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The protein encoded by ARSA hydrolyzes cerebroside sulfate to cerebroside and sulfate. Additionally we are shipping Arylsulfatase A Kits (38) and Arylsulfatase A Proteins (16) and many more products for this protein.
Showing 10 out of 112 products:
Mouse (Murine) Polyclonal Arylsulfatase A Primary Antibody for ELISA, WB - ABIN238536
Sevin, Benraiss, Van Dam, Bonnin, Nagels, Verot, Laurendeau, Vidaud, Gieselmann, Vanier, De Deyn, Aubourg, Cartier: Intracerebral adeno-associated virus-mediated gene transfer in rapidly progressive forms of metachromatic leukodystrophy. in Human molecular genetics 2005
Show all 5 references for ABIN238536
Cow (Bovine) Polyclonal Arylsulfatase A Primary Antibody for WB - ABIN2785757
Saito, Ohno, Sugawara, Sakuraba: Structural and clinical implications of amino acid substitutions in N-acetylgalactosamine-4-sulfatase: insight into mucopolysaccharidosis type VI. in Molecular genetics and metabolism 2008
Mouse (Murine) Polyclonal Arylsulfatase A Primary Antibody for IP, ELISA - ABIN2000133
Laidler: [Arylsulfatase A--physico-chemical properties and the use of enzyme radioimmunoassay in medical diagnosis]. in Folia medica Cracoviensia 1993
Multipotential Neural precursors deficient in arylsulfatase A show a higher ratio of long versus short fatty acid sulfatides, reduction in PDGFRa (show PDGFRA Antibodies), decreased AKT (show AKT1 Antibodies) phosphorylation, and increased exosomal shedding of PDGFRa (show PDGFRA Antibodies).
Sperm arylsulfatase A binds to mZP2 and mZP3 glycoproteins in a nonenzymatic manner.
Sulfogalactosylglycerolipid was a physiological substrate of Sertoli lysosomal arylsulfatase A
study provides the first proof of cognitive deficit and impaired synaptic plasticity in an MLD (show MBP Antibodies) mouse model.
ArsA plays a role as a novel component of the extracellular matrix which could be very useful for clarifying the mechanisms underlying some of the syndromes caused by functional deficiency of the Ars (show SLURP1 Antibodies) genes.
Data demonstrate a delay in myelin formation in ASA-deficient mice at 2 weeks of age, as a consequence of inability to degrade sulfatide.
Since high cholesterol levels are important for myelination, and various cellular processes, like vesicular trafficking and signal transduction, reduced cholesterol levels might be an important factor in the molecular pathology of MLD (show MBP Antibodies).
ASA-deficient [ASA(-/-)] mice overexpressing the sulfatide synthesizing enzymes causes hyperexcitability and axonal degeneration in a mouse model of metachromatic leukodystrophy
The increasing sulfatide storage in ASA(-/-) mice leads to neurological symptoms and morphological alterations that are reminiscent of human MLD (show MBP Antibodies).
Safety of Arsa overexpression for gene therapy of metachromatic leukodystrophy was evaluated.
Data indicate a significant correlation between the mutation of c.622delC(p.His208Metfs*46) in the arylsulfatase A (ARSA) gene and the phenotype OF metachromatic leukodystrophy.
Sixteen novel mutations that cause metachromatic leukodystrophy have been identified in the arylsulfatase A gene.
Studied brain uptake in the rhesus monkey of a fusion protein of arylsulfatase a and a monoclonal antibody against the human insulin receptor (show INSR Antibodies).
HSPA2 (show HSPA2 Antibodies) regulates the expression of sperm surface receptors involved in human sperm-oocyte recognition, such as arylsulfatase A and SPAM1 (show SPAM1 Antibodies).
The interaction between SPAM1 (show SPAM1 Antibodies), ARSA and HSPA2 (show HSPA2 Antibodies) in a multimeric complex mediating sperm-egg interaction.
This is the first report that human adipocytes express functional DAR (show ATP2A2 Antibodies) and ARSA, suggesting a regulatory role for peripheral DA in adipose functions.
The purpose was to estimate the birth prevalence of Metachromatic leukodystrophy in Poland by determining population frequency of the common pathogenic ARSA gene mutations and to compare this estimate with epidemiological data.
The presence of two most common mutations associated with Arylsulfatase A pseudodeficiency was analyzed in 56 patients with diagnosis of relapsing-remitting multiple sclerosis, by polymerase chain reaction restriction fragment length polymorphism method.
cationization of ASA and an increase of the mannose 6-phosphate content of the enzyme may promote blood-to-brain transfer of ASA, thus leading to an improved therapeutic efficacy of enzyme replacement therapy behind the BBB (show ALMS1 Antibodies).
ARSA mutations in the Indian population were characterized. 4 new variant & 5 pseudodeficiency alleles were found. Protein modeling showed loss of interactions leading to conformation change.
The protein encoded by this gene hydrolyzes cerebroside sulfate to cerebroside and sulfate. Defects in this gene lead to metachromatic leucodystrophy (MLD), a progressive demyelination disease which results in a variety of neurological symptoms and ultimately death. Alternatively spliced transcript variants have been described for this gene.
, Arylsulfatase A