Human ALKBH2 blocking peptide (CDBP0377)

Synthetic Human ALKBH2 blocking peptide for BL

Product Overview
Blocking peptide for anti-ALKBH2 antibody
Target
ALKBH2
Nature
Synthetic
Species Reactivity
Human
Tag/Conjugate
Unconjugated
Application Notes
For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not suitable for human or animal consumption.
Procedure
None
Format
Liquid
Concentration
200 μg/ml
Size
50 μg
Buffer
PBS containing 0.02% sodium azide
Preservative
0.02% Sodium Azide
Storage
Store at -20℃, stable for one year.
UniProt ID
Antigen Description
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 [PubMed 12486230]).
Function
DNA-N1-methyladenine dioxygenase activity; cytosine C-5 DNA demethylase activity; cytosine C-5 DNA demethylase activity; ferrous iron binding; metal ion binding; oxidoreductase activity; oxidoreductase activity, acting on single donors with incorporation
Synonyms
ALKBH2; alkB, alkylation repair homolog 2 (E. coli); alpha-ketoglutarate-dependent dioxygenase alkB homolog 2; ABH2; MGC90512; oxy DC1; 2OG-Fe(II) oxy DC1; alkylated DNA repair protein alkB homolog 2; FLJ99103;

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References


Oncometabolite D-2-Hydroxyglutarate Inhibits ALKBH DNA Repair Enzymes and Sensitizes IDH Mutant Cells to Alkylating Agents

CELL REPORTS

Authors: Wang, Pu; Wu, Jing; Ma, Shenghong; Zhang, Lei; Yao, Jun; Hoadley, Katherine A.; Wilkerson, Matthew D.; Perou, Charles M.; Guan, Kun-Liang; Ye, Dan; Xiong, Yue

Chemotherapy of a combination of DNA alkylating agents, procarbazine and lomustine (CCNU), and a microtubule poison, vincristine, offers a significant benefit to a subset of glioma patients. The benefit of this regimen, known as PCV, was recently linked to IDH mutation that occurs frequently in glioma and produces D-2-hydroxyglutarate (D-2-HG), a competitive inhibitor of a-ketoglutarate (a-KG). We report here that D-2-HG inhibits the a-KG-dependent alkB homolog (ALKBH) DNA repair enzymes. Cells expressing mutant IDH display reduced repair kinetics, accumulate more DNA damages, and are sensitized to alkylating agents. The observed sensitization to alkylating agents requires the catalytic activity of mutant IDH to produce D-2-HG and can be reversed by the deletion of mutant IDH allele or overexpression of ALKBH2 or AKLBH3. Our results suggest that impairment of DNA repair may contribute to tumorigenesis driven by IDH mutations and that alkylating agents may merit exploration for treating IDH-mutated cancer patients.

Down-regulation of ALKBH2 increases cisplatin sensitivity in H1299 lung cancer cells

ACTA PHARMACOLOGICA SINICA

Authors: Wu, Shuang-shuang; Xu, Wei; Liu, Shan; Chen, Bo; Wang, Xue-li; Wang, Yan; Liu, Shi-feng; Wu, Jian-qing

Aim: To elucidate the combined effect of alkylated DNA repair protein alkB homolog 2 (ALKBH2)-targeting gene therapy and cisplatin (cDDP) chemotherapy on the non-small cell lung cancer (NSCLC) H1299 cell line. Methods: ALKBH2 was down-regulated in H1299 cells by lentivirus-mediated RNA interference (RNAi). Changes in ALKBH2 expression were determined using real-time RT-PCR and western blotting. Cell viability was evaluated using MTT assay. DNA synthesis in proliferating cells was determined using BrdU incorporation assay. Cell apoptosis was determined using flow cytometry. Results: Lentivirus-mediated ALKBH2 silencing alone did not induce apoptosis or attenuate the growth potential of H1299 cells within five days post-infection. Combined treatment modalities with lentivirus-mediated ALKBH2 down-regulation and cDDP (333 mu mol/L) were significantly more potent in inhibiting cell growth and inducing apoptosis than mono-chemotherapy. Conclusion: Combined treatment modalities of ALKBH2 knockdown and cDDP chemotherapy have the potential to improve the efficacy in the treatment of NSCLC.

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