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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Arylsulfatase A

arylsulfatase A
Top mentioned proteins: Transcription Factor DP1, ACID, HAD, CAN, sulfatase
Papers on arylsulfatase A
Lacritin and other autophagy associated proteins in ocular surface health.
Laurie et al., Hyderābād, India. In Exp Eye Res, Mar 2016
Mutation of arylsulfatase A, arylsulfatase B, ceroid-lipofuscinosis neuronal 3, mucolipin, or Niemann-Pick disease type C1 respectively underlie several diseases of apparently insufficient autophagic flux that affect the eye, including: metachromatic leukodystrophy, mucopolysaccharidosis type VI, juvenile-onset Batten disease, mucolipidosis IV, and Niemann-Pick type C associated with myelin sheath destruction of corneal sensory and ciliary nerves and of the optic nerve; corneal clouding, ocular hypertension, glaucoma and optic nerve atrophy; accumulation of 'ceroid-lipofuscin' in surface conjunctival cells, and in ganglion and neuronal cells; decreased visual acuity and retinal dystrophy; and neurodegeneration.
Mutation Update of ARSA and PSAP Genes Causing Metachromatic Leukodystrophy.
Biffi et al., Milano, Italy. In Hum Mutat, Jan 2016
The disease is caused by variants in the ARSA gene, which codes for the lysosomal enzyme arylsulfatase A, or, more rarely, in the PSAP gene, which codes for the activator protein saposin B. In this Mutation Update, an extensive review of all the ARSA- and PSAP-causative variants published in the literature to date, accounting for a total of 200 ARSA and 10 PSAP allele types, is presented.
Sulfatide Analysis by Mass Spectrometry for Screening of Metachromatic Leukodystrophy in Dried Blood and Urine Samples.
Gelb et al., Sherbrooke, Canada. In Clin Chem, Jan 2016
BACKGROUND: Metachromatic leukodystrophy (MLD) is an autosomal recessive disorder caused by deficiency in arylsulfatase A activity, leading to accumulation of sulfatide substrates.
Heat Shock Protein member A2 forms a stable complex with angiotensin converting enzyme and protein disulfide isomerase A6 in human spermatozoa.
Nixon et al., Newcastle, Australia. In Mol Hum Reprod, Jan 2016
Moreover, our recent work has shown that defective HSPA2 function induced by oxidative stress leads to the aberrant surface expression of one of its interacting proteins, arylsulfatase A, and thus contributes to a loss of sperm-zona pellucida adhesion.
Determination of arylsulfatase A pseudodeficiency allele and haplotype frequency in the Tunisian population.
Abdelhak et al., Tunisia. In Neurol Sci, Dec 2015
UNASSIGNED: Arylsulfatase A (ASA) is a lysosomal enzyme involved in the catabolism of cerebroside sulfate.
A Rare Case of Metachromatic Leukodystrophy Confirmed by Arylsulfatase A.
Ahmed et al., Dhaka, Bangladesh. In Mymensingh Med J, Oct 2015
Metachromatic leukodystrophy (MLD) is the rare neurometabolic disease caused by the deficiency of a lysosomal enzyme arylsulfatase A (ARSA) activity.
Volumetric MRI data correlate to disease severity in metachromatic leukodystrophy.
Wolf et al., Amsterdam, Netherlands. In Ann Clin Transl Neurol, Sep 2015
OBJECTIVE: Metachromatic leukodystrophy (MLD) is an inherited lysosomal disorder due to a deficiency in arylsulfatase A with progressive demyelination and neurological decline.
Metachromatic leukodystrophy: Disease spectrum and approaches for treatment.
Wolf et al., Amsterdam, Netherlands. In Best Pract Res Clin Endocrinol Metab, Mar 2015
Metachromatic leukodystrophy is an inherited lysosomal disorder caused by recessive mutations in ARSA encoding arylsulfatase A. Low activity of arylsulfatase A results in the accumulation of sulfatides in the central and peripheral nervous system leading to demyelination.
Lentiviral hematopoietic stem cell gene therapy benefits metachromatic leukodystrophy.
Naldini et al., Milano, Italy. In Science, 2013
Metachromatic leukodystrophy (MLD) is an inherited lysosomal storage disease caused by arylsulfatase A (ARSA) deficiency.
Developing therapeutic approaches for metachromatic leukodystrophy.
Maegawa et al., Baltimore, United States. In Drug Des Devel Ther, 2012
Metachromatic leukodystrophy (MLD) is an autosomal recessive lysosomal disorder caused by the deficiency of arylsulfatase A (ASA), resulting in impaired degradation of sulfatide, an essential sphingolipid of myelin.
Lysosomal leukodystrophies: Krabbe disease and metachromatic leukodystrophy.
Kohlschütter, Hamburg, Germany. In Handb Clin Neurol, 2012
In metachromatic leukodystrophy, deficient activity of arylsulfatase A, or lack of a cofactor, causes accumulation of sulfatide in various tissues and diffuse demyelination.
In vivo gene therapy of metachromatic leukodystrophy by lentiviral vectors: correction of neuropathology and protection against learning impairments in affected mice.
Naldini et al., Milano, Italy. In Nat Med, 2001
Metachromatic leukodystrophy (MLD) is a lipidosis caused by deficiency of arylsulfatase A (ARSA).
Mucopolysaccharidosis: secondarily induced abnormal distribution of lysosomal isoenzymes.
Hooft et al., In Science, 1973
Total activities of acid hydrolases in liver of two patients with mucopolysaccharidosis are decreased for beta-galactosidase, alpha-galactosidase, and arylsulfatase A; total activities of four other hydrolases are normal or increased.
Correction of abnormal cerebroside sulfate metabolism in cultured metachromatic leukodystrophy fibroblasts.
Kihara et al., In Science, 1971
Cultured fibroblasts derived from patients with late infantile metachromatic leukodystrophy incorporated arylsulfatase A from the growth medium.
Metachromatic leukodystrophy: diagnosis with samples of venous blood.
Brady et al., In Science, 1968
Arylsulfatase A and B have been demonstrated in preparations of human leukocytes.
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