Glucose-6-phosphate isomerase (GPI) is a homodimeric enzyme ubiquitously present in most organisms. GPI catalyzes the interconversion between glucose-6-phosphate and fructose-6-hosphate, the second step of the glycolytic pathway. In mammals, Glucose-6-phosphate isomerase also acts as an autocrine motility factor (AMF), a neuroleukin, and a maturation factor. GPI deficiency is the second most common erythroenzymopathy of glycolytic enzymes after pyruvate kinase deficiency. Inherited deficiency of the enzymatic activity of GPI causes hereditary nonspherocytic hemolytic anemia (HNSHA) in humans, a severe deficiency that can be associated with hydrops fetalis (a-thalassaemia), immediate neonatal death, and neurological impairment.
Proprietà fisiche
C-terminal histidine-tagged
Definizione di unità
One unit will convert 1.0 mmole of D-fructose 6-phosphate to D-glucose 6-phosphate per inute at pH 7.4 at 25 °C.
Stato fisico
Supplied as a solution in 50 mM Tris-HCl pH 7.5, and 50% glycerol
Thrombopoietin (TPO), a hematopoietic growth factor produced predominantly by the liver, is essential for thrombopoiesis. Prevailing theory posits that circulating TPO levels are maintained through its clearance by platelets and megakaryocytes via surface c-Mpl receptor internalization. Interestingly, we found a
Thrombosis and haemostasis, 117(1), 66-74 (2016-10-14)
Currently, molecular diagnosis of haemophilia A and B (HA and HB) highlights the excess risk-inhibitor development associated with specific mutations, and enables carrier testing of female relatives and prenatal or preimplantation genetic diagnosis. Molecular testing for HA also helps distinguish
Soluble factors released from irradiated human mesenchymal stromal cells (MSC) may induce genetic instability in human CD34+ cells, potentially mediating hematologic disorders. Recently, we identified four key proteins in the secretome of X-ray-irradiated MSC, among them three endoplasmic reticulum proteins
The endothelium monolayer lining in the luminal side of blood vessels provides critical antithrombotic functions. Damage to these cells will expose a highly thrombogenic subendothelium, which leads to pathological vascular changes. Using combined tissue engineering and ligand-receptor targeting strategy, we
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