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Render Timestamp: 2024-11-21T13:42:38.670Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-05-10 06:57:11.745
Product last modified at: 2024-11-04T12:30:47.706Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

Mcl-1 (D2W9E) Rabbit mAb (Pacific Blue Conjugate) #85415

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  • F

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa)
    Source/Isotype Rabbit IgG
    Application Key:
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Description

    This Cell Signaling Technology® antibody is conjugated to Pacific Blue™ fluorescent dye under optimal conditions. This antibody conjugate is expected to exhibit the same species cross-reactivity as the unconjugated Mcl-1 (D2W9E) Rabbit mAb #94296.

    Product Usage Information

    Application Dilution
    Flow Cytometry (Fixed/Permeabilized) 1:50

    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.

    Protocol

    Specificity / Sensitivity

    Mcl-1 (D2W9E) Rabbit mAb (Pacific Blue™ 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 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.
    Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
    Pacific Blue is a trademark of Life Technologies Corporation.
    All other trademarks are the property of their respective owners. Visit our Trademark Information page.