PMID: 15691589,12605597,9733516 These include the ¡Ædesensitization¡Ç of the initial pro-apoptotic signaling pathway (although the mechanisms of this have been little studied), the inhibition of procaspase processing and caspase activity and the expression of anti-apoptotic genes of the Inhibitor of Apoptosis (IAP) family

PMID: 15691589 The active sites of caspase enzymes contain a cysteine residue that is susceptible to S-nitrosylation by NO in the procaspase and active forms of the proteins.

PMID: 15691589 This occurs through a mechanism that involves nitrosylation of the proteasome and of the p50 and p65 subunits at their DNA binding domains; inhibiting their transcriptional activity.

PMID: 15691589 This occurs through a mechanism that involves nitrosylation of the proteasome and of the p50 and p65 subunits at their DNA binding domains; inhibiting their transcriptional activity.

PMID: 15691589,9422508 This potent anti-inflammatory molecule efficiently inhibits IKappaB kinase (IKK) activation, as well as the transcriptional activity of several factors such as NF-KappaB, AP-1 and Stat-1alpha

PMID: 15691589 Moreover, 15-dPGJ2 synergizes with NO by enhancing the synthesis of reactive oxygen species, in particular oxygen superoxide.

PMID: 15691589,11086094,10593878,11175752,12893946,12727142 Superoxide rapidly reacts withNO to produce peroxynitrite, one of the most potent oxidants released by cells, and exhibits both pro-apoptotic and necrotic effects

PMID: 15691589,10669746,12612088,12524534 These nuclear receptors ? respectively activated by fatty acids/prostanoids and oxysterols ? exert an important down-regulatory control on the transcriptional activity of pro-inflammatory genes and on transcription factors such as NF-KappaB, Stat-1alpha, and AP-1

PMID: 15691589,10669746,12612088,12524534 These nuclear receptors ? respectively activated by fatty acids/prostanoids and oxysterols ? exert an important down-regulatory control on the transcriptional activity of pro-inflammatory genes and on transcription factors such as NF-KappaB, Stat-1alpha, and AP-1

PMID: 15691589,10669746,12612088,12524534 These nuclear receptors ? respectively activated by fatty acids/prostanoids and oxysterols ? exert an important down-regulatory control on the transcriptional activity of pro-inflammatory genes and on transcription factors such as NF-KappaB, Stat-1alpha, and AP-1

PMID: 15691589 Figure 3

PMID: 15691589,7528106 For example, moderate NO concentrations inhibit basal apoptosis in B lymphocytes, apoptosis induced by the potent cytokine TGF-beta in hepatocytes, and Fas-dependent apoptosis in several cellular models of inflammation

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589,7528106 For example, moderate NO concentrations inhibit basal apoptosis in B lymphocytes, apoptosis induced by the potent cytokine TGF-beta in hepatocytes, and Fas-dependent apoptosis in several cellular models of inflammation

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589,12605597,9733516 These include the ¡Ædesensitization¡Ç of the initial pro-apoptotic signaling pathway (although the mechanisms of this have been little studied), the inhibition of procaspase processing and caspase activity and the expression of anti-apoptotic genes of the Inhibitor of Apoptosis (IAP) family

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Figure 3

PMID: 15691589 Elevated nitric oxide synthesis after the induced expression of NOS-2 by activated macrophages is one of the main cytostatic, cytotoxic, and pro-apoptotic mechanisms participating in the innate response in many mammals PMID: 15691589 A process that can be demonstrated when NO synthesis is suppressed via treatment of cells with a selective NOS-2 inhibitor such as N-(3-aminomethylbenzyl)acetamidine (1400 W) or l-N6-(1-iminoethyl)lysine (l-NIL).

PMID: 15691589,11129661 The pro-apoptotic activity of NO has been well documented and involves the release of cytochrome c from the mitochondria, increased expression of the tumor suppressor p53 and accumulation and targeting of pro-apoptotic members of the Bcl-2 family, in particular Bax, which is translocated to the mitochondria

PMID: 15691589 In contrast, molecules that release NO in a sustained way, or induction of NOS-2 expression by treatment with lipopolysaccharide (LPS) and IFN- gamma, do not provoke this response

PMID: 15691589 In contrast, molecules that release NO in a sustained way, or induction of NOS-2 expression by treatment with lipopolysaccharide (LPS) and IFN- gamma, do not provoke this response

PMID: 15691589 The active sites of caspase enzymes contain a cysteine residue that is susceptible to S-nitrosylation by NO in the procaspase and active forms of the proteins.