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. Author manuscript; available in PMC: 2013 Nov 14.
Published in final edited form as: Exp Biol Med (Maywood). 2009 Aug 5;234(11):10.3181/0811-RM-339. doi: 10.3181/0811-RM-339

Figure 1.

Figure 1

Mechanisms for γ-globin gene activation via NO signaling. Shown is a model of how hydroxyurea (HU) and detanonoate (DE) act as nitric oxide (NO) donors. The level of γ-globin transcription is increased by cyclic guanosine monophosphate (cGMP) signaling triggered by the conversion of guanosine triphosphate (GTP) to cGMP by soluble guanosine cyclase (sGC). Nitric oxide synthase (NOS) inhibitors NG-monomethyl-L-arginine (L-NMMA), NG-nitro-L-arginine methyl ester (L-NAME), and NG-nitro-L-arginine (L-NNA) are shown in gray along with the sGC inhibitor 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one (ODQ).