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AMPD3 encodes a member of the AMP deaminase gene family. De plus, nous expédions AMPD3 Protéines (6) et et beaucoup plus de produits pour cette protéine.
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N-terminal sequence and distal histidine residues are responsible for pH-regulated cytoplasmic membrane binding
mtDNA deletion coordinately induces AMP deaminase to contribute to the loss of atrial adenine nucleotides through degrading AMP excessively.
The primary underlying mechanism for increased catabolic flow through the AMP deaminase reaction in circulating erythrocytes of individuals with familial phosphofructokinase deficiency is Ca2+-calmodulin activation of AMP deaminase isoform E.
may control the systemic metabolic status by changing AMPK activity through the AMP level.
This is a first report evidencing the pattern of AMPD genes expression in neoplastic human liver.
Data show that AMP deaminase 3 (Ampd3)-/-/5'-nucleotidase (CD73)-/- knockout mice are more sensitive to AMP-induced hypometabolism than mice with a single enzyme deficiency, which are more sensitive than wild type.
depletion of the epigenome modifier histone deacetylase 3 (HDAC3) specifically in skeletal muscle causes severe systemic insulin resistance in mice but markedly enhances endurance and resistance to muscle fatigue, despite reducing muscle force. This is due to lower glucose utilization and greater lipid oxidation in HDAC3-depleted muscles, a fuel switch caused by the activation of anaplerotic reactions driven by Ampd3.
Mice carrying the mutation exhibit rapid RBC turnover, with increased erythropoiesis, dramatically shortened RBC lifespan, and signs of increased RBC senescence/eryptosis, suggesting a key role for AMPD3 in determining RBC half-life. Mice were also found to be resistant to infection with the rodent malaria Plasmodium chabaudi.
Erythrocytes from Ampd3(-/-) mice exhibited higher half-saturation pressure of oxygen.
effect of AMP-deaminase 3 knock-out in mice on enzyme activity in heart and other organs
AMP deaminase-deficient models demonstrate for the first time that AMPD3 plays a critical role in remote reperfusion lung injury via generation of inosine monophosphate (IMP).
AMPD3 deficiency increases the level of ATP in erythrocytes, but does not improve anemia due to pyruvate kinase deficiency and leads to erythrocyte dysfunction.
Along with the activation of AMPD3, ischemia-reperfusion-induced lung inflammation is associated with increased MPO activity and TNF-alpha level.
This gene encodes a member of the AMP deaminase gene family. The encoded protein is a highly regulated enzyme that catalyzes the hydrolytic deamination of adenosine monophosphate to inosine monophosphate, a branch point in the adenylate catabolic pathway. This gene encodes the erythrocyte (E) isoforms, whereas other family members encode isoforms that predominate in muscle (M) and liver (L) cells. Mutations in this gene lead to the clinically asymptomatic, autosomal recessive condition erythrocyte AMP deaminase deficiency. Alternatively spliced transcript variants encoding different isoforms of this gene have been described.
adenosine monophosphate deaminase (isoform E)
, AMP deaminase 3
, adenosine monophosphate deaminase 3
, erythrocyte adenosine monophosphate deaminase
, AMP deaminase 3-like
, AMP aminohydrolase
, erythrocyte AMP deaminase
, erythrocyte type AMP deaminase
, erythrocyte-specific AMP deaminase
, myoadenylate deaminase
, AMP deaminase H-type
, heart-type AMPD