Render Target: STATIC
Render Timestamp: 2024-11-21T13:53:13.848Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-08-01 15:32:49.187
Product last modified at: 2024-11-18T22:45:07.594Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Mcl-1 Antibody #4572

Filter:
  • WB

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 40
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    Mcl-1 Antibody detects endogenous levels of human Mcl-1. The antibody does not cross-react with other Bcl-2 family members at physiological levels.

    Species Reactivity:

    Human

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ser121 of human Mcl-1. Antibodies are purified by protein A and peptide affinity chromatography.

    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 mcl-1 gene shows that Mcl-1 plays an important role in early lymphoid development and in the maintenance of mature lymphocytes (13).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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