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Key Documents

MAB16200

Sigma-Aldrich

Anti-MGMT Antibody, clone MT3.1

clone MT3.1, Chemicon®, from mouse

Synonym(s):

O-6-methylguanine-DNA Methyltransferase, Methylated-DNA--Protein-cysteine Methyltransferase

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

MT3.1, monoclonal

species reactivity

human

manufacturer/tradename

Chemicon®

technique(s)

flow cytometry: suitable
immunocytochemistry: suitable
immunohistochemistry: suitable (paraffin)
immunoprecipitation (IP): suitable
western blot: suitable

isotype

IgG1

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... MGMT(4255)

General description

O6-Methylguanine-DNA Methyltransferase (MGMT) is a ubiquitous DNA repair protein that removes O6-alkyl-guanine, primarily O6 methylguanine lesions from damaged DNA. It is a major contributor to cellular protection from the mutagenic, carcinogenic, and cytotoxic effects of DNA alkylation. The mechanism of MGMT action is based on the transfer of the alkyl group from the DNA to a unique acceptor cysteine residue in the protein, forming a stable thioether linkage. MGMT is frequently classified as a suicide protein. The repair capacity for O6- methylguanine is dependent on the number of MGMT molecules in the cell. There is a correlation between the occurrence of cancer in various tissues and the lack of the MGMT enzyme. High levels of MGMT result in reduced tumor events and resistance of tumors to alkylating agents.

Specificity

MGMT is a 22 kDa DNA repair protein that is present in all normal tissues; however, in a subset of human tumours MGMT is completely absent. Thus, antibody MAB16200 may be helpful in utilizing MGMT as a marker of malignant or pre-malignant cells. Because MGMT repairs the potentially cytotoxic antitumour lesions induced in DNA by certain cancer chemotherapeutic alkylating agents (e.g. BCNU, CCNU, DTIC, procarbazinc, temozolomide), tumours lacking or having low levels of MGMT will predictably be responsive to drug therapy. Conversely, tumours with high MGMT levels will likely be drug resistant. The MGMT antibody may also be used to gauge the effectiveness of MGMT modulators, such as O-6-benzylguanine, which lead to rapid degradation of the inactivated protein.

Immunogen

Made against recombinant human MGMT (O-6-methylguanine-DNA methyltransferase) expressed in E. coli.

Application

Flow Cytometry:
An independent laboratory used a previous lot on flow cytometry (Gerson, 1996).

Immunoprecipitation:
A previous lot of this antibody was used on Immunoprecipitation.

Immunohistochemistry:
A previous lot of this antibody was used on paraffin embedded sections.

Optimal working dilutions must be determined by end user.
Research Category
Epigenetics & Nuclear Function
Research Sub Category
Cell Cycle, DNA Replication & Repair
Use Anti-MGMT Antibody, clone MT3.1 (mouse monoclonal antibody) validated in FC, ICC,IHC(P), IP, WB to detect MGMT also known as O-6-methylguanine-DNA Methyltransferase, Methylated-DNA--Protein-cysteine Methyltransferase.
Useful for detection of MGMT in human tissues, tumours, cells, or xenograft lines. Gives weak cross-reactivity with MGMT from mouse, hamster and rat cells.

Quality

Evaluated by Western Blot on Jurkat lysates.

Western Blot Analysis:
1:500 dilution of this antibody detected MGMT on 10 µg of Jurkat lysates.

Target description

22-25 kDa

Physical form

Format: Purified
Protein A purified
Purified mouse monoclonal IgG1 in buffer containing 0.02 M PB, pH 7.6, 0.25 M NaCl containing 0.1% sodium azide.

Storage and Stability

Stable for 1 year at 2-8ºC from date of receipt.

Analysis Note

Control
Positive Control: Tonsil tissue, HeLa cells, CEM-CCRF cells.
Negative Control: TK6 cells.

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

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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Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 2

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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Brian R Rood et al.
Neuro-oncology, 6(3), 200-207 (2004-07-29)
DNA methylation and epigenetic inactivation of the O6-methylguanine methyltransferase (MGMT) gene induces MGMT deficiency, reducing the tumor cell's DNA repair capacity and increasing its susceptibility to alkylating chemotherapeutic agents. Consequently, adult patients whose tumors are deficient in MGMT have better
V Shilpa et al.
The Indian journal of medical research, 140(5), 616-623 (2015-01-13)
Epigenetic alterations, in addition to multiple gene abnormalities, are involved in the genesis and progression of human cancers. Aberrant methylation of CpG islands within promoter regions is associated with transcriptional inactivation of various tumour suppressor genes. O 6-methyguanine-DNA methyltransferase (MGMT)
Volumetric and MGMT parameters in glioblastoma patients: survival analysis.
Iliadis, G; Kotoula, V; Chatzisotiriou, A; Televantou, D; Eleftheraki, AG; Lambaki et al.
BMC Cancer null
Simone Frandsen et al.
Frontiers in oncology, 9, 1425-1425 (2020-01-11)
Background: Gliosarcoma (GS) is a rare histopathologic variant of glioblastoma (GBM) characterized by a biphasic growth pattern consisting of both glial and sarcomatous components. Reports regarding its relative prognosis compared to conventional GBM are conflicting and although GS is treated
Hirofumi Hirano et al.
Molecular and clinical oncology, 6(3), 321-326 (2017-04-30)
We herein present an autopsy case of a glioma patient who received long-term treatment with temozolomide (TMZ). The patient, a 35-year-old man with a hypointense tumor of the left frontal lobe, without contrast enhancement following gadolinium (Gd) administration on T1-weighted

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