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Human Polyclonal DDH Primary Antibody for WB - ABIN514921
Ebert, Kisiela, Wsól, Maser: Proteasome inhibitors MG-132 and bortezomib induce AKR1C1, AKR1C3, AKR1B1, and AKR1B10 in human colon cancer cell lines SW-480 and HT-29. in Chemico-biological interactions 2011
Show all 3 Pubmed References
Human Polyclonal DDH Primary Antibody for ELISA, WB - ABIN560581
Buytaert, Matroule, Durinck, Close, Kocanova, Vandenheede, de Witte, Piette, Agostinis: Molecular effectors and modulators of hypericin-mediated cell death in bladder cancer cells. in Oncogene 2008
Show all 2 Pubmed References
Decreased invasion caused by AKR1C1 knockdown suggests a novel role of AKR1C1 in cancer invasion, which is probably due to the regulation of Rac1 (show RAC1 Antibodies), Src (show SRC Antibodies), or Akt (show AKT1 Antibodies). An inflammatory cytokine, interleukin-1beta, was found to increase AKR1C1 in bladder cancer cell lines.
Data show that increased levels of AKR1C1/C2 enhanced the sensitivity of esophageal squamous cell carcinoma (ESCC) cells to ethyl-3,4-dihydroxybenzoate (EDHB).
the present study suggests that AKR1C1, AKR1C2 (show AKR1C2 Antibodies), AKR1C3 (show AKR1C3 Antibodies), and AKR1C4 (show AKR1C4 Antibodies) are closely associated with drug resistance to both CDDP and 5FU, and that mefenamic acid, an inhibitor of AKR1C, restores sensitivity through inhibition of drug-resistance in human cancer cells.
Activation of AKR1C1/ERbeta (show ESR2 Antibodies) induces apoptosis by downregulation of c-FLIP (show CFLAR Antibodies) in prostate cancer cells.
results suggest a gender-specific modulatory effect of AKR1C1 on anxiety levels, most likely through changes in progesterone and allopregnanolone levels within and outside the brain
Studies indicate that mutations in aldo-keto reductase family 1 (AKR1) enzymes AKR1C1 and AKR1C4 (show AKR1C4 Antibodies) are responsible for sexual development dysgenesis and mutations in AKR1D1 (show AKR1D1 Antibodies) are causative in bile-acid deficiency.
activation of the Nrf2 (show GABPA Antibodies)/AKR1C axis may contribute to oxaliplatin resistance in gastric carcinoma
The involvement of up-regulated AKR1C1, AKR1C3 (show AKR1C3 Antibodies) and proteasome in CDDP resistance of colon cancers.
Which promoted significant reduction of AKR1C1 and AKR1C2 (show AKR1C2 Antibodies) expression.
Data suggest that interleukin-1beta facilitates progesterone metabolism in cervical fibroblasts by regulating expression of AKR1C1 and AKR1C2 (show AKR1C2 Antibodies).
This gene encodes a member of the aldo/keto reductase superfamily, which consists of more than 40 known enzymes and proteins. These enzymes catalyze the conversion of aldehydes and ketones to their corresponding alcohols by utilizing NADH and/or NADPH as cofactors. The enzymes display overlapping but distinct substrate specificity. This enzyme catalyzes the reaction of progesterone to the inactive form 20-alpha-hydroxy-progesterone. This gene shares high sequence identity with three other gene members and is clustered with those three genes at chromosome 10p15-p14.
20 alpha-hydroxysteroid dehydrogenase
, 20-alpha-hydroxysteroid dehydrogenase
, aldo-keto reductase C
, aldo-keto reductase family 1 member C1
, chlordecone reductase homolog HAKRC
, dihydrodiol dehydrogenase 1
, dihydrodiol dehydrogenase 1/2
, dihydrodiol dehydrogenase 1; 20-alpha (3-alpha)-hydroxysteroid dehydrogenase
, dihydrodiol dehydrogenase isoform DD1
, hepatic dihydrodiol dehydrogenase
, high-affinity hepatic bile acid-binding protein
, indanol dehydrogenase
, trans-1,2-dihydrobenzene-1,2-diol dehydrogenase
, type II 3-alpha-hydroxysteroid dehydrogenase
, aldo-keto reductase family 1 member C1 homolog