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1 ation were unabated following treatment with manumycin.
2                                         Both manumycin (7.5 mg/kg/dose) and paclitaxel (20 mg/kg/dose
3 kinase kinase 1/2 [MEK1/2] upstream of ERK), manumycin A (Ras inhibitor), BAY43-9006 (Raf-1 inhibitor
4      To identify the molecular mechanisms of manumycin A action, cultured human HepG2 hepatoma cells
5              Furthermore, the Ras inhibitors manumycin A and a dominant-negative form of Ras (RasN17)
6                                We found that manumycin A caused a rapid and potent inhibition of IKK
7 ase (FNTA) by siRNA and the enzyme inhibitor manumycin A caused elevation of ApoA-I secretion from he
8                                              Manumycin A is a potent and selective farnesyltransferas
9 eta constructs, and a striking difference in manumycin A sensitivity was observed.
10 beta dimers were observed in the presence of manumycin A that could be blocked by dithiothreitol.
11          Most importantly, administration of manumycin A to mice xenografted with murine B16F10 tumor
12                                        Thus, manumycin A with its epoxyquinoid moieties plays an impo
13 ly than JAK2 V617F, and inhibition of Ras by manumycin A, a farnesyltransferase inhibitor, ameliorate
14 in transfected HEK293 cells was inhibited by manumycin A, BAY43-9006, U0126, and transfection with a
15 typic dimerization of IKKbeta in response to manumycin A, whereas substitution of Cys-662 and -716 co
16 aptor protein IKKgamma/NEMO was disrupted in manumycin A-treated cells.
17         Thus, we investigated the effects of manumycin (a farnesyl:protein transferase inhibitor), al
18 moted cell growth; dominant negative RhoB or manumycin, a farnesyltransferase inhibitor that targets
19                                    Moreover, manumycin, a specific inhibitor of FTase, was effective
20  Ras protein farnesyl transferase inhibitors manumycin-A and FTI-277.
21       The Ras farnesyl transferase inhibitor manumycin-A, and a dominant-negative form of Ras (RasN17
22  in phosphorylation of SMAD2 were reduced by manumycin-A, suggesting that Ras-dependent transduction
23 paclitaxel treatments seemed as effective as manumycin against ARO cells and more effective than eith
24                         In contrast, neither manumycin alone, paclitaxel alone, doxorubicin alone, no
25 oceramide, an inactive form of ceramide, and manumycin, an inhibitor of neutral sphingomyelinase.
26                           The combination of manumycin and paclitaxel is also effective in vivo with
27                                     Combined manumycin and paclitaxel treatments seemed as effective
28  The in vivo effect and toxicity of combined manumycin and paclitaxel treatments were evaluated in a
29                          Cell treatment with manumycin blocked insulin's ability to suppress pro-apop
30                               In conclusion, manumycin can inhibit the growth of ATC both in vitro an
31               Using synchronized BY-2 cells, manumycin completely blocked mitosis when added at the e
32                              In combination, manumycin enhanced the effect of paclitaxel in all six o
33                  Asukamycin, a member of the manumycin family metabolites, is an antimicrobial and po
34 p. asukaensis ATCC 29757 and a member of the manumycin family of antibiotics, is assembled from three
35  of farnesylated Ras was causally related to manumycin-induced apoptosis and showed that the response
36 of the potent farnesyltransferase inhibitor, manumycin, on insulin antiapoptotic function.
37 nst ARO cells and more effective than either manumycin or paclitaxel alone against KAT-4 cells.
38 ion of Akt was blocked by 4 h treatment with manumycin (P < 0.01), a kinetic too rapid to be explaine
39                    After an 18-h incubation, manumycin plus paclitaxel caused enhanced activation of
40                                              Manumycin plus paclitaxel has enhanced cytotoxic effects
41 one, doxorubicin alone, nor doxorubicin plus manumycin produced significant specific cleavage of PARP
42  whereas blocking protein farnesylation with manumycin severely disrupted the antiapoptotic capacity
43 locked by the farnesyl transferase inhibitor manumycin, suggesting a role for Ras in the actions of G
44 tion of short-lived farnesylated proteins by manumycin suppresses the antiapoptotic action of insulin
45 ed apoptosis and showed that the response to manumycin was found to be independent of K-Ras function
46 ssay of cell viability and light microscopy, manumycin was shown to decrease the number of viable cel

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