|1.||Isaacs, John T: 7 articles (05/2015 - 07/2003)|
|2.||Denmeade, Samuel R: 7 articles (05/2015 - 07/2003)|
|3.||Jiang, Chen Chen: 7 articles (01/2015 - 10/2007)|
|4.||Zhang, Xu Dong: 7 articles (01/2015 - 10/2007)|
|5.||Hersey, Peter: 5 articles (09/2009 - 10/2007)|
|6.||Saatcioglu, Fahri: 4 articles (01/2011 - 02/2002)|
|7.||Denmeade, S R: 4 articles (05/2002 - 06/2000)|
|8.||Prevarskaya, Natalia: 3 articles (11/2013 - 07/2004)|
|9.||Pariente, José A: 3 articles (09/2009 - 08/2006)|
|10.||Thorne, Rick F: 3 articles (08/2008 - 11/2007)|
01/01/2009 - "Overexpression of SERCA2 abrogated the protective effects of HAX-1 on cell survival, after hypoxia/reoxygenation or thapsigargin treatment. "
02/01/2010 - "Suppression of Ca2+ release by thapsigargin did not alter the response of ICa to anoxia, suggesting a mandatory role for Ca2+ influx and not Ca2+-induced Ca2+ release (CICR) in O2 regulation of the channel. "
04/17/2009 - "However, the cellular changes and apoptotic events that occurred following thapsigargin treatment, were completely inhibited by hypoxia, including loss of mitochondrial transmembrane potential (MTP), ROS generation and JNK phosphorylation. "
04/17/2009 - "Hypoxia protects articular chondrocytes from thapsigargin-induced apoptosis."
01/01/2008 - "At modeling of endoplasmatic reticulum (ER) stress by it classic inducer thapsigargin, anoxia-reoxygenation and simultaneous inhibition ofproteasomal proteolysis, autophagy and apoptosis a diversity of ultrastructural peculiarities was shown. "
09/01/2015 - "This study aimed to evaluate the potential involvement of O-demethyldemethoxycurcumin, an analog of curcuminoids, on thapsigargin-induced apoptosis in cultured neuroblastoma (SK-N-SH) cells through the ER stress signaling pathway. "
08/01/2000 - "In this study we found that SH-SY5Y neuroblastoma cell division was blocked by entry into a quiescent G0-like state by thapsigargin, a high specific SERCA inhibitor, highlighting the regulatory role of SERCA in cell cycle progression. "
06/01/2007 - "In addition, SH-20148 demonstrated a neuroprotective effect against thapsigargin-induced neuronal cell death in neuroblastoma SH-SY5Y cells. "
05/15/2005 - "Caspases-2, -3, and -7 are involved in thapsigargin-induced apoptosis of SH-SY5Y neuroblastoma cells."
06/18/2004 - "Differential thapsigargin-sensitivities and interaction of Ca2+ stores in human SH-SY5Y neuroblastoma cells."
12/15/2014 - "However, in our study, persistent ER stress induced by multiple administrations of low-dose thapsigargin (Tg) accelerated tumor growth in mice. "
05/01/2015 - "Targeting thapsigargin towards tumors."
01/01/2015 - "This review will describe the discovery of the new drug, the on-going elucidation of the biosynthesis of thapsigargin in the plant and attempts to supply the global market with a novel potent anti-cancer drug. "
01/01/2014 - "Combined treatment with the ER stressor thapsigargin and the mitochondrial Hsp90 inhibitor gamitrinib augmented interorganelle stress signaling by elevating CHOP expression, and showed synergistic cytotoxic activity exclusively in cancer cells in vitro and in vivo. "
01/01/2013 - "Sec62 is essential for cell migration and protects tumor cells against thapsigargin-induced ER stress, which are both linked to cytosolic Ca²⁺. "
|4.||Brain Ischemia (Cerebral Ischemia)
12/31/2010 - "Because endoplasmic reticulum (ER) stress has been implicated in neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and cerebral ischemia, we investigated the effects of baicalein on apoptotic death of HT22 mouse hippocampal neuronal cells induced by thapsigargin (TG) and brefeldin A (BFA), two representative ER stress inducers. "
02/01/2002 - "Calcium measurements with fura-2 acetoxymethylester revealed that oxygen-glucose deprivation caused a significant reduction in thapsigargin-releasable endoplasmic reticular stores of Ca2+. These studies suggest that an important component of the neuronal toxicity in cerebral ischemia is due to disruption of calcium homeostasis, particularly to the depletion of intracellular Ca2+ stores."
10/01/2001 - "Increased intracellular Ca(2+) was detected 10-15 s after the onset of ischemia; the initial increase was inhibited by preperfusion with thapsigargin. "
09/11/2008 - "Pretreatment with tunicamycin or thapsigargin significantly ameliorated renal dysfunction and injury after ischemia-reperfusion. "
01/01/2000 - "Pretreatment of lungs with thapsigargin abolished the increase in free iron with ischemia indicating that this effect is dependent on Ca2+ release from intracellular stores. "
07/10/1999 - "Ischemia from 5 to 60 min had no significant effect on thapsigargin sensitive ATPase activity. "
04/01/1998 - "Therefore, using the isolated working rat heart model, we investigated the effect of Thapsigargin (TH)-induced SR calcium diminution on the myocardial protection when added either before onset of ischemia or at time of reperfusion under conditions of normothermic ischemia. "
|3.||Fura-2 (Fura 2)
|9.||Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)
|10.||Glutamic Acid (Glutamate)
|4.||Heterologous Transplantation (Xenotransplantation)