PD 98059

05/01/2014 - "Subsequently, the PASMCs were divided into five groups: the normoxia group, the hypoxia group, the hypoxia + Tau group, the hypoxia + Tau + PD98059 group and the hypoxia + PD98059 group. "
07/01/2013 - "Pretreatment with 30 µM PD98059, an inhibitor of ERK1/2, significantly reduced hypoxia-stimulated periostin expression (P < 0.01). "
04/27/2012 - "Primary cultures of adult rat ventricular myocytes (ARVMs) were exposed to 3 h of hypoxia followed by 30, 60, 90 and 120 min of reoxygenation in presence of a vehicle, NO donor (GSNO, 50 μmol/L) and inhibitors of ERK1/2 (PD98059, 10 μmol/L). "
06/01/2008 - "The effects of KGF on TER and ZO-1 localization in cells exposed to hypoxia were inhibited by PD98059, an inhibitor of ERK signaling. "
06/07/2007 - "Conversely, treatment of tumour cells with the MEK1/2 inhibitors PD98059 or U0216, or expression of a dominant-negative form of ERK1 blocked HIF-1 activation in hypoxia without affecting HIF-1alpha induction, localization or binding of HIF-1beta. "

01/01/2004 - "Finally, administration of PD98059 during ischemia-reperfusion diminished the protective effects of IPC and APC. "
03/31/2009 - "Sixty-four isolated TAC mouse hearts were mounted onto the Langendorff perfusion system and randomly divided into 4 equal group: (1) I/R group undergoing stable perfusion for 30 min, ischemia for 30 min, and re-perfusion for 120 min (an I/R cycle) to cause hypertrophic myocardium I/R injury, (2) IPost group undergoing ischemia for 10s and reperfusion for 10s, totally 3 cycles (60s) before reperfusion for 120 min, (3) I/R+ PD98059 (an ERK1/2 inhibitor) group undergoing perfusion of Krebs-Henseleit (KH) buffer with PD98059 10(-5)mol/L for 15 min and perfusion of KH buffer without PD98059 at the beginning of re-perfusion, and (4) IPost + PD98059 group undergoing 3 cycles of IPost and perfusion of KH buffer with PD98059 10(-5)mol/L for 15 min at the beginning of re-perfusion. "
02/01/2008 - "Langendorff perfused C57/BL mouse hearts were divided to 6 groups: (1) control: 30 min global ischemia and 2 h reperfusion (I/R); (2) IPC with 3 episodes, IPC with 3 episodes of 10 s of ischemia and 10 s reperfusion after 30 min ischemia and before 2 h reperfusion; (3) IPC with 6 episodes, IPC with six episodes of 10 s of ischemia and 10 s reperfusion after 30 min ischemia and before 2 h reperfusion; (4) delayed IPC, IPC with 3 episodes of 10 s of ischemia and 10 s reperfusion after 30 min ischemia and at one minute after reperfusion; (5) IPC + ERK1/2 inhibitor PD98059 (10(-5) mol/L for 15 min); (6) I/R + ERK1/2 inhibitor PD98059 (10(-5) mol/L for 15 min). "
07/01/2000 - "Neither PD98059 nor IPC altered alpha BC phosphorylation during prolonged ischemia. "
03/31/2000 - "Hearts isolated from rats treated with PD98059 and subjected to global ischemia (30 minutes)/reoxygenation (1 hour) showed a diminished functional recovery compared with the vehicle group. "

07/01/2015 - "In addition, PD98059, a specific ERK inhibitor, increased the sensitivity of cancer cells to a lower concentration of ATO treatment. "
03/01/2012 - "Tumor cell migration was inhibited by the treatment with PD98059, ERK inhibitor, NAC or DPI, well-known ROS scavengers. "
01/01/2010 - "Administration of the ERK inhibitor PD98059 to tumor bearers attenuates muscle depletion and weakness, while restoring normal atrogin-1 expression. "
01/01/2010 - "Inhibition of MEK with PD98059 did not affect tumor growth in any tested variant. "
01/01/2007 - "PD-98059 inhibited CCN2-induced proliferation (-12 +/- 3%, P < 0.05) and ERK1/2 phosphorylation (-34 +/- 5%, P < 0.05) in tumor cells. "

12/25/2015 - "Further, PD 98059, the inhibitor of ERK1/2, significantly abolished the BPA induced up regulation of ERRγ and proliferation of breast cancer cells. "
06/01/2007 - "We observed that 5 mum Tam rapidly induced sustained activation of ERK1/2 in ER-positive breast cancer cell lines (MCF-7 and T47D) and that PD98059 (inhibitor of ERK activation) was able to protect MCF-7 cells against Tam-induced death. "
02/01/2008 - "In this study, we evaluated the proliferative behavior of PMA-treated MCF-7 breast cancer cell and found that: PMA induced growth arrest and inhibited cell death; PMA activated ERKs, which, in turn, induced p21; and inhibitors of ERK (PD98059) and PKC (GF109203X) prevented p21 induction and abolished the PMA survival effect. "
01/01/2014 - "MCF-7 breast cancer cells were treated with ERKl/2 inhibitor (PD98059) or CANP inhibitor (calpeptin) before exposure to 1×10(-8) M E2. "
08/01/2005 - "Moreover, in MCF-7 human breast cancer cells mAChR stimulation induced an increase of protein synthesis and cell proliferation, and these effects were prevented by PD098059, a specific inhibitor of the mitogen activated kinase kinase. "

02/01/2015 - "In congruence, IT administration of PD98059 before incision delayed mechanical hyperalgesia after incision; however, administration after incision had only a modest effect on mechanical hyperalgesia. "
02/01/2015 - "In addition, PD98059 did not affect non-evoked pain behaviour or heat hyperalgesia after incision. "
02/01/2015 - "In behavioural experiments, the effect of PD98059 administered 1 h before or after incision on non-evoked pain behaviour and mechanical and heat hyperalgesia was assessed. "
02/01/2009 - "We examined the effect of intraplantar injection of an ERK1/2 inhibitor, PD98059, and a p38 inhibitor, SB202190, on BV-induced PSN, mechanical hyperalgesia, and inflammatory swelling. "
12/06/2006 - "Spinal administration of PD 98059 dose-dependently reduced SNBs, and attenuated both mechanical allodynia and heat hyperalgesia induced by DHPG. "