NO-cGMP signaling pathway

Denninger JW, Marietta MA. Guanylate cyclase and the NO/cGMP signalling pathway. Biochem Biophys Acta 1999 1411 334. 

Another possible way of regulating cADPR levels in cells is via the NO/cGMP signaling pathway (see Section III.E). However, since NO is a potent smooth muscle relaxing agent, it may be considered an unlikely pathway leading to Ca + mobilization in smooth muscle. However, a possible role for a NO/cGMP/... 

Denninger, J.W. and Marietta, M.A. (1999). Guanylate cyclase and the. NO/cGMP signaling pathway. Biochim. Biophys. Acta 1411(2-3), 334—350. 

Role of the Canonical NO/cGMP/cGK Pathway in Retrograde Signalling... 

Another mechanism to increase NO signaling is to enhance the downstream NO signaling pathway. Inhibitors of type 5 phosphodiesterase such as sildenafil result in prolongation of the duration of NO-induced cGMP elevations in a variety of tissues (see Chapter 12). 

Furthermore, the LPS signal transduction involves the activation of G proteins, of phospholipases C and D, the formation of diacyl-glycerol (DG) and inositol triphosphate (IP3). DG mediates the stimulation of protein kinase C (PKC) and IP3 induces an increase of cytosolic Ca++ The LPS signaling pathway also involves tyrosine kinases, constitutive nitric oxide (NO) synthase (cNOS), cGMP-dependent protein kinase, Ca channels, calmodulin and calmodulin kinase [27,28], as well as the MAP kinases [29] ERK1, ERK2 and p38 [23], The intracellular events in response to LPS are due to lipid A because they are inhibited by polymyxin B which is known to bind lipid A [27] and they are reproduced by lipids A [30,31]. 

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