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Data show that the three DNA repair enzymes ALKBH2, ALKBH3, and AlkB are not only able to repair DNA adducts, but also can edit the epigenetic modification and generate the corresponding oxidative derivatives.
These results revealed that N3-ethylthymidine , but not other DNA lesions, could be repaired by Alkbh2 and Alkbh3 in mammalian cells.
studies reveal the ALKBH2 binding interface of PCNA and indicate that both germline and somatic ALKBH2 variants could have cellular effects on ALKBH2 function in DNA repair.
It was shown for first time that DNA glycosylase ALKBH2 can repair DNA adduct 1,N2-ethenoguanine.
ABH2 knockdown impairs rDNA transcription and leads to increased single-stranded and double-stranded DNA breaks in the rDNA genes.
Overexpression of ALKBH2 is associated with enhanced resistance to temozolomide in glioblastoma.
ALKBH2 is an upstream molecule of the oncoprotein, MUC1, and regulates cell cycle and EMT, resulting in progression of urothelial carcinomas.
combination of duplex interrogation and oxidation chemistry allows ALKBH2 to detect and process diverse lesions efficiently and correctly
The non-enzymatic binding of AAG to 3,N(4)-ethenocytosine specifically blocks ALKBH2-catalyzed repair of 3,N(4)-ethenocytosine but not that of methylated ALKBH2 substrates.
X-ray absorption spectroscopy structural investigation of early intermediates in the mechanism of DNA repair by human ABH2
ABH2 is downregulated in a subset of gastric cancers, and might be involved in the molecular mechanism of gastric cancer through inhibiting the proliferation of gastric cancer cells.
This work has provided a detailed understanding of the structural features of the single-stranded DNA and double-stranded DNA preferences of ABH2 and ABH3.
Divergent sequences outside of the active site determine substrate specificities of ABH2.
Tumour protein (TP53) is directly involved by binding to the promoter of ALKBH2 in mediating photofrin-mediaated photodynamic therapy in U87 glioma cells.
Data show that the JMJD1A/ABH2 family of dioxygenases is highly sensitive to inhibition by carcinogenic nickel ions.
first crystal structure of ABH2
ABH2 is active in the direct reversal of epsilon A lesions, and that ABH2, together with the alkyl-N-adenine-DNA glycosylase, which is the most effective enzyme for the repair of epsilon A, comprise the cellular defense against epsilon A lesions
Mutations of ABH2 is associated with pediatric brain tumors.
ALKBH2 and ALKBH3 provide cancer protection similar to that of the DNA glycosylase AAG and display apparent epistasis with Aag
Although both Alkbh2 and Alkbh3 can protect against methyl methanesulfonate-induced cell death, only Alkbh2 shows statistically significant protection against mutations following treatment with this exogenous methylating agent.
The Escherichia coli AlkB protein protects against the cytotoxicity of methylating agents by repair of the specific DNA lesions generated in single-stranded DNA. ALKBH2 and ALKBH3 (MIM 610603) are E. coli AlkB homologs that catalyze the removal of 1-methyladenine and 3-methylcytosine (Duncan et al., 2002
alkB, alkylation repair homolog 2 (E. coli)
, alpha-ketoglutarate-dependent dioxygenase alkB homolog 2
, alpha-ketoglutarate-dependent dioxygenase alkB homolog 2-like
, 2OG-Fe(II) oxy DC1
, DNA oxidative demethylase ALKBH2
, alkylated DNA repair protein alkB homolog 2
, oxy DC1
, AlkB homolog 2