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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 (Biotinylated) #68542

Filter:
  • WB
Western Blotting Image 1: Mcl-1 (D2W9E) Rabbit mAb (Biotinylated)
Western blot analysis of extracts from U-937 and 3T3 cells using Mcl-1 (D2W9E) Rabbit mAb (Biotinylated).

To Purchase # 68542

Cat. # Size Qty. Price Ships
68542S 100 µl
$452 Jan 9

Supporting Data

REACTIVITY H M R
SENSITIVITY Endogenous
MW (kDa) 40 (human), 35 (mouse)
Source/Isotype Rabbit IgG
Application Key:
  • WB-Western Blotting 
Species Cross-Reactivity Key:
  • H-Human 
  • M-Mouse 
  • R-Rat 

Product Information

Product Description

This Cell Signaling Technology antibody is conjugated to biotin under optimal conditions. The biotinylated antibody is expected to exhibit the same species cross-reactivity as the unconjugated Mcl-1 (D2W9E) Rabbit mAb #94296.
MW (kDa) 40 (human), 35 (mouse)

Product Usage Information

Application Dilution
Western Blotting 1:1000

Storage

Supplied in 136 mM NaCl, 2.6 mM KCI, 12 mM sodium phosphate (pH 7.4) dibasic, 2 mg/ml BSA, and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

Protocol

Specificity / Sensitivity

Mcl-1 (D2W9E) Rabbit mAb (Biotinylated) 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.
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