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Catalyzes the methylation of 5-carboxymethyl uridine to 5-methylcarboxymethyl uridine at the wobble position of the anticodon loop in tRNA. Zusätzlich bieten wir Ihnen ALKBH8 Proteine (4) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal ALKBH8 Primary Antibody für EIA, WB - ABIN452732
Shimada, Nakamura, Anai, De Velasco, Tanaka, Tsujikawa, Ouji, Konishi: A novel human AlkB homologue, ALKBH8, contributes to human bladder cancer progression. in Cancer research 2009
Cow (Bovine) Polyclonal ALKBH8 Primary Antibody für WB - ABIN2776625
Ota, Suzuki, Nishikawa, Otsuki, Sugiyama, Irie, Wakamatsu, Hayashi, Sato, Nagai, Kimura, Makita, Sekine, Obayashi, Nishi, Shibahara, Tanaka, Ishii, Yamamoto, Saito, Kawai, Isono, Nakamura, Nagahari et al.: Complete sequencing and characterization of 21,243 full-length human cDNAs. ... in Nature genetics 2003
findings suggest that the high expression of ALKBH8 is critical for the growth and progression of bladder cancer
Many euk (zeige ALKBH Antikörper)aryotic tRNAs contain the wobble modification 5-m (zeige MCM5 Antikörper)ethoxycarbonylmethyl-uridine (mcm5U). It is demonstrated that (R)- and (S)-5-methoxycarbonylhydroxymethyluridine (mchm5U), hydroxylated forms of mcm(5)U, are present in mammalian tRNA-Arg(UCG), and tRNA-Gly(UCC), respectively. It is shown that the hydroxylation reaction leading to the formation of (S)-mchm5U is catalyzed by the oxygenase (AlkB) domain of ALKBH8.
The methyltransferase domain of ALKBH8 is demonstrated to be a functional homologue of the Saccharomyces cerevisiae Trm9 protein, mediating the last step in the formation of the wobble uridine modification 5-methoxycarbonylmethyl-uridine in tRNA. This modification is shown to be important for efficient selenoprotein synthesis. ALKBH8 knock-out mice are generated and described.
Data show that human AlkB (zeige ALKBH Antikörper) homolog 8 (ABH8) catalyzes tRNA methylation to generate 5-methylcarboxymethyl uridine (mcm(5 (zeige MCM5 Antikörper))U) at the wobble position of certain tRNAs, a critical anticodon loop modification linked to DNA damage survival.
Findings indicate a role for ALKBH8 in urothelial carcinoma cell survival mediated by NOX-1 (zeige NOX1 Antikörper)-dependent ROS (zeige ROS1 Antikörper) signals, further suggesting therapeutic strategies in human bladder cancer by inducing JNK (zeige MAPK8 Antikörper)/p38 (zeige CRK Antikörper)/gammaH2AX (zeige H2AFX Antikörper)-mediated cell death by silencing of ALKBH8.
Alkbh8 and tRNA modifications as central regulators of cellular oxidative stress responses in mammalian systems.
The AlkB (zeige ALKBH Antikörper) domain of ALKBH8 specifically hydroxylates mcm(5 (zeige MCM5 Antikörper))U into (S)-mchm(5)U in tRNA-Gly(UCC).
Data show that ALKBH8 is a tRNA methyltransferase required for the final step in the biogenesis of mcm5U.
Catalyzes the methylation of 5-carboxymethyl uridine to 5-methylcarboxymethyl uridine at the wobble position of the anticodon loop in tRNA. Catalyzes the last step in the formation of 5-methylcarboxymethyl uridine at the wobble position of the anticodon loop in target tRNA. Has a preference for tRNA(Arg) and tRNA(Glu), and does not bind tRNA(Lys). Required for normal survival after DNA damage. May inhibit apoptosis and promote cell survival and angiogenesis (By similarity).
AlkB homologue 8
, S-adenosyl-L-methionine-dependent tRNA methyltransferase ABH8
, alkylated DNA repair protein alkB homolog 8
, probable alpha-ketoglutarate-dependent dioxygenase ABH8
, tRNA (carboxymethyluridine(34)-5-O)-methyltransferase ABH8