CST, 74857W2, Mcl-1 (D2W9E) Rabbit Monoclonal Antibody (SignalFlex™ mFluor™ Red 780 Conjugate)

Monoclonal Antibody for studying MCL1 mouse. Highly specific and rigorously validated in-house, Mcl-1 (D2W9E) Rabbit Monoclonal Antibody (SignalFlex^™ mFluor^™ Red 780 Conjugate) (CST #74857) is ready to ship. Product Usage Information SignalFlex™ conjugates are produced using highly validated Cell Signaling Technology ® primary antibodies and conjugation methods that have been rigorously tested, ensuring high-quality conjugates and lot-to-lot consistency. These conjugates are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity. However, they are not tested on specific assays. Optimal dilutions/concentrations should be determined by the end user. When performing flow cytometry, we recommend using an isotype control conjugate at the same concentration as the antibody conjugate. Storage Supplied in PBS (pH 7.2), less than 0.1% sodium azide, and 2 mg/mL BSA. Store at 4°C. Do not aliquot the antibody. Protect from light. Do not freeze. Specificity / Sensitivity Mcl-1 (D2W9E) Rabbit mAb (SignalFlex™ mFluor™ Red 780 Conjugate) recognizes endogenous levels of total Mcl-1 protein. Species Reactivity: Human, Mouse, Rat Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro60 of mouse 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 AW556805; Bcl-2-related protein EAT/mcl1; Induced myeloid leukemia cell differentiation protein Mcl-1 homolog; Mcl-; Mcl-1; Mcl1; myeloid cell leukemia sequence 1 Specification REACTIVITY: H M R SENSITIVITY: Endogenous Source/Isotype: Rabbit IgG