M8434
Anti-Mcl-1 antibody produced in rabbit
IgG fraction of antiserum, buffered aqueous solution
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About This Item
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biological source
rabbit
conjugate
unconjugated
antibody form
IgG fraction of antiserum
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 40-42 kDa
species reactivity
human
technique(s)
immunoprecipitation (IP): 100-150 μg using lysate of mitochondria from 2.5 to 5.0 × 107 HeLa cells
microarray: suitable
western blot: 1:8,000 using a HeLa cell (human epithelioid carcinoma) mitochondria extract
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... CLEC4D(338339)
mouse ... Clec4d(17474)
rat ... Clec4d(362432)
Related Categories
General description
Anti-Mcl-1 is developed in rabbit using a synthetic peptide corresponding to an internal region of Mcl-1 of human origin with N-terminal added cysteine, conjugated to maleimide activated keyhole limpet hemocyanin (KLH), as immunogen. MCL1 apoptosis regulator, BCL2 family member (Mcl-1) is expressed in many normal and neoplastic cells and is especially abundant in skeletal and cardiac muscle and in germinal centers of lymphoid tissues.
Mcl-1 is a member of Bcl-2 family that contains 3 Bcl-2 homology (BH) domains, BH1, BH2 and BH3, originally identified as an upregulated gene in human myeloid leukemia cell line (ML-1) in response to PMA. It is regulated transcriptionally and post-transcriptionally to enhance the cell survival. Mcl-1 is induced rapidly through cytokine-mediated survival pathways. Additionally, the upstream half of Mcl-1 RNA contains PEST (pro (P) Glu (E), Ser (S) and Thr (T) ) sequences and exhibits rapid turn-over. Increased expression of Mcl-1 maintains cell viability, decreased expression promotes cell death. Mcl-1 is reported to exhibit differentiation stage-specific expression in hematopoietic lineages and epithelial cells. A splice variant of Mcl-1, Mcl-1s promotes cell death. Often, the expression of Mcl-1 is induced via the MAPK signalling pathway acting on SRF/Elk-1 or Akt/CREB regulated pathway. Mcl-1 is expressed in many normal and neoplastic cells and is especially abundant in skeletal and cardiac muscle and in germinal centers of lymphoid tissues. It is predominantly expressed in the mitochondria but in neutrophils it seems to be mainly located in nuclear fractions.
Specificity
Anti-Mcl-1 specifically recognizes Mcl-1 in tissue and cell extracts (40 to 42 kDa doublet).
Immunogen
synthetic peptide corresponding to an internal region of Mcl-1 of human origin (amino acids 121-139). This sequence is highly similar in mouse and rat.
Application
A minimum working dilution of 1:8000 is determined by immunoblotting using HeLa human epithelioid carcinoma mitochondria extract. It may also be used for detection by immunoblotting in Human melanoma cell lines, Human colon adenocarcinoma HT-29 and SW620 cells. Mcl-1 is immunoprecipitated from the lysate of mitochondria from 2.5 to 5.0x10 7 HeLa cells using 100 to 150 μg of the antibody. The antibody is suitable for protein microarray applications.
Anti-Mcl-1 antibody produced in rabbit has been used in immunoblotting.
Biochem/physiol Actions
MCL1 apoptosis regulator, BCL2 family member (Mcl-1) exhibits great lability presumably due to its PEST sequence (P, Pro; E, Glu; S, Ser; T, Thr). Unlike the stable Bcl-2 protein, Mcl-1 exhibits great lability presumably due to its PEST sequence (P, Pro; E, Glu; S, Ser; T, Thr). Mcl-1, like Bcl-2, promotes cell viability under conditions which otherwise cause apoptosis. MCL1 acts as a chaperone of fortilin by binding and stabilizing it. It also interacts and negatively regulates the proliferating cell nuclear antigen (PCNA).
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Signal Word
Warning
Hazard Statements
Precautionary Statements
Hazard Classifications
Acute Tox. 4 Dermal - Acute Tox. 4 Oral - Aquatic Chronic 3
Storage Class Code
10 - Combustible liquids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Kung-Wen Lu et al.
International journal of molecular sciences, 23(18) (2022-09-24)
Some clinically used anti-cancer drugs are obtained from natural products. Allyl isothiocyanate (AITC), a plant-derived compound abundant in cruciferous vegetables, has been shown to possess an anti-cancer ability in human cancer cell lines in vitro, including human brain glioma cells.
Immunohistochemical analysis of Mcl-1 protein in human tissues. Differential regulation of Mcl-1 and Bcl-2 protein production suggests a unique role for Mcl-1 in control of programmed cell death in vivo.
Krajewski S, et al.
The American Journal of Pathology, 146(6), 1309-1309 (1995)
Different modulation of TRAIL-induced apoptosis by inhibition of pro-survival pathways in TRAIL-sensitive and TRAIL-resistant colon cancer cells
Vaculova A, et al.
Febs Letters, 580(28-29), 6565-6569 (2006)
D A Moulding et al.
Blood, 92(7), 2495-2502 (1998-09-25)
Human neutrophils possess a very short half-life because they constitutively undergo apoptosis. Cytokines, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), and other agents can rescue neutrophils from apoptosis but the molecular mechanisms involved in this rescue are undefined. Here, we show
Differences in TRAIL-induced changes of Mcl-1 expression among distinct human colon epithelial cell lines
Vaculova A, et al.
Experimental Cell Research, 315(19), 3259-3266 (2009)
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