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anti-Mouse (Murine) AGL Antikörper:
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Human Polyclonal AGL Primary Antibody für IF, WB - ABIN1882062
Hansen, Lundin, Markussen, Thorsby: T cell receptor usage by HLA-DQw8-specific T cell clones. in International immunology 1992
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Human Polyclonal AGL Primary Antibody für IF, WB - ABIN389030
Parker, Kong, Walsh, Salajegheh, Moghadaszadeh, Amato, Nazareno, Lin, Krastins, Sarracino, Beggs, Pinkus, Greenberg: Fast-twitch sarcomeric and glycolytic enzyme protein loss in inclusion body myositis. in Muscle & nerve 2009
Show all 9 Pubmed References
Human Polyclonal AGL Primary Antibody für IP, WB - ABIN343185
Parker, Koay, Gilbert-Wilson, Waddington, Stapleton: AMP-activated protein kinase does not associate with glycogen alpha-particles from rat liver. in Biochemical and biophysical research communications 2007
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The study identified 31 novel mutations and extended the mutation spectrum of AGL in Chinese patients with glycogen (zeige GYS1 Antikörper) storage disease type III.
Our study establishes HAS2 (zeige HAS2 Antikörper)-mediated HA synthesis as a driver of growth of bladder cancer with low AGL and provides preclinical rationale for personalized targeting of HAS2 (zeige HAS2 Antikörper)/HA signaling in patients with low amylo-alpha-1-6-glucosidase-4-alpha-glucanotransferase -expressing tumors.
AGL loss causes high SHMT2 (zeige SHMT2 Antikörper) expression and consequently increases glycine-dependent nucleotide synthesis leading to bladder cancer growth.
Point mutations in AGL gene are associated with glycogen (zeige GYS1 Antikörper) storage disease type IIIa in a Chinese family.
AGL haplotype analyses suggested that c.1019delA and c.958+1G>A are founder mutations in Turkish patients, while p.R864X is a recurrent mutation.
A homozygous frameshift deletion, c.4456delT, in exon 33 of the AGL gene in Inuit children determines the cause of glycogen (zeige GYS1 Antikörper) storage disease type IIIa and confirms a founder effect.
study identified 10 different mutations in 8 Korean Glycogen (zeige GYS1 Antikörper) storage disease type III patients; 5 mutations are novel and include 1 nonsense (c.1461G>A, p.W487X), 3 splicing (c.293+4_293+6delAGT in IVS4, c.460+1G>T in IVS5, c.2682-8A>G in IVS21) and 1 missense mutation (c.2591G>C, p.R864P)
Characterization of a novel homozygous single point mutation at the polypyrimidine tract of intron 21 of the AGL gene in two consanguineous siblings with glycogen (zeige GYS1 Antikörper) storage disease type III.
We found that most patients with macular telangiectasia-2 possess retinal autoantibodies, the most prevalent of which were directed against AGL, RBP3 (zeige E2F1 Antikörper), and CK-B.
A founder effect discovered amongst Tunisian patients with glycogen (zeige GYS1 Antikörper) storage disease type III and a c.3216_3217delGA mutation in the AGL gene.
This gene encodes the glycogen debrancher enzyme which is involved in glycogen degradation. This enzyme has two independent catalytic activities which occur at different sites on the protein: a 4-alpha-glucotransferase activity and a amylo-1,6-glucosidase activity. Mutations in this gene are associated with glycogen storage disease although a wide range of enzymatic and clinical variability occurs which may be due to tissue-specific alternative splicing. Alternatively spliced transcripts encoding different isoforms have been described.
amylo-1, 6-glucosidase, 4-alpha-glucanotransferase (glycogen debranching enzyme, glycogen storage disease type III)
, glycogen debranching enzyme
, amylo-1, 6-glucosidase, 4-alpha-glucanotransferase
, amylo-alpha-1, 6-glucosidase, 4-alpha-glucanotransferase
, glycogen storage disease type III
, glycogen debrancher
, amylo-1,6-glucosidase, 4-alpha-glucanotransferase
, Glycogen debrancher