Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P04040 (
Catalase
)
3,577
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The viability of neutrophils in the condition under which they kill neoplastic cells was studied. In the presence of phorbol myristate acetate (PMA) the 51Cr-release by human neutrophils was markedly stimulated. The PMA-induced 51Cr-release by neutrophils correlated well with the number of nonviable neutrophils as determined by the uptake of trypan blue. Phorbol myristate acetate had no effect on the 51Cr-release by lymphocytes,
LPC
-1 myeloma cells, ovarian ascites tumor cells, or neutrophils from a patient with chronic granulomatous disease. This suggests that the effect of PMA is not due to its nonspecific toxic effect; instead, it is dependent on the reactive oxygen species produced by the normal neutrophils.
Catalase
, cytochrome C, histidine, and methionine inhibited the PMA-induced 51Cr-release by human neutrophils, whereas superoxide dismutase, myeloperoxidase inhibitors, and some hydroxyl radical scavengers or singlet oxygen quenchers had no effect. The clumping of neutrophils induced by PMA was also important in the PMA-induced 51Cr-release by human neutrophils.
...
PMID:Phorbol myristate acetate induced neutrophil autotoxicity. 719 15
Altered redox state modulates the expression levels of endothelial K
Ca
2.3 and K
Ca
3.1 (K
Ca
s) in normal pregnancy (NP) and preeclampsia (PE), thereby regulating vascular contractility. The mechanisms underlying K
Ca
s endocytosis and transportation remain unknown. We investigated the regulation of K
Ca
s expression in plasma membrane (PM) during NP and PE. Cultured human uterine artery endothelial cells were incubated in serum from normal nonpregnant women and women with NP or PE, or in oxidized LDL-, or lysophosphatidylcholine- (LPC-) containing a medium for 24 hours. NP serum elevated PM levels of K
Ca
s and reduced caveolin-1 and clathrin levels. PE serum, oxidized LDL, or
LPC
reduced PM levels of K
Ca
s and elevated caveolin-1, clathrin, Rab5c, and early endosome antigen-1 (EEA1) levels. Reduced K
Ca
s levels by PE serum or
LPC
were reversed by inhibition of caveolin-1, clathrin, or EEA1.
Catalase
and glutathione peroxidase 1 (GPX1) knockdown elevated PM-localized K
Ca
s levels and reduced caveolin-1 and clathrin levels. Elevated K
Ca
2.3 levels upon catalase and GPX1 knockdown were reversed by PEG-catalase treatment. An H
2
O
2
donor reduced clathrin and Rab5c. In contrast, elevated clathrin, caveolin-1, or colocalization of caveolin-1 with K
Ca
3.1 by PE serum or
LPC
was reversed by NADPH oxidase inhibitors or antioxidants. A superoxide donor xanthine+xanthine oxidase elevated caveolin-1 or Rab5c levels. We concluded that K
Ca
s are endocytosed in a caveola- or a clathrin-dependent manner and transported in a Rab5c- and EEA1-dependent manner during pregnancy. The endocytosis and transportation processes may slow down via H
2
O
2
-mediated pathways in NP and may be accelerated via superoxide-mediated pathways in PE.
...
PMID:Internalization and Transportation of Endothelial Cell Surface K
Ca
2.3 and K
Ca
3.1 in Normal Pregnancy and Preeclampsia. 3187 52
