• Corpus ID: 32871783

Effect of NPC-15199 on Ca2+ levels in renal tubular cells.

  title={Effect of NPC-15199 on Ca2+ levels in renal tubular cells.},
  author={C-R Jan and Bang Ping Jiann and Hong‐Tai Chang and Changsong Yu and Yih-Chau Lu and J H Yeh and Wei-C Chen and Y P Law and Jong‐Khing Huang},
  journal={The Chinese journal of physiology},
  volume={45 3},
In Madin-Darby canine kidney (MDCK) cells, effect of NPC-15199 on intracellular Ca2+ concentration ([Ca2+]i) was investigated by using fura-2. NPC-15199 (100-1000 microM) caused a rapid and sustained increase of [Ca2+]i in a concentration-dependent manner (EC50=500 microM). NPC-15199-induced [Ca2+]i rise was prevented by 70% by removal of extracellular Ca2+, but was not changed by dihydropyridines, verapamil and diltiazem. In Ca2+-free medium, carbonylcyanide m-chlorophenylhydrazone (CCCP; 2… 
Effect of diethylstilbestrol on Ca2+ handling and cell viability in human breast cancer cells.
In human breast cancer cells, the effect of the widely prescribed estrogen diethylstilbestrol (DES) on intracellular Ca2+ concentrations ([Ca2+]i) and cell viability was explored by using fura-2 and
Effect of gossypol on intracellular Ca2+ regulation in human hepatoma cells.
The results suggest that in human hepatocytes, gossypol induced a [Ca2+]i increase by causing store Ca2+ release from the endoplasmic reticulum in a phospholipase C-independent manner, and by inducing Ca2- influx.
Effect of NPC15199 on [Ca²⁺]i and viability in SCM1 human gastric cancer cells.
Together, in SCM1 cells, NPC15199 induced [Ca²⁺]i rises that involved Ca�⁺ entry through PKC-insensitive non-store-operated Ca¬⁺ channels and PLC-independent Ca²⁚ release from the endoplasmic reticulum, and induced Caµ⁺-independent cell death.


Mechanism of bifonazole-induced [Ca2+]i increases in MDCK renal tubular cells.
Together, bifonazole increased [Ca2+]i in renal tubular cells by inducing intracellular Ca2+ release and extracellular Ca1+ influx and inositol 1,4,5-trisphosphate may be involved in bif onazole-induced Ca2+.
NPC-14686, a novel anti-inflammatory agent, increased intracellular Ca(2+) concentrations in MDCK renal tubular cells.
NPC-15199, a novel anti-inflammatory agent, mobilizes intracellular Ca2+ in bladder female transitional carcinoma (BFTC) cells.
The findings suggest that in BFTC bladder cancer cells, NPC-15199 induced Ca2- release from the endoplasmic reticulum and activating Ca2+ entry.
Effect of diethylstilbestrol (DES) on intracellular Ca2+ levels in renal tubular cells
Intracellular calcium concentrations in human bladder tumor cells could be increased by NPC‐14686, a novel antiinflammatory agent
The findings suggest that in T24 bladder tumor cells NPC‐14686 induced Ca2+ release followed by Ca2-i increase, which was unlinked to IP3 and the [Ca2+]i signal could be modulated by protein kinase C.
Dual effect of tamoxifen, an anti-breast-cancer drug, on intracellular Ca(2+) and cytotoxicity in intact cells.
It was found that tamoxifen increased [Ca(2+)](i) in MDCK cells by releasing Ca(2+) from multiple Ca-2+) stores in a manner independent of the production of inositol 1,4, 5-trisphosphate and also by triggering Ca( 2+) influx from extracellular space.
Thapsigargin, a tumor promoter, discharges intracellular Ca2+ stores by specific inhibition of the endoplasmic reticulum Ca2(+)-ATPase.
The results suggest that thapsigargin increases the concentration of cytosolic free Ca2+ in sensitive cells by an acute and highly specific arrest of the endoplasmic reticulum Ca 2+ pump, followed by a rapid Ca2+.
MK-886, a leukotriene biosynthesis inhibitor, as an activator of Ca(2+) mobilization in Madin-Darby canine kidney (MDCK) cells.
  • C. Jan, C. Tseng
  • Biology, Chemistry
    The Journal of pharmacology and experimental therapeutics
  • 2000
The effect of 3-¿1-(p-chlorobenzyl)-5-(isopropyl)-3-tert-butylthioindol-2-yl-2, 2-dimethylpropanoic acid (MK-886), a leukotriene biosynthesis inhibitor, on Ca(2+) mobilization in Madin- Darby canine