3.4.22.40: bleomycin hydrolase
This is an abbreviated version!
For detailed information about bleomycin hydrolase, go to the full flat file.
Word Map on EC 3.4.22.40
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3.4.22.40
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luteinizing
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paraoxonase
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thiolactone
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helveticus
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peplomycin
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lutropins
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corneocytes
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homocysteinylation
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beta-naphthylamide
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medicine
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hcy-thiolactone
- 3.4.22.40
-
luteinizing
- paraoxonase
- thiolactone
- helveticus
- peplomycin
-
lutropins
- corneocytes
-
homocysteinylation
- beta-naphthylamide
- medicine
-
hcy-thiolactone
Reaction
Inactivates bleomycin B2 (a cytotoxic glycometallopeptide) by hydrolysis of a carboxyamide bond of beta-aminoalanine, but also shows general aminopeptidase activity. The specificity varies somewhat with source, but amino acid arylamides of Met, Leu and Ala are preferred =
Synonyms
aminopeptidase C, aminopeptidase H, ApsC, BANA-hydrolase, BH, BH protein, Bleomycin hydrolase, BLH, Blh1p, BLM hydrolase, Blmh, BLMH protein, BMH, citrulline aminopeptidase, Gal6p, Hcy-thiolactonase, homocysteine thiolactonase, HTLase, hydrolase H, More, PEPC, yBLH, yeast cysteine protease
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medicine
medicine
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is thought to be the major cause of tumor cell resistance to bleomycin chemotherapy
medicine
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ectopic expression of enzyme alters processing of amyloid precursor protein and increases significantly release of beta-amyloid
medicine
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ectopic expression of enzyme increases the secretion of amyloid precursor protein, increase is blocked in mutant C73S
medicine
patient study, patients with testicular germ-cell cancer treated with bleomycin-containing chemotherapy, response to chemotherapy determined by gene polymorphisms involved in metabolism of cytotoxic drugs analyzed, importance for risk classification and selection for alternative treatment strategies suggested
medicine
the bleomycins (BLMs) are widely used in combination therapies for the treatment of various cancers. Dose-dependent and cumulative pulmonary toxicity is the major cause of BLM-associated morbidity, limiting the broad uses of BLMs as anticancer drugs. Opportunities to overcome bleomycin-induced pulmonary toxicity in chemotherapies, potentially by exploring BLM B2 as the preferred congener, engineering designer bleomycins with optimized activity for recombinant human bleomycin hydrolase (rhBLMH), or co-administrating rhBLMH directly into the lung as a potential protein therapeutic