|Other Names||Dehydrogenase/reductase SDR family member 2, mitochondrial, 111-, Dicarbonyl reductase HEP27, Protein D, DHRS2|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Displays NADPH-dependent dicarbonyl reductase activity in vitro with 3,4-Hexanedione, 2,3-Heptanedione and 1-Phenyl-1,2- propanedione as substrates. No reductase activity is displayed in vitro with steroids, retinoids and sugars as substrates. Attenuates MDM2-mediated p53/TP53 degradation, leading to p53/TP53 stabilization and increased transcription activity, resulting in the accumulation of MDM2 and CDKN1A/p21.|
|Cellular Location||Mitochondrion matrix. Nucleus. Note=A minor fraction of the protein is translocated from the mitochondria to the nucleus, after cleavage of the targeting signal|
|Tissue Location||Widely expressed, with highest levels in liver and kidney, followed by heart, spleen, skeletal muscle and placenta. In hemopoietic cells, expressed in dendritic cells, but not in monocytes, macrophages, granulocytes, nor in B and T lymphocytes.|
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Provided below are standard protocols that you may find useful for product applications.
DHRS2 displays NADPH-dependent dicarbonyl reductase activity in vitro with 3,4-Hexanedione, 2,3-Heptanedione and 1-Phenyl-1,2-propanedione as substrates. DHRS2 do not reductase activity is displayed in vitro with steroids, retinoids and sugars as substrates. This protein may inhibit cell replication.
Monge, M., et al. Carcinogenesis 30(8):1288-1297(2009)Persson, B., et al. Chem. Biol. Interact. 178 (1-3), 94-98 (2009) Shafqat, N., et al. Cell. Mol. Life Sci. 63(10):1205-1213(2006)
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