CST, 14765T, Phospho-Mcl-1 (Thr163) (D5M9D) Rabbit Monoclonal Antibody

Monoclonal Antibody for studying MCL1 (Thr163) phosphate. Validated for Western Blotting,Immunoprecipitation. Available in 2 sizes. Highly specific and rigorously validated in-house, Phospho-Mcl-1 (Thr163) (D5M9D) Rabbit Monoclonal Antibody (CST #14765) is ready to ship. Product Usage Information Western Blotting: 1:1000 Immunoprecipitation: 1:50 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at -20°C. Do not aliquot the antibody. Protocol Available protocols: Western Blotting, Immunoprecipitation Specificity / Sensitivity Phospho-Mcl-1 (Thr163) (D5M9D) Rabbit Monoclonal Antibody 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. Species Reactivity: Human Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Thr163 of human Mcl-1 protein. Background 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 posttranslational 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 gene shows that Mcl-1 plays an important role in early lymphoid development and in the maintenance of mature lymphocytes (13). Alternate Names Bcl-2-like protein 3; Bcl-2-related protein EAT/mcl1; BCL2 family apoptosis regulator; Bcl2-L-3; BCL2L3; EAT; Induced myeloid leukemia cell differentiation protein Mcl-1; Mcl-1; MCL1; MCL1 apoptosis regulator, BCL2 family member; MCL1-ES; MCL1, BCL2 family apoptosis regulator; mcl1/EAT; MCL1L; MCL1S; MGC104264; MGC1839; myeloid cell leukemia 1; myeloid cell leukemia ES; myeloid cell leukemia sequence 1 (BCL2-related); myeloid cell leukemia sequence 1, isoform 1; TM Specification REACTIVITY: H SENSITIVITY: Endogenous MW (kDa): 40 Source/Isotype: Rabbit IgG