Rabbit MCL1 Polyclonal Antibody | anti-MCL1 antibody

Anti-MCL1 Antibody

Cat. Num. AAA419445

• Gene Names: Mcl1; Mcl-1; AW556805
• Reactivity: Human, Mouse, Rat
• Applications: Western Blot, Immunohistochemistry
• Purity: Affinity Purification
• Synonyms: MCL1; Polyclonal Antibody; Anti-MCL1 Antibody; anti-MCL1 antibody

• Host: Rabbit
• Reactivity: Human, Mouse, Rat
• Clonality: Polyclonal
• Isotype: IgG
• Specificity: Western blot analysis of extracts of various cell lines, using MCL1 antibody.
• Purity/Purification: Affinity Purification
• Form/Format: Liquid
• Concentration: 1mg/ml (varies by lot)
• Sequence Length: 65

• Applicable Applications for anti-MCL1 antibody: Western Blot (WB), Immunohistochemistry (IHC)
• Application Notes: WB: 1:500 - 1:1000; IHC: 1:50 - 1:100
• Immunogen: Recombinant protein of human MCL1
• Storage Buffer: PBS with 0.02% sodium azide,50% glycerol, pH7.3.
• Preparation and Storage: Store at -20 degree C (regular) and -80 degree C (long term). Avoid freeze / thaw cycles.

Western Blot (WB)

Related Product Information for anti-MCL1 antibody

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).

NCBI and Uniprot Product Information

• NCBI GI #: 3360506
• NCBI GeneID: 17210
• Molecular Weight: 30,930 Da
• NCBI Official Full Name: MCL1, partial
• NCBI Official Synonym Full Names: myeloid cell leukemia sequence 1
• NCBI Official Symbol: Mcl1
• NCBI Official Synonym Symbols: Mcl-1; AW556805
• NCBI Protein Information: induced myeloid leukemia cell differentiation protein Mcl-1 homolog
• UniProt Protein Name: Induced myeloid leukemia cell differentiation protein Mcl-1 homolog
• Protein Family: Minichromosome loss protein
• UniProt Gene Name: Mcl1

Uniprot Description

MCL1: a myeloid cell leukemia protein of the Bcl-2 family of proteins. Two alternatively spliced transcripts encoding distinct isoforms have been identified. The longer gene product (isoform 1) enhances cell survival by inhibiting apoptosis while the alternatively spliced shorter gene product (isoform 2) promotes apoptosis and is death-inducing.

Protein type: Apoptosis; Channel, misc.; Inhibitor; Membrane protein, integral; Mitochondrial

Chromosomal Location of Human Ortholog: 3 F2.1|3 40.74 cM

Cellular Component: cytoplasm; cytosol; membrane; mitochondrial matrix; mitochondrial outer membrane; mitochondrion; nucleus

Molecular Function: BH domain binding; BH3 domain binding; protein binding; protein dimerization activity; protein heterodimerization activity; protein homodimerization activity

Biological Process: apoptotic mitochondrial changes; DNA damage response, signal transduction resulting in induction of apoptosis; negative regulation of apoptosis; negative regulation of autophagy; response to cytokine stimulus