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anti-Human MGMT Antikörper:
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Human Monoclonal MGMT Primary Antibody für CyTOF, FACS - ABIN151202
Kokkinakis, Ahmed, Delgado, Fruitwala, Mohiuddin, Albores-Saavedra: Role of O6-methylguanine-DNA methyltransferase in the resistance of pancreatic tumors to DNA alkylating agents. in Cancer research 1998
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Human Monoclonal MGMT Primary Antibody für WB - ABIN1882265
Tano, Shiota, Collier, Foote, Mitra: Isolation and structural characterization of a cDNA clone encoding the human DNA repair protein for O6-alkylguanine. in Proceedings of the National Academy of Sciences of the United States of America 1990
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Human Monoclonal MGMT Primary Antibody für WB - ABIN1882266
Rydberg, Spurr, Karran: cDNA cloning and chromosomal assignment of the human O6-methylguanine-DNA methyltransferase. cDNA expression in Escherichia coli and gene expression in human cells. in The Journal of biological chemistry 1990
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Human Monoclonal MGMT Primary Antibody für IHC (p), IHC - ABIN152115
Takeshita, Inoshita, Taguchi, Okuda, Fukuhara, Oyama, Ohashi, Sano, Takeuchi, Yamada: High incidence of low O(6)-methylguanine DNA methyltransferase expression in invasive macroadenomas of Cushing's disease. in European journal of endocrinology 2009
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Monoclonal MGMT Primary Antibody für FACS, IHC (fro) - ABIN534106
Roth, Xu, Luo, Kelley: Human-yeast chimeric repair protein protects mammalian cells against alkylating agents: enhancement of MGMT protection. in Cancer gene therapy 2003
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Human Polyclonal MGMT Primary Antibody für FACS, IHC (p) - ABIN391514
Kim, Suh, Choi, Kang, Shin, Lee, Moon, Kim: Inactivation of O6-methylguanine-DNA methyltransferase in soft tissue sarcomas: association with K-ras mutations. in Human pathology 2009
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Human Polyclonal MGMT Primary Antibody für IF (p), IHC (p) - ABIN730768
Oláh, Kálmán, Tóth, Zvara, Sántha, Ivitz, Janka, Pákáski: Proteomic Analysis of Cerebrospinal Fluid in Alzheimer's Disease: Wanted Dead or Alive. in Journal of Alzheimer's disease : JAD 2014
Low MGMT promoter methylation is associated with glioblastoma.
MGMT Gene Promoter Methylation Status - Assessment of Two Pyrosequencing Kits and Three Methylation-specific PCR Methods for their Predictive Capacity in Glioblastomas.
In patients with neuroendocrine neoplasms, response to therapy, progression free survival and overall survival was correlated to MGMT promoter methylation status
The first evidence for non-repair functions of MGMT in cell cycle and highlight the involvement of PCNA in MGMT downregulation, with p21 attenuating the process.
The methylation of the MGMT promoter is uncommon, or occurs at a low frequency in meningiomas. There is no convincing rationale to test such tumors for their MGMT methylation status in a clinical setting
Data revealed that MGMT gene methylation was higher in non-small-cell lung carcinoma (NSCLC) tissue samples than normal. Also advanced stage NSCLC patients showed higher methylation than early stage patients without impacting patients survival. These results provided clear evidence about the association of MGMT hypermethylation with increased risk of NSCLC. [review]
There is no difference in the expression of Integrin alphavbeta3 between tumor samples from glioblastomas patients with methylated or unmethylated promoter regions in the (6)O-methylguanine methyltransferase (MGMT).
Germline variants in MGMT gene are associated with prostate cancer.
Promoter Hypermethylation of MGMT Gene is associated with Colorectal Cancer.
Our study confirmed that the independent prognostic role of MGMT methylation status. An average level of methylation between all investigated CpGs of 9% may help discriminating between methylated and unmethylated tumors.
results indicated that the MGMT rs12917 TT genotype increases the risk of Head and neck squamous cell carcinoma
Strong MGMT expression was associated with survival in pancreatic ductal adenocarcinoma
MGMT promoter methylation may be correlated with the tumorigenesis of ovarian cancer. It was associated with tumor histotypes, but not correlated with clinical stage and tumor grade.
use a compendium of brain MRI scans collected from The Cancer Imaging Archive (TCIA) combined with methylation data from The Cancer Genome Atlas (TCGA) to predict the methylation state of the MGMT regulatory regions in glioblastoma patients
In summary of this results and the published data clearly indicate that MGMT promoter methylation is a rare event in DMG patients supporting the idea that analyzing the MGMT promoter status would only be recommended in H3 K27M-wildtype GBM.
The changes in MGMT expression reflect the impairment of DNA repair, which probably serves as a stage in the development and progression of endometriosis.
MGMT methylation was observed in 37% of cases with primary CNS diffuse large B-cell lymphoma
Methylguanine methyltransferase (MGMT) is a key gene that encodes for a protein that repairs DNA.
Study provides evidence that low-expression of TET1 in oral squamous cell carcinoma (OSCC) stem cells may stimulate MGMT promoter methylation, while inhibiting MGMT mRNA expression, which ultimately strengthens the sensitivity of OSCC stem cells in regards to chemotherapeutics.
High MGMT expression is associated with glioblastoma multiforme resistance to temozolomide
This study shows that when cell death and cell cycle arrest pathways are inhibited, p53 can still mediate MGMT-dependent repair, to promote cell survival upon DNA damage.
Snell, GHKRO, and PAPPA-KO mice express high levels of two proteins involved in DNA repair, O-6-methylguanine-DNA methyltransferase (MGMT) and N-myc downstream-regulated gene 1 (NDRG1).
This study demonstrates for the first time a non-linear dose-response for alkylation-induced colorectal carcinogenesis and reveals DNA repair by MGMT, but not AAG, as a key node in determining a carcinogenic threshold.
Findings suggest that O6-methylguanine-DNA methyltransferase (MGMT)-mediated temozolomide resistance is associated with increased histone acetylation.
Loss of MGMT expression and high Ezrin protein expression leads to esophageal cancer.
Both base excision repair and O6-methylguanine-DNA methyltransferase protect against methylation-induced colon carcinogenesis.
ta indicate that Zik1 and Gja9 demonstrated cancer-specific aberrant DNA methylation, whereas, Cdkn2a/p16, Igfbp3, Mgmt, Id4, and Cxcr4 were methylated in both the AOM tumors and normal colon mucosa.
Roles of MGMT and MLH1 proteins in alkylation-induced apoptosis and mutagenesis.
Repression of MGMT is associated with precancerous conditions in hyperplastic mucosa adjacent to colon cancer
GAMT and AGAT mRNA are up-regulated 5.4- and 1.9-fold respectively in adult mdx muscle compared to C57
In vivo selection of MD9-P140K-transduced BM cells was more efficient following submyeloablative than myeloablative therapy.
MGMT-deficient cells would likely exhibit an increased mutational burden, but only following exposures to specific environmental mutagens such as the tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK).
Mgmt suppresses intestinal cancer associated with exogenous alkylating agents.
IFN-beta appears to sensitize neuroblastoma cells to the cytotoxic effects of temozolomide through attenuation of MGMT expression
In the fetal brain, mRNA expression of AGAT increased steadily across the second half of pregnancy. In the fetal kidney and liver, AGAT mRNA and protein expression were also relatively low until 34-37 days gestation.
Involved in the cellular defense against the biological effects of O6-methylguanine (O6-MeG) in DNA. Repairs alkylated guanine in DNA by stoichiometrically transferring the alkyl group at the O-6 position to a cysteine residue in the enzyme. This is a
, O6-methylguanine-DNA methyltransferase
, methylated-DNA--protein-cysteine methyltransferase
, methylguanine-DNA methyltransferase
, O-6-alkylguanine-DNA alkyltransferase
, 0-6-methylguanine-DNA methyltransferase
, O(6)-alkylguanine-DNA alkyltransferase
, O6-alkylguanine-DNA alkyltransferase
, O6-methylguanine-DNA methyltranferase