Product Pathways - Apoptosis
Phospho-Mcl-1 (Thr163) (D5M9D) Rabbit mAb #14765
|14765S||100 µl ( 10 western blots )||￥3,900.00 现货查询||购买询价|
|14765||carrier free & custom formulation / quantity||email request|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation,
Specificity / Sensitivity
Phospho-Mcl-1 (Thr163) (D5M9D) Rabbit mAb recognizes endogenous levels of Mcl-1 protein only when phosphorylated at Thr163. This antibody also cross-reacts with an unidentified protein of 70 kDa in some cell lines.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Thr163 of human Mcl-1 protein.
Western blot analysis of extracts from KARPAS-299 and Raji cell lines, untreated (-) or treated with TPA #4174 (200 nM, 30 min; +), using Phospho-Mcl-1 (Thr163) (D5M9D) Rabbit mAb (upper) and β-Actin (D6A8) Rabbit mAb #8457 (lower).
Immunoprecipitation of phospho-Mcl-1 (Thr163) from KARPAS-299 cells treated with TPA #4174 (200 nM, 30 min) using Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (lane 2) or Phospho-Mcl-1 (Thr163) (D5M9D) Rabbit mAb (lane 3). Lane 1 represents 10% input. Western blot was perform using Phospho-Mcl-1 (Thr163) (D5M9D) Rabbit mAb. Mouse Anti-rabbit IgG (Conformation Specific) (L27A9) mAb #3678 was used as a secondary antibody to avoid cross reactivity with IgG heavy and light chains.
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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- Zhou, P. et al. (1997) Blood 89, 630-43.
- Wang, J.M. et al. (1999) Mol Cell Biol 19, 6195-206.
- Jourdan, M. et al. (2003) Oncogene 22, 2950-9.
- Chao, J.R. et al. (1998) Mol Cell Biol 18, 4883-98.
- Domina, A.M. et al. (2000) J Biol Chem 275, 21688-94.
- 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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