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GLA encodes a homodimeric glycoprotein that hydrolyses the terminal alpha-galactosyl moieties from glycolipids and glycoproteins. Additionally we are shipping GLA Kits (37) and GLA Proteins (17) and many more products for this protein.
Showing 10 out of 83 products:
Human Polyclonal GLA Primary Antibody for EIA, WB - ABIN453055
Ioannou, Zeidner, Grace, Desnick: Human alpha-galactosidase A: glycosylation site 3 is essential for enzyme solubility. in The Biochemical journal 1998
Show all 2 references for ABIN453055
Chicken Polyclonal GLA Primary Antibody for WB - ABIN2785641
Auray-Blais, Cyr, Ntwari, West, Cox-Brinkman, Bichet, Germain, Laframboise, Melançon, Stockley, Clarke, Drouin: Urinary globotriaosylceramide excretion correlates with the genotype in children and adults with Fabry disease. in Molecular genetics and metabolism 2008
Fabry disease, an X-linked disorder of glycosphingolipids that is caused by mutations of the GLA (show NAT8 Antibodies) gene that codes for alpha-galactosidase A, leads to dysfunction of many cell types and includes a systemic vasculopathy.
Study describes 5 novel mutations found in the GLA (show NAT8 Antibodies) gene of patients with clinical diagnosis of Fabry disease.
GLA (show NAT8 Antibodies) gene variations correlate with globotriaosylceramide and globotriaosylsphingosine analog levels in urine and plasma
results directly implicated the GLA (show NAT8 Antibodies) mutation p.E66Q as the genetic etiology of the Chinese renal variant FD pedigree.
This study indicated that the p.E66Q variant of GLA (show NAT8 Antibodies) does not affect the progression of chronic kidney disease.
Thus, inheritance of the CIH caused an mRNA deregulation altering the GLA (show NAT8 Antibodies) expression pattern, producing a tissue glycolipid storage.
data strongly suggest that the GLA (show NAT8 Antibodies) p.(Arg118Cys) variant does not segregate with Fabry disease clinical phenotypes in a Mendelian fashion, but might be a modulator of the multifactorial risk of cerebrovascular disease
In Fabry disease patients, the alpha-galactosidase A-10T allele appears to be causal for neurological manifestations.
Some clinical cases of some members of a Sicilian family to express phenotypical variability of Anderson-Fabry disease in subjects with the same genetic mutation in alpha galactosidase A gene, are reported.
Case Report: immunohistologically detected synaptopodin (show SYNPO Antibodies) upregulation in foamy podocytes in Fabry disease due to novel alpha-galactosidase A mutation.
In oocyte meiosis, GM130 (show GOLGA2 Antibodies) localization and expression patterns are regulated by FMNL1 (show FMNL1 Antibodies).
The histological changes in Gla KO mice better resemble the type 2 later-onset phenotype observed in patients with residual alpha-galactosidase A activity.
our findings imply that the alpha-GalA KO mouse is a good model in which to study the peripheral small fiber neuropathy exhibited by FD patients
we demonstrate an age-dependent microvasculopathy of the mesenteric artery in a murine model of Fabry disease (galactosidase A-knockout mice) resulting from dysregulation of the vascular homeostatic enzyme endothelial nitric oxide synthase (eNOS (show NOS3 Antibodies))
GM130 (show GOLGA2 Antibodies) regulates microtubule organization and might cooperate with the MAPK (show MAPK1 Antibodies) pathway to play roles in spindle organization, migration and asymmetric division during mouse oocyte maturation
It suggested that there could be a combination of GLA deficiency and FVL (show F5 Antibodies) or other thrombosis-related gene defect in patients with genetic severe early-onset thrombosis.
present Toll (show TLR4 Antibodies)-like receptor-dependent negative regulation of alpha-Gal-A as a mechanistic link between pathogen recognition and self lipid antigen induction for natural killer T cells
Developed a novel recombinant lentiviral vector that engineers expression of alpha-galactosidase. Analysis of tissues at 26 wks demonstrated similar alpha-gal A enzyme activities but enhanced Gb3 reduction in hearts and kidneys compared with control.
alpha-galactosidase A deficiency could be an important genetic modifier for the enhanced thrombosis associated with FV Leiden associated thrombosis.
The adeno (show ADORA2A Antibodies)-associated virus (AAV) vector containing the alpha-gal A gene was injected into the right quadriceps muscles of Fabry knockout mice.
This gene encodes a homodimeric glycoprotein that hydrolyses the terminal alpha-galactosyl moieties from glycolipids and glycoproteins. This enzyme predominantly hydrolyzes ceramide trihexoside, and it can catalyze the hydrolysis of melibiose into galactose and glucose. A variety of mutations in this gene affect the synthesis, processing, and stability of this enzyme, which causes Fabry disease, a rare lysosomal storage disorder that results from a failure to catabolize alpha-D-galactosyl glycolipid moieties.
, galactosidase alpha
, Alpha-galactosidase A
, alpha-D-galactosidase A
, alpha-galactosidase A-like
, alpha-galactosidase A
, agalsidase alfa
, alpha-D-galactoside galactohydrolase 1
, alpha-gal A
, alpha-D-galactoside galactohydrolase
, 130 kDa cis-Golgi matrix protein
, Golgin subfamily A member 2
, SY11 protein