translational level. First, Mcl-1 has an extended amino-terminal PEST region, which is responsible for its relatively short half-life (1,2). Second, unlike other family members, Mcl-1 is rapidly transcribed via a PI3K/Akt dependent pathway, resulting in its increased expression during myeloid differentiation and cytokine stimulation (1,5-7). Mcl-1 is phosphorylated in response to treatment with phorbol ester, microtubule-damaging agents, oxidative stress, and cytokine withdrawal (8-11). Phosphorylation at Thr163, the conserved MAP kinase/ERK site located within the PEST region, slows Mcl-1 protein turnover (10) but may prime the GSK-3 mediated phosphorylation at Ser159 that leads to Mcl-1 destabilization (11). Mcl-1 deficiency in mice results in peri-implantation lethality (12). In addition, conditional disruption of the corresponding mcl-1 gene shows that Mcl-1 plays an important role in early lymphoid development and in the maintenance of mature lymphocytes (13).
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- Inoshita, S. et al. (2002) J Biol Chem 277, 43730-4.
- Domina, A.M. et al. (2004) Oncogene 23, 5301-15.
- Maurer, U. et al. (2006) Mol Cell 21, 749-60.
- Rinkenberger, J.L. et al. (2000) Genes Dev 14, 23-7.
- Opferman, J.T. et al. (2003) Nature 426, 671-6.
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For Research Use Only. Not For Use In Diagnostic Procedures.
Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
XP is a registered trademark of Cell Signaling Technology, Inc.
Alexa Fluor is a registered trademark of Life Technologies Corporation.
The Alexa Fluor dye conjugates in this product are sold under license from Life Technologies Corporation, for research use only excluding use in combination with DNA microarrays and high content screening (HCS).
Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.
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