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Murine aldo-keto reductase family 1 subfamily B: identification of AKR1B8 as an ortholog of human AKR1B10
被引:25
|作者:
Joshi, Amit
[1
]
Rajput, Sandeep
[1
]
Wang, Chun
[1
]
Ma, Jun
[1
]
Cao, Deliang
[1
]
机构:
[1] So Illinois Univ, Sch Med, Simmons Cooper Canc Inst, Dept Med Microbiol Immunol & Cell Biol, Springfield, IL 62794 USA
关键词:
acetyl-CoA carboxylase-alpha;
aldo-keto reductase family 1 member B8 (AKR1B8);
aldo-keto reductase family 1 member B10 (AKR1B10);
AKR1B8;
knockdown;
mouse ortholog;
MOUSE VAS-DEFERENS;
BREAST-CANCER;
PROTEIN;
GROWTH;
GENE;
SUPERFAMILY;
B10;
CELLS;
OVEREXPRESSION;
CARCINOMAS;
D O I:
10.1515/BC.2010.144
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Aldo-keto reductase family 1 member B10 (AKR1B10), over-expressed in multiple human cancers, might be implicated in cancer development and progression via detoxifying cytotoxic carbonyls and regulating fatty acid synthesis. In the present study, we investigated the ortholog of AKR1B10 in mice, an ideal modeling organism greatly contributing to human disease investigations. In the mouse, there are three aldo-keto reductase family 1 subfamily B (AKR1B) members, i.e., AKR1B3, AKR1B7, and AKR1B8. Among them, AKR1B8 has the highest similarity to human AKR1B10 in terms of amino acid sequence, computer-modeled structures, substrate spectra and specificity, and tissue distribution. More importantly, similar to human AKR1B10, mouse AKR1B8 associates with murine acetyl-CoA carboxylase-a and mediates fatty acid synthesis in colon cancer cells. Taken together, our data suggest that murine AKR1B8 is the ortholog of human AKR1B10.
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页码:1371 / 1378
页数:8
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