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Glucosidase, Alpha, Acid Proteins (GAA)

GAA encodes acid alpha-glucosidase, which is essential for the degradation of glycogen to glucose in lysosomes. Additionally we are shipping GAA Antibodies (50) and GAA Kits (16) and many more products for this protein.

list all proteins Gene Name GeneID UniProt
GAA 367562 Q6P7A9
GAA 14387 P70699
GAA 2548 P10253
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Top GAA Proteins at antibodies-online.com

Showing 9 out of 14 products:

Catalog No. Origin Source Conjugate Images Quantity Supplier Delivery Price Details
HOST_Escherichia coli (E. coli) Human His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Log in to see 39 to 44 Days
$9,248.02
Details
HOST_Escherichia coli (E. coli) Mouse His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Log in to see 39 to 44 Days
$9,248.02
Details
HOST_Escherichia coli (E. coli) Rat His tag,T7 tag 100 μg Log in to see 11 to 13 Days
$816.20
Details
HOST_Escherichia coli (E. coli) Mouse His tag 100 μg Log in to see 11 to 13 Days
$827.20
Details
HOST_Escherichia coli (E. coli) Human His tag 100 μg Log in to see 11 to 13 Days
$880.00
Details
HOST_Wheat germ Human GST tag 10 μg Log in to see 9 Days
$405.71
Details
HOST_Escherichia coli (E. coli) Rat Un-conjugated   100 μg Log in to see 9 to 19 Days
$983.48
Details
HOST_Escherichia coli (E. coli) Mouse Un-conjugated   100 μg Log in to see 9 to 19 Days
$999.22
Details
HOST_Escherichia coli (E. coli) Human Un-conjugated   100 μg Log in to see 9 to 19 Days
$1,046.42
Details

GAA Proteins by Origin and Source

Origin Expressed in Conjugate
Rat (Rattus)

Mouse (Murine)

Human ,
,

More Proteins for Glucosidase, Alpha, Acid (GAA) Interaction Partners

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

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

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

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

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

Human Glucosidase, Alpha, Acid (GAA) interaction partners

  1. 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.

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

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

  4. 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.

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

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

  7. 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.

  8. 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.

  9. 7 of 27 in: Gene. 2014 Mar (show IRF1 Proteins) 1;537(1) Novel GAA sequence variant c.1211 A>G reduces enzyme activity but not protein expression in infantile and adult onset Pompe disease.

  10. This study demonstrates that the c.-32-13T>G mutation of GAA gene abrogates the binding of the splicing factor (show SLU7 Proteins) U2AF65 (show U2AF59 Proteins) to the polypyrimidine tract of exon 2 and that several splicing factors affect exon 2 inclusion.

GAA Protein Profile

Protein 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.

Gene names and symbols associated with Glucosidase, Alpha, Acid Proteins (GAA)

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

Protein level used designations for Glucosidase, Alpha, Acid Proteins (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

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