1 ins with Cys28 is more than 90% inhibited by mersalyl.

2 by the no Cys mutant shows 40% inhibition by mersalyl.

3 cid (pCMBS), p-chloromercuribenzoate (pCMB), mersalyl acid and HgCl2, but not by the stilbene anion e

4 kers p-hydroxymercuribenzoic acid (PHMB) and mersalyl acid inhibited PrP(Sc) amplification in vitro,

5                   Fe-S cluster disruption by mersalyl acid inhibits heme reduction by HPhenH(2), sugg

6 by n-butylmalonate, p-chloromercuribenzoate, mersalyl, and to a lesser extent pyridoxal 5'-phosphate

7 98059 markedly reduced induction of HIF-1 by mersalyl but not by hypoxia.

8  by a channel or a carrier, was inhibited by mersalyl but not by N-ethylmaleimide or sulfobetaine - p

9 f the insulin-like growth factor-1 receptor, mersalyl did not induce HIF-1 activity or VEGF mRNA expr

10 eport here that the organomercurial compound mersalyl induced expression of VEGF and enolase 1 mRNA,

11                  These results indicate that mersalyl induces expression of HIF-1 and a subset of hyp

12                                     However, mersalyl inhibited endogenous EPO mRNA expression induce

13 nduced pore by Pi is seen in the presence of mersalyl, suggesting a second mechanism of action.

14 s selectively disassembled by titration with mersalyl to give E3(apoFeS).

15 m the EPO and VEGF genes was also induced by mersalyl treatment.