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2 survival in cardiomyocytes were inhibited by Pifithrin-a, a p53 inhibitor, suggesting that Lats2 stim
8 tified the tetrahydrobenzothiazole analogue, pifithrin-alpha (2), as a p53 inhibitor that was effecti
9 l animals or wild-type p53 mice treated with pifithrin-alpha (a p53 blocker) were irradiated (five 10
12 ibitors of the tumor suppressor protein p53, pifithrin-alpha (PFT-alpha) and Z-1-117, are highly effe
15 otective activity of the previously reported pifithrin-alpha (PFT-alpha, 1), various derivatives and
18 tream target of Rig-G, and p53 inhibition by pifithrin-alpha caused abrogation of tumor-suppressive e
21 -Ala-Asp-fluoromethylketone or p53 inhibitor pifithrin-alpha markedly prevented mitochondrial release
27 short-term treatment with the p53 inhibitor Pifithrin-alpha partially and transiently rescued the my
30 , the inhibition of p53 by the p53 inhibitor pifithrin-alpha protected against PA-induced apoptosis.
31 stent with activation of AP-1 and NF-kappaB, pifithrin-alpha was also able to enhance the UV-induced
33 either by administration of a p53 inhibitor (pifithrin-alpha), or by crossing Foxe3-/- mice with p53-
35 ions in p53 as well as in cells treated with pifithrin-alpha, a chemical inhibitor of p53 that decrea
38 during cisplatin treatment was attenuated by pifithrin-alpha, a pharmacological inhibitor of p53, whi
41 treatment of mouse epidermal Cl41 cells with pifithrin-alpha, an inhibitor for p53-dependent transcri
42 ficiency, caused by germ-line mutation or by pifithrin-alpha, an inhibitor of p53-dependent apoptosis
44 g inhibitors of p53-dependent transcription, pifithrin-alpha, and a genetic approach (overexpressing
47 eath was provided by use of a p53 inhibitor, pifithrin-alpha, in organotypic slice cultures of mouse
49 for p53 was tested using the p53 inhibitor, pifithrin-alpha, or using stable transfectants of a v-MY
51 t of pol eta(-/-) mice with a p53 inhibitor, pifithrin-alpha, reduced adipocyte senescence and attenu
53 We utilized the small molecule inhibitor, pifithrin-alpha, to inhibit p53 signaling, and nutlin-3a
54 ce the apoptosis of LNCaP cells treated with pifithrin-alpha, which prevents p53 accumulation, or of
55 f macrophages in the kidneys of p53(-/-) and pifithrin-alpha-treated mice after ischemic injury were
57 nally, models of peritonitis in p53(-/-) and pifithrin-alpha-treated mice confirmed the anti-inflamma
66 ciency of p53 or pharmacologic inhibition by pifithrin impairs thrombus resolution and is associated
68 the mitochondrial translocation of p53 with pifithrin mu prevents the formation of p53/Bak complexes
69 elective for the inward-facing state) and/or pifithrin-mu (an HSP70 inhibitor) restored folding of, a
70 the heat shock protein 70 (HSP70) inhibitor pifithrin-mu such that endoplasmic reticulum export of a
72 y this flow-through fraction is inhibited by pifithrin-mu, a small molecule inhibitor of Hsp70, sugge
75 efficacy of administering the small-molecule pifithrin (PFT)-mu, an inhibitor of mitochondrial p53 ac
78 s-infected cells, which could be reversed by pifithrin-u, a p53-heat shock protein 70 (HSP70) signali