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IFNB1 — NOS2
Text-mined interactions from Literome
Diefenbach et al., Science 1999
(Leishmaniasis, Cutaneous) :
Activation of Tyk2 in NK cells by
IFN-alpha/beta also
required NOS2
Yao et al., J Interferon Cytokine Res 2001
:
Regulation by
IFN-beta of inducible
nitric oxide synthase and interleukin-12/p40 in murine macrophages cultured in the presence of Chlamydia pneumoniae antigens
Hua et al., J Neurochem 2002
:
In primary cultures of human astrocytes, we determined the
effects of
IFN-beta on astrocyte cytokine [tumor necrosis factor-alpha ( TNF-alpha ) and interleukin (IL)-6 ] and
inducible nitric oxide synthase (iNOS) expression by ribonuclease protection assay and ELISA ... We found that
IFN-beta inhibited astrocyte
cytokine/iNOS induced by IL-1 plus IFN-gamma, but in the absence of IFN-gamma, IFN-beta enhanced IL-1 induced cytokine/iNOS expression
Utaisincharoen et al., Clin Exp Immunol 2004
(Melioidosis) :
Induction of
iNOS expression and antimicrobial activity by
interferon (IFN)-beta is distinct from IFN-gamma in Burkholderia pseudomallei infected mouse macrophages
Zheng et al., J Biol Chem 2006
(Bone Resorption) :
Thus, RANKL induced
IFN-beta triggers
iNOS/NO as an important negative feedback signal during osteoclastogenesis
Fujihara et al., J Biol Chem 1994
:
The
role of endogenous tumor necrosis factor alpha (TNF-alpha) and
interferon-beta (IFN-beta) in lipopolysaccharide (LPS) induced activation of the
inducible nitric-oxide synthase (i-NOS) gene was investigated ... These data thus suggest that endogenous
IFN-beta , but not TNF-alpha, produced by LPS stimulated J774 cells specifically
contributes , probably in an auto/paracrine fashion, to the activation of the
i-NOS gene expression by LPS
Chen et al., Infect Immun 1996
:
Further, exogenous
IFN-beta potentiated
iNOS mRNA expression in macrophages from young mice
López-Collazo et al., J Immunol 1998
:
Evaluation of the transcriptional activity using run-on assays indicated that
IFN-alpha/beta inhibited the transcription of
iNOS ... These results suggest that in the
presence of
IFN-alpha/beta , the activity of the
iNOS promoter is impaired, and this attenuated nitric oxide synthase expression could be important in pathophysiologic situations in which secretion of type I IFNs occurs