- CITATIONS: 4
|Application ||WB, IHC-P, FC, E|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||37337 Da|
|Antigen Region||191-226 aa|
|Other Names||Induced myeloid leukemia cell differentiation protein Mcl-1, Bcl-2-like protein 3, Bcl2-L-3, Bcl-2-related protein EAT/mcl1, mcl1/EAT, MCL1, BCL2L3|
|Target/Specificity||This MCL1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 191-226 amino acids from human MCL1.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||MCL1 Antibody (BH3 Domain Specific) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Involved in the regulation of apoptosis versus cell survival, and in the maintenance of viability but not of proliferation. Mediates its effects by interactions with a number of other regulators of apoptosis. Isoform 1 inhibits apoptosis. Isoform 2 promotes apoptosis.|
|Cellular Location||Membrane; Single-pass membrane protein. Cytoplasm. Mitochondrion. Nucleus, nucleoplasm. Note=Cytoplasmic, associated with mitochondria|
Provided below are standard protocols that you may find useful for product applications.
The Mcl-1 protein belongs to the Bcl-2 family. Alternative splicing occurs at this locus and two transcript variants 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.
Crossley, L.J., J. Leukoc. Biol. 74(4):583-592 (2003).
Kotelkin, A., et al., J. Virol. 77(17):9156-9172 (2003).
Erwert, R.D., et al., Microb. Pathog. 35(2):87-93 (2003).
Liu, H., et al., Blood 102(1):344-352 (2003).
Nijhawan, D., et al., Genes Dev. 17(12):1475-1486 (2003).
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