Product Pathways - Apoptosis
Phospho-Mcl-1 (Ser64) Antibody #13297
|13297S||100 µl (10 western blots)||---||In Stock||---|
|13297||carrier free and custom formulation / quantity||email request|
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Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting
Specificity / Sensitivity
Phospho-Mcl-1 (Ser64) Antibody recognizes endogenous levels of Mcl-1 protein only when phosphorylated at Ser64. Non-specific bands of unknown origin are detected in some cell lines at 70 and 140 kDa.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser64 of human Mcl-1 protein.
Western blot analysis of extracts from HCT 116 and KARPAS-299 cells, untreated (-) or treated with MG-132 #2194 (10 μM, overnight; +) using Phospho-Mcl-1 (Ser64) Antibody (left). Phospho-specificity is demonstrated by antibody competition with peptides specific for phospho-Mcl-1 (Ser64) (middle) or non-phospho-Mcl-1 (Ser64) (right).
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).
Phosphorylation of Mcl-1 at Ser64 can target it for ubiqutination and destruction by the tumor suppressor protein FBW7 (14,15)
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