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Arylsulfatase A Variants in Patients with Alcoholism
Alcoholism: Clinical and Experimental Research, 1984Leukocytes from 200 mentally ill patients and 100 normal controls were analyzed for eiectrophoretic variants of arylsulfatase A. Four different variant forms were found in 15 subjects. There is a relatively high occurrence of the arylsulfatase A variants in patients with alcoholism. Twenty‐one per cent (12/56) of patients with alcoholism have a variant
A R, Hulyalkar, R, Nora, P, Manowitz
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Proteolytic processing of human lysosomal arylsulfatase A
Biochimica et Biophysica Acta (BBA) - Protein Structure and Molecular Enzymology, 1992Arylsulfatase A purified from human placenta contained an unreported component with an apparent molecular mass of 7 kDa in addition to the two known components with apparent molecular masses of 58 and 50 kDa. The detailed relationship between the 58 kDa component and the 50 kDa component is as yet unknown. The present study was undertaken to define the
T, Fujii +6 more
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Sulfhydryl groups of rabbit liver arylsulfatase A
Biochimica et Biophysica Acta (BBA) - Protein Structure and Molecular Enzymology, 1985Rabbit liver arylsulfatase A (aryl-sulfate sulfhydrolase, EC 3.1.6.1) monomers of 130 kDa contain two free sulfhydryl groups as determined by spectrophotometric titration using 5,5'-dithiobis(2-nitrobenzoate) and by labeling with the fluorescent probe 5-(iodoacetamidoethyl)aminonaphthalene-1-sulfonic acid.
A, Waheed, R L, Van Etten
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Apparent arylsulfatase A activity in excretory fluids
Experientia, 1977Arylsulfatase activity has been demonstrated in rat and human parotid and submandibular saliva indicating that oral bacteria are not the only source of salivary sulfatase activity. Activity was also observed in human sweat, tears and in snake venom.
R V, Watson, A D, Landman
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The purification of arylsulfatases A and B
Biochemical Medicine, 1984Abstract Arylsulfatases A and B (arylsulfate sulfohydrolase, EC 3.1.6.1) are isoenzymatical. Both enzymes are located mainly in the liver, though they are widely distributed in mammalian tissues [rabbit liver (1), ox liver (2), human kidney (3), human brain (4), and human liver (5)].
T, Ozeki, M, Kan, K, Ohuchi, K, Iwaki
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Gene Therapy, 2000
A deficiency of arylsulfatase A (ASA) results in the lysosomal lipid storage disease metachromatic leukodystrophy. The disease mainly affects the central nervous system causing a progressive demyelination. A therapeutic effect will depend on the delivery of the deficient enzyme to the central nervous system. We have transplanted ASA-deficient mice with
U, Matzner +4 more
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A deficiency of arylsulfatase A (ASA) results in the lysosomal lipid storage disease metachromatic leukodystrophy. The disease mainly affects the central nervous system causing a progressive demyelination. A therapeutic effect will depend on the delivery of the deficient enzyme to the central nervous system. We have transplanted ASA-deficient mice with
U, Matzner +4 more
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Human Genetics, 1986
It had been shown previously that arylsulfatase A activity was attenuated in pseudo arylsulfatase A deficiency fibroblasts and that subunits of the enzyme were smaller than subunits of the enzyme in normal fibroblasts. Attenuated enzyme activity has now been affirmed in other tissues.
H, Kihara, W E, Meek, A L, Fluharty
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It had been shown previously that arylsulfatase A activity was attenuated in pseudo arylsulfatase A deficiency fibroblasts and that subunits of the enzyme were smaller than subunits of the enzyme in normal fibroblasts. Attenuated enzyme activity has now been affirmed in other tissues.
H, Kihara, W E, Meek, A L, Fluharty
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Arylsulfatase A in multiple sclerosis
Neurologija. Supplement, 2006The aim of this study was to elucidate possible involvement of a lysosomal enzyme arylsulfatase A (ASA) in complex pathogenesis and clinical features of multiple sclerosis (MS). Low ASA activities have been reported in healthy individuals due to condition termed ASA pseudodeficiency (ASA-PD).
Mlinac Jerković, Kristina +2 more
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Arylsulfatase A (ASA) defect and psychiatric illness
Molecular and Chemical Neuropathology, 1990The detection of homozygous (disease state) and heterozygous (carrier) forms of metachromatic leukodystrophy (MLD) and their prevalence among psychiatric individuals are reviewed. Levels of Arylsulfatase A (ASA) activity in peripheral leukocytes, mixed white cell populations, and lymphocytes are compared in normal and psychiatric patients.
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