Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normal human granulocytes obtained by Ficoll-Hypaque sedimentation were subjected to mild hypotonic shock and disruption by shear. The homogenate was fractionated by differential centrifugation and equilibrium ultracentrifugation to yield a plasma membrane preparation constituting 1% of the total cellular protein and enriched fifteen- and six-fold in alkaline phosphatase and Mg2+-adenosine triphosphatase activities, respectively. Granulocytes obtained from patients with chronic myeloid leukemia (CML) were identically processed. The protein constituents of both the normal and CML granulocyte plasma membranes were resolved by two-dimensional polyacrylamide gel electrophoresis. Comparison of the stained gels revealed CML-associated quantitative changes in four out of the fifteen protein spots examined. Thus, this analysis has permitted identification of those protein moieties that deserve attention for further isolation and purification.
 ...
PMID:Plasma membranes from normal and chronic myeloid leukemic granulocytes: isolation and two-dimensional polyacrylamide gel electrophoretic analysis. 385 66

During allergic disease, leucocytes infiltrate the affected tissues and release their mediators and cytokines. In this way, the local inflammatory process is induced and maintained. Basophilic granulocytes have been demonstrated in lung and sputum of allergic asthmatics, in nasal mucosa and secretion of allergic rhinitis patients, and in skin lesions of atopic dermatitis patients. The number of basophils correlates with the severity of the disease. Analysis of mediator profiles and cellular contents of lavages of nose, skin and lung during allergic late-phase reactions (LPR) have demonstrated histamine, but not tryptase or prostaglandin D2. The histamine-containing cells have been characterized as basophilic granulocytes. This indicates that infiltrating basophils but not mast cells are activated and release their inflammatory contents in the LPR. We are interested in the cellular mechanisms that determine the degranulation of basophils during LPR. Basophil activators, such as allergens and activated complement, are not present at these sites. However, cytokines that prime basophils but do not induce degranulation, such as interleukin-5 (IL-5) and granulocyte/macrophage colony-stimulating factor (GM-CSF), have been detected at sites of LPR. We have now observed that after emptying intracellular Ca2+ stores by means of the Ca2+ adenosine triphosphatase (ATPase) inhibitor, thapsigargin, basophils become extremely sensitive to stimuli that do not affect the Ca2+ stores themselves but that induce degranulation, such as the phorbolester, phorbol myristate acetate (PMA). The most interesting finding was that although both thapsigargin and IL-3, IL-5 or GM-CSF do not induce basophil degranulation by themselves, a 2 min preincubation of basophils with thapsigargin followed by addition of one of these cytokines resulted in extensive histamine release: IL-3 induced 71 +/- 7% histamine release (conc1/2max 6 pM), IL-5 induced 43 +/- 8% histamine release (conc1/2max 41 pM) and GM-CSF induced 57 +/- 10% histamine release (conc1/2max 140 pM). Interestingly, the effect of thapsigargin could be mimicked by platelet-activating factor (PAF) (range 10(-9) to 10(-6) M), although to a lesser extent. Our results indicate that basophil degranulation in tissues during late-phase reactions might be caused by a combination of mediators or cytokines depleting Ca2+ stores, as platelet-activating factor or thapsigargin do, concurrent with activation by interleukin-3, interleukin-5 or granulocyte/macrophage colony-stimulating factor. The response of the basophils towards these cytokines might also be influenced by cell adhesion events, such as binding of basophils via integrins. This is the subject of further study.
 ...
PMID:The role of basophils in allergic disease. 887 Oct 57

The effects of Ku Ding tea (Lactuca taiwaniana Maxim) and milk powder on biochemical and immunological parameters of Sprague-Dawley rats were investigated and the possibility of use of Ku Ding tea to reduce physiological discomfort of drinking milk powder was assessed. Eighty rats were randomly assigned to four treatments: basal diet (control), basal diet plus whole milk powder (WM), basal diet plus Ku Ding tea (KD) and basal diet plus whole milk powder and Ku Ding tea (MK). Data was collected on animals' final body weight, hematological values, blood biochemical parameters, antioxidation parameters and immune organ weight index. Results showed that final body weight of male KD was significantly lower than that of WM. White blood cell count, monocyte count and granulocyte count of KD rats were significantly lower than those of WM. Compared to the control, single milk powder supplementation numerically increased plasma malondialdehyde. The malondialdehyde in the male KD and MK rats were lower than those in WM and control, although the differences were not significant. No significant differences were found in Na(+)K(+)-adenosine triphosphatase activity, spleen and thymus index in each group. Consumption of Ku Ding tea appeared to lower lipid peroxidation that was induced by milk powder in the rats.
 ...
PMID:Milk powder induced lipid peroxidation reduction using Ku Ding tea (Lactuca taiwaniana Maxim) in rats. 2357 69