Browse our anti-GAA (GAA) Antibodies

Full name:
anti-Glucosidase, Alpha, Acid Antibodies (GAA)
On are 72 Glucosidase, Alpha, Acid (GAA) Antibodies from 16 different suppliers available. Additionally we are shipping GAA Kits (23) and GAA Proteins (16) and many more products for this protein. A total of 120 GAA products are currently listed.
E430018M07Rik, LYAG

Most Popular Reactivities for anti-GAA (GAA) Antibodies

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anti-Rat (Rattus) GAA Antibodies:

anti-Mouse (Murine) GAA Antibodies:

anti-Human GAA Antibodies:

All available anti-GAA Antibodies

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Top referenced anti-GAA Antibodies

  1. Human Monoclonal GAA Primary Antibody for ELISA, WB - ABIN560974 : Xiao, Westbroek, Motabar, Lea, Hu, Velayati, Zheng, Southall, Gustafson, Goldin, Sidransky, Liu, Simeonov, Tamargo, Ribes, Matalonga, Ferrer, Marugan: Discovery of a novel noniminosugar acid ? glucosidase chaperone series. in Journal of medicinal chemistry 2012 (PubMed)
    Show all 2 references for 560974

  2. Human Polyclonal GAA Primary Antibody for IHC (p), WB - ABIN656475 : Aoyama, Ozer, Demirkol, Ebara, Murase, Podskarbi, Shin, Gokcay, Okubo: Molecular features of 23 patients with glycogen storage disease type III in Turkey: a novel mutation p.R1147G associated with isolated glucosidase deficiency, along with 9 AGL mutations. in Journal of human genetics 2009 (PubMed)
    Show all 2 references for 656475

More Antibodies against GAA Interaction Partners

Mouse (Murine) Glucosidase, Alpha, Acid (GAA) interaction partners

  1. GAA enzyme deficiency leads to glycogen (show GYS1 Antibodies) accumulation in the trachea and bronchi and impairs the ability of lower airway smooth muscle to regulate calcium and respond appropriately to bronchodilator or constrictors.

  2. GAA deficiency results in reduced mTORC1 activation that is partly responsible for the skeletal muscle wasting phenotype and can be amerliorated by leucine supplementation.

  3. Results describe the inhibitory effects of Chana series chalcone derivatives on the activities of alpha-glucosidase (show AGLU Antibodies) and DPP-4 (show DPP4 Antibodies), and on adipocyte differentiation.

  4. Power and torque did not change with age in control animals, but declined significantly in acid 1-4 alpha-glucosidase (show AGLU Antibodies) knockout mice in three age groups.

  5. These studies suggest that hyase enhances penetration of enzyme into the tissues including muscle during ERT (show ELF3 Antibodies) and therefore hyase pretreatment may be important in treating Pompe disease.

Human Glucosidase, Alpha, Acid (GAA) interaction partners

  1. This is the first report of the alpha-glucosidase (show AGLU Antibodies) inhibitory activity of compounds 20, 26, and 29, and the findings support the important role of Eremanthus species as novel sources of new drugs and/or herbal remedies for treatment of type 2 diabetes.

  2. Compared with controls, GAA gene expression levels in coronary artery disease (CAD (show CAD Antibodies)) patients were significantly increased, suggesting that GAA may be involved in the CAD (show CAD Antibodies) development.

  3. Study reports on the clinical, biochemical, morphological, muscle imaging, and genetic findings of six adult Pompe patients from five unrelated families with the c.-32-13T>G GAA gene mutation in homozygous state. All patients had decreased GAA activity and elevated creatine kinase levels.

  4. glycogen (show GYS1 Antibodies) storage disease type II is caused by deficiency of GAA activity resulting from mutation of GAA gene

  5. RT-PCR followed by DNA sequence analysis of patients with Pompe disease revealed new variant in GAA gene resulting in aberrant splicing event.

  6. Findings indicate that GAA c.2238G > C (p.W746C) novel mutation is the most common mutation in mainland Chinese late-onset Pompe patients, as observed in Taiwanese patients expanding the genetic spectrum of the disease.

  7. this study shows several alterations distributed along the GAA gene in a sample of Brazilian families.

  8. GAA deficiency results in reduced mTORC1 activation that is partly responsible for the skeletal muscle wasting phenotype and can be amerliorated by leucine supplementation.

  9. The phenotype LO-GSDII with GAA mutation in the North of Italy seems not significantly different from other LO-GSDII populations in Europe or the USA.

  10. Data shows the largest informative family with late-onset Pompe disease described in the literature showing a peculiar complex set of mutations of GAA gene that may partially elucidate the clinical heterogeneity of this family.

Cow (Bovine) Glucosidase, Alpha, Acid (GAA) interaction partners

  1. The lethal mutation 1057DeltaTA of GAA is present in the Droughtmaster breed, with pathology identical to that reported in pure Brahman animals.

GAA Antigen Profile

Antigen Summary

This gene encodes acid alpha-glucosidase, which is essential for the degradation of glycogen to glucose in lysosomes. Different forms of acid alpha-glucosidase are obtained by proteolytic processing. Defects in this gene are the cause of glycogen storage disease II, also known as Pompe's disease, which is an autosomal recessive disorder with a broad clinical spectrum. Three transcript variants encoding the same protein have been found for this gene.

Alternative names and synonyms associated with GAA

  • glucosidase, alpha, acid (Gaa) antibody
  • glucosidase, alpha; acid (GAA) antibody
  • E430018M07Rik antibody
  • LYAG antibody

Protein level used designations for GAA

acid (Pompe disease, glycogen storage disease type II) , acid alpha-glucosidase , acid maltase , glucosidase, alpha; acid (Pompe disease, glycogen storage disease type II) , lysosomal alpha-glucosidase , aglucosidase alfa

367562 Rattus norvegicus
14387 Mus musculus
2548 Homo sapiens
483352 Canis lupus familiaris
280798 Bos taurus
100173365 Pongo abelii
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