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Adenosine monophosphate deaminase 1 catalyzes the deamination of AMP to IMP in skeletal muscle and plays an important role in the purine nucleotide cycle. Additionally we are shipping Adenosine Monophosphate Deaminase 1 Proteins (5) and many more products for this protein.
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Human Polyclonal AMPD1 Primary Antibody for IHC, ELISA - ABIN1534626
Gregory, Barlow, McLay, Kaul, Swarbreck, Dunham, Scott, Howe, Woodfine, Spencer, Jones, Gillson, Searle, Zhou, Kokocinski, McDonald, Evans, Phillips, Atkinson, Cooper, Jones, Hall, Andrews, Lloyd et al.: The DNA sequence and biological annotation of human chromosome 1. ... in Nature 2006
Show all 2 references for ABIN1534626
Cow (Bovine) Polyclonal AMPD1 Primary Antibody for ELISA - ABIN408637
Hand, Roth, Roltsch, Park, Kostek, Ferrell, Brown: AMPD1 gene polymorphism and the vasodilatory response to ischemia. in Life sciences 2006
Cow (Bovine) Polyclonal AMPD1 Primary Antibody for IHC (p), WB - ABIN4280395
Coley, Rayavarapu, Pandey, Sabina, Van der Meulen, Ampong, Wortmann, Rawat, Nagaraju: The molecular basis of skeletal muscle weakness in a mouse model of inflammatory myopathy. in Arthritis and rheumatism 2012
Variations in AMPD1, CPT2 (show CPT2 Antibodies), and PGYM genes are not associated with the onset, susceptibility, or severity of chronic fatigue syndrome.
Common polymorphism of the AMPD1 gene (C34T) is strongly associated with essential hypertension.
AMPD1 could have a profound influence on cholinergic neurotransmission and sleep; further studies are mandatory
AMPD1 34C>T variant is associated with higher infection susceptibility to community acquired pneumonia but not to ventilator associated pneumonia in sepsis pateints
Mutational variants in AMPD1 contribute to autism risk in Han Chinese population, via mitochondria dysfunction and cell necrosis.
The best response to creatine in terms of physical performance was presented by AMPD1 CC genotype.
The present study demonstrated a positive effect of C34T AMPD1 gene polymorphism in aortic stiffness and in inflammatory status in a high risk population of CAD (show CAD Antibodies) subjects.
Our other studies on the metabolic impact of AMPD1 C34T mutation revealed decrease in AMPD activity.
AMPD1 gene polymorphism C34T can be considered as a marker of liability to the high-speed and strength muscular activity.
In a study of a Spanish and 2 North African cohorts, frequency of the AMPD1 C34T mutation was lower in Berbers compared with the Alpujarra cohort. The GDF8 (show MSTN Antibodies) K153R substitution showed little variability among the three cohorts.
The deduced amino acid sequence of AMPD1 contains an AMP (show TMPRSS5 Antibodies) deaminase signature sequence (SLSTDDP). RT-PCR analyses showed that AMPD1 was expressed specifically in skeletal muscle.
Our results indicate that the deletion mutation in the AMPD1 gene is associated with production traits, and may be used for marker-assisted selection in beef cattle breeding programs.
These results suggest that the 18-bp deletion mutation in AMPD1 may influence the carcass traits in Qinchuan cattle.
AMPD1 deficiency activates AMPK (show PRKAA1 Antibodies)/Akt (show AKT1 Antibodies)/mTORC1/p70 S6 kinase (show PRKACB Antibodies) axis in skeletal muscle after high fat diet challenge, but not in normal chow diet. These changes may contribute to improve insulin (show INS Antibodies) resistance.
Disruption of the AMPD1 gene leads to a less severe state of insulin (show INS Antibodies) resistance, improved glucose tolerance and enhanced insulin (show INS Antibodies) clearance in mice fed a high-fat diet. Data suggest that AMPD may be a new drug target for reversing insulin (show INS Antibodies) resistance.
AMPD1 deficiency is acquired prior to overt muscle inflammation and is responsible, at least in part, for the muscle weakness that occurs in the mouse model of myositis.
Adenosine monophosphate deaminase 1 catalyzes the deamination of AMP to IMP in skeletal muscle and plays an important role in the purine nucleotide cycle. Two other genes have been identified, AMPD2 and AMPD3, for the liver- and erythocyte-specific isoforms, respectively. Deficiency of the muscle-specific enzyme is apparently a common cause of exercise-induced myopathy and probably the most common cause of metabolic myopathy in the human. Alternatively spliced transcript variants encoding different isoforms have been identified in this gene.
, N-acetylmuramoyl-L-alanine amidase
, Negative regulator of beta-lactamase expression
, adenosine monophosphate deaminase 1
, AMP deaminase 1-like
, adenosine monophosphate deaminase 1 (isoform M)
, AMP deaminase 1
, adenosine monophosphate deaminase-1 (muscle)
, myoadenylate deaminase
, skeletal muscle AMPD