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Literature summary extracted from

  • Matsunaga, T.; Hojo, A.; Yamane, Y.; Endo, S.; El-Kabbani, O.; Hara, A.
    Pathophysiological roles of aldo-keto reductases (AKR1C1 and AKR1C3) in development of cisplatin resistance in human colon cancers (2013), Chem. Biol. Interact., 202, 234-242.
    View publication on PubMed

Application

EC Number Application Comment Organism
1.1.1.64 medicine exposure of HCT-15 cells to cisplatin results in aquisition of cisplatin resistance and concomitant induction of isoform AKR1C3 and aldo-keto reductase AKR1C1 expression. The resistance lowers the sensitivity toward cellular damages evoked by oxidative stress-derived aldehydes, 4-hydroxy-2-nonenal and 4-oxo-2-nonenal that are detoxified by AKR1C1 and AKR1C3. Overexpression of AKR1C1 or AKR1C3 in the parental HCT15 cells mitigates the cytotoxicity of the aldehydes and cisplatin. Knockdown of both AKR1C1 and AKR1C3 in the resistant cells or treatment of the cells with specific inhibitors of the aldo-keto reductases increases the sensitivity to ciplatin toxicity. Pretreatment of the resistant cells with proteasome inhibitor Z-Leu-Leu-Leu-al augments the cisplatin sensitization elicited by aldo-keto reductase inhibitors Homo sapiens
1.1.1.213 medicine exposure of HCT-15 cells to cisplatin results in aquisition of cisplatin resistance and concomitant induction of isoform AKR1C3 and aldo-keto reductase AKR1C1 expression. The resistance lowers the sensitivity toward cellular damages evoked by oxidative stress-derived aldehydes, 4-hydroxy-2-nonenal and 4-oxo-2-nonenal that are detoxified by AKR1C1 and AKR1C3. Overexpression of AKR1C1 or AKR1C3 in the parental HCT15 cells mitigates the cytotoxicity of the aldehydes and cisplatin. Knockdown of both AKR1C1 and AKR1C3 in the resistant cells or treatment of the cells with specific inhibitors of the aldo-keto reductases increases the sensitivity to ciplatin toxicity. Pretreatment of the resistant cells with proteasome inhibitor Z-Leu-Leu-Leu-al augments the cisplatin sensitization elicited by aldo-keto reductase inhibitors Homo sapiens
1.1.1.239 medicine exposure of HCT-15 cells to cisplatin results in aquisition of cisplatin resistance and concomitant induction of isoform AKR1C3 and aldo-keto reductase AKR1C1 expression. The resistance lowers the sensitivity toward cellular damages evoked by oxidative stress-derived aldehydes, 4-hydroxy-2-nonenal and 4-oxo-2-nonenal that are detoxified by AKR1C1 and AKR1C3. Overexpression of AKR1C1 or AKR1C3 in the parental HCT15 cells mitigates the cytotoxicity of the aldehydes and cisplatin. Knockdown of both AKR1C1 and AKR1C3 in the resistant cells or treatment of the cells with specific inhibitors of the aldo-keto reductases increases the sensitivity to ciplatin toxicity. Pretreatment of the resistant cells with proteasome inhibitor Z-Leu-Leu-Leu-al augments the cisplatin sensitization elicited by aldo-keto reductase inhibitors Homo sapiens

KM Value [mM]

EC Number KM Value [mM] KM Value Maximum [mM] Substrate Comment Organism Structure
1.1.1.64 0.0031
-
 4-oxo-2-nonenal pH 7.4, 25°C Homo sapiens
1.1.1.213 0.0031
-
 4-oxo-2-nonenal pH 7.4, 25°C Homo sapiens
1.1.1.239 0.0031
-
 4-oxo-2-nonenal pH 7.4, 25°C Homo sapiens

Organism

EC Number Organism UniProt Comment Textmining
1.1.1.64 Homo sapiens P42330
-
-
1.1.1.213 Homo sapiens P42330
-
-
1.1.1.239 Homo sapiens P42330
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
1.1.1.64 colon
-
 Homo sapiens
-
1.1.1.64 HCT-15 cell
-
 Homo sapiens
-
1.1.1.213 colon
-
 Homo sapiens
-
1.1.1.213 HCT-15 cell
-
 Homo sapiens
-
1.1.1.239 colon
-
 Homo sapiens
-
1.1.1.239 HCT-15 cell
-
 Homo sapiens
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
1.1.1.64 4-oxo-2-nonenal + NADPH + H+
-
 Homo sapiens 4-hydroxy-2-nonenal + NADP+
-
 ?
1.1.1.213 4-oxo-2-nonenal + NADPH + H+
-
 Homo sapiens 4-hydroxynonenal + NADP+
-
 ?
1.1.1.239 4-oxo-2-nonenal + NADPH + H+
-
 Homo sapiens 4-hydroxy-2-nonenal + NADP+
-
 ?

Turnover Number [1/s]

EC Number Turnover Number Minimum [1/s] Turnover Number Maximum [1/s] Substrate Comment Organism Structure
1.1.1.64 0.148
-
 4-oxo-2-nonenal pH 7.4, 25°C Homo sapiens
1.1.1.213 0.148
-
 4-oxo-2-nonenal pH 7.4, 25°C Homo sapiens
1.1.1.239 0.148
-
 4-oxo-2-nonenal pH 7.4, 25°C Homo sapiens

Expression

EC Number Organism Comment Expression
1.1.1.64 Homo sapiens exposure of HCT-15 cells to cisplatin results in aquisition of cisplatin resistance and concomitant induction of isoform AKR1C3 and aldo-keto reductase AKR1C1 expression up
1.1.1.213 Homo sapiens exposure of HCT-15 cells to cisplatin results in aquisition of cisplatin resistance and concomitant induction of isoform AKR1C3 and aldo-keto reductase AKR1C1 expression up
1.1.1.239 Homo sapiens exposure of HCT-15 cells to cisplatin results in aquisition of cisplatin resistance and concomitant induction of isoform AKR1C3 and aldo-keto reductase AKR1C1 expression up

General Information

EC Number General Information Comment Organism
1.1.1.64 physiological function exposure of HCT-15 cells to cisplatin results in aquisition of cisplatin resistance and concomitant induction of isoform AKR1C3 and aldo-keto reductase AKR1C1 expression. The resistance lowers the sensitivity toward cellular damages evoked by oxidative stress-derived aldehydes, 4-hydroxy-2-nonenal and 4-oxo-2-nonenal that are detoxified by AKR1C1 and AKR1C3. Overexpression of AKR1C1 or AKR1C3 in the parental HCT15 cells mitigates the cytotoxicity of the aldehydes and cisplatin. Knockdown of both AKR1C1 and AKR1C3 in the resistant cells or treatment of the cells with specific inhibitors of the aldo-keto reductases increases the sensitivity to ciplatin toxicity Homo sapiens
1.1.1.213 physiological function exposure of HCT-15 cells to cisplatin results in aquisition of cisplatin resistance and concomitant induction of isoform AKR1C3 and aldo-keto reductase AKR1C1 expression. The resistance lowers the sensitivity toward cellular damages evoked by oxidative stress-derived aldehydes, 4-hydroxy-2-nonenal and 4-oxo-2-nonenal that are detoxified by AKR1C1 and AKR1C3. Overexpression of AKR1C1 or AKR1C3 in the parental HCT15 cells mitigates the cytotoxicity of the aldehydes and cisplatin. Knockdown of both AKR1C1 and AKR1C3 in the resistant cells or treatment of the cells with specific inhibitors of the aldo-keto reductases increases the sensitivity to ciplatin toxicity Homo sapiens
1.1.1.239 physiological function exposure of HCT-15 cells to cisplatin results in aquisition of cisplatin resistance and concomitant induction of isoform AKR1C3 and aldo-keto reductase AKR1C1 expression. The resistance lowers the sensitivity toward cellular damages evoked by oxidative stress-derived aldehydes, 4-hydroxy-2-nonenal and 4-oxo-2-nonenal that are detoxified by AKR1C1 and AKR1C3. Overexpression of AKR1C1 or AKR1C3 in the parental HCT15 cells mitigates the cytotoxicity of the aldehydes and cisplatin. Knockdown of both AKR1C1 and AKR1C3 in the resistant cells or treatment of the cells with specific inhibitors of the aldo-keto reductases increases the sensitivity to ciplatin toxicity Homo sapiens

kcat/KM [mM/s]

EC Number kcat/KM Value [1/mMs-1] kcat/KM Value Maximum [1/mMs-1] Substrate Comment Organism Structure
1.1.1.64 47.8
-
 4-oxo-2-nonenal pH 7.4, 25°C Homo sapiens
1.1.1.213 47.8
-
 4-oxo-2-nonenal pH 7.4, 25°C Homo sapiens
1.1.1.239 47.8
-
 4-oxo-2-nonenal pH 7.4, 25°C Homo sapiens