Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.1.1 (asparaginase)
 2,695 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twice a week plasma (Pl.)-fibronectin was determined quantitatively in the course of disease with immunoelectrophoresis according to Laurell in 12 patients suffered from acute non-lymphoblastic leukemia (ANLL) and in 12 patients affected with acute lymphoblastic leukemia (ALL). At diagnosis Pl.-fibronectin concentration was found to be significantly lowered only in those patients affected with ANLL. During the induction therapy Pl.-Fibronectin could be observed to decline significantly in all patients: in acute non-lymphoblastic leukemia from mean 270 micrograms/ml, s 93 micrograms/ml, to mean 185 micrograms/ml, s 89 micrograms/ml (p less than 0.01), and in acute lymphoblastic leukemia from mean 290 micrograms/ml, s 98 micrograms/ml, to mean 180 micrograms/ml, s 94 micrograms/ml (p less than 0.01). After administering L-asparaginase there is a strong decline of Pl.-fibronectin. Pl.-fibronectin concentration could be observed to be significantly lower in patients without remission in comparison to those with remission. A correlation between Pl.-fibronectin concentration and tumour mass could not be identified.
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PMID:[Plasma fibronectin in acute leukemia. Effects of the cytostatic therapy on plasma fibronectin level]. 244 8

The thrombocyte count, the factor XIII (F XIII) activity, the concentration of fibrinogen (F I), prothrombin (F II), fibronectin (CIG), albumin and the proteinase inhibitors antithrombin III (AT III), alpha 2-macroglobulin (A2M), alpha 1-antitrypsin (A1A) and Cl-esterase inactivator (Cl-INA) were determined in ten children with acute lymphoblastic leukaemia (ALL). Changes due to the disease and to therapy were observed. Before the start of treatment the patients had thrombocytopenia secondary to the disease, and the proteinase inhibitors--especially Cl-INA and A1A--were raised. During the induction phase the thrombocyte count rose but there was also a marked increase in the concentration of F II and CIG. During the consolidation phase there was a general fall in protein concentration under L-asparaginase medication. The cause was attributed to a disorder of protein synthesis. The concentration of the factors studied rose again during maintenance therapy.
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PMID:Coagulation factors and proteinase inhibitors in the plasma of children with acute lymphoblastic leukoses. Behaviour before and during treatment according to Protocol I of the Cooperative Leukaemia Study COALL-80. 608 31

The glycoprotein fibronectin is, as well as by various other cells, also produced in leucocytes and is said to play an important role in malignant transformation of cells. Therefore, the behaviour of plasma fibronectin and of factor VIII R:AG was investigated in acute leukaemia in order to prove their significance as prognostic and therapeutic markers (method: electroimmunoassay). In patients with acute myeloid leukaemia (n = 29) and acute lymphoblastic leukaemia (n = 11) no significant changes in fibronectin concentration could be evaluated. Fibronectin levels declined significantly only during therapy with asparaginase in patients with acute lymphoblastic leukaemia, probably as a result of disturbed synthesis in the liver. Using crossed immunoelectrophoresis against fibronectin antiserum, one normal and one slower migrating antigen (FN:C) could be observed in nearly all plasma samples in patients with acute leukaemia. By means of in vitro tests with highly purified substances and intermediate gel electrophoresis it could be shown that FN:C represents fibronectin which has bound fibrinogen, probably crosslinked by activated factor XIII. Factor VIII R:AG was found to be greatly raised in patients with acute leukaemia--up to 1400% of the normal level. Increased levels correlated well with a worsening of the disease. The protein seems to be suitable for estimating the activity and prognosis of acute leukaemia.
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PMID:Fibronectin and factor VIII-related antigen in acute leukaemia. 640 58

Porphyromonas gingivalis is a well-adapted pathogen of the periodontal pocket distinguished by its wide array of proteolytic activities and its ability to adhere to multiple substrata in the oral cavity. Microbial proteins with binding functions (such as adhesins and enzymes) very often contain critical tyrosine residues, supported by one or more asparagines in the binding cleft. This study investigates the reduction in adhesiveness and in proteolytic activity after treating P. gingivalis with the tyrosine- and asparagine-targeting enzymes polyphenol oxidase (PPO) and asparaginase (ASG). Cysteine protease activity was reduced by pretreatment with both enzymes, while the trypsin-like activity was affected only by PPO. Adhesion to buccal epithelial cells, laminin and fibronectin as well as hemagglutination was reduced by one or both of the enzymes. PPO, but not ASG, reduced the coaggregation of P. gingivalis with Actinomyces naeslundii. Treatment with these enzymes might provide an alternative to traditional antimicrobial strategies.
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PMID:Virulence factors of Porphyromonas gingivalis are modified by polyphenol oxidase and asparaginase. 1293 May 24