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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 Antibodies (127) and GLA Kits (34) and many more products for this protein.
Showing 10 out of 18 products:
Human GLA Protein expressed in Human Cells - ABIN2005026
Koide, Ishiura, Iwai, Inoue, Kaneda, Okada, Uchida: A case of Fabry's disease in a patient with no alpha-galactosidase A activity caused by a single amino acid substitution of Pro-40 by Ser. in FEBS letters 1990
Show all 5 Pubmed References
Human GLA Protein expressed in Wheat germ - ABIN1355176
Corchero, Mendoza, Lorenzo, Rodríguez-Sureda, Domínguez, Vázquez, Ferrer-Miralles, Villaverde: Integrated approach to produce a recombinant, His-tagged human ?-galactosidase A in mammalian cells. in Biotechnology progress 2011
Four patients had non-amenable mutant forms of a-Gal (show GAL Proteins) based on the validated cell-based assay conducted after treatment initiation and were excluded from primary efficacy analyses only.
Mesenchymal stem cells with reduced GLA (show NAT8 Proteins) activity are prone to apoptosis and senescence due to impaired autophagy and DNA repair capacity.
we review the various types of GLA (show NAT8 Proteins) variants and recommend that pathogenicity be considered only when associated with elevated globotriaosylceramide in disease-relevant organs and tissues as analyzed by mass spectrometry.
findings revealed the alternative splicing mechanism of GLA (show NAT8 Proteins) (IVS4+919G>A), and a potential treatment for this specific genetic type of Fabry disease by amiloride in the future
Results found a novel heterozygous stop codon mutation in exon 1 of the GLA (show NAT8 Proteins) gene in female patients with Fabry Disease with methylation in the non-mutated allele thought to be associated with the clinical severity of the disease.
Study described the demographic data, wide clinical spectrum of phenotypes, and GLA (show NAT8 Proteins) mutation spectrum of Fabry disease in Korea. Most of the patients had classical Fabry disease, with a 4 times higher incidence than that of late-onset Fabry disease, indicating an underdiagnosis of mild, late-onset Fabry disease.
we reviewed other small molecules that were reported to have a stabilizing effect on some GLA (show NAT8 Proteins) missense mutations in vitro and might be developed to act in synergy or as an alternative to 1-deoxygalactonojirimycin
No pathogenic mutations in the coding regions of the GLA (show NAT8 Proteins) gene were identified in this group of patients and thus no Fabry disease was found in this study.
High desphospho-uncarboxylated matrix Gla protein (show MGP Proteins) level, reflecting a poor vitamin K status, seems to be associated with kidney damage and may be also a marker of cardiovascular risk in CKD patients
Case Report: Kidney transplantation from a mother with unrecognized Fabry disease to her son with low alpha-galactosidase A activity.
the GM130 (show GOLGA2 Proteins)-deficient mouse provides a valuable model for investigating the etiology of human globozoospermia.
Mice with alpha-galactosidase A deficiency show age-dependent and distinct deficits of the sensory system.
In oocyte meiosis, GM130 (show GOLGA2 Proteins) localization and expression patterns are regulated by FMNL1 (show FMNL1 Proteins).
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 Proteins))
GM130 (show GOLGA2 Proteins) regulates microtubule organization and might cooperate with the MAPK (show MAPK1 Proteins) 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 Proteins) or other thrombosis-related gene defect in patients with genetic severe early-onset thrombosis.
present Toll (show TLR4 Proteins)-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.
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