Mammalian Mitogen-Activated Protein Kinase Signal Transduction Pathways Activated by Stress and Inflammation

Kyriakis, John; Avruch, Joseph

doi:10.1152/physrev.2001.81.2.807

Cited by 3,047 publications

(2,751 citation statements)

References 365 publications

(918 reference statements)

Supporting

Mentioning

2,660

Contrasting

Unclassified

Order By: Relevance

“…Activation of JNK regulates activator protein-1 (AP-1) transcription in response to environmental stress such as UV radiation [48]. Increased AP-1 activity has been implicated in inflammation, metastasis and angiogenesis, and also in the promotion and progression of various types of cancers [49][50][51]. Therefore, higher levels of ERK1/2, JNK and p38 activation may promote skin diseases in obese mice.…”

Section: Discussionmentioning

confidence: 99%

Obesity increases the risk of UV radiation-induced oxidative stress and activation of MAPK and NF-κB signaling

Katiyar

Meeran

2007

Free Radical Biology and Medicine

View full text Add to dashboard Cite

Obesity has been implicated in several diseases including cancer, however, the relationship of obesity and susceptibility to ultraviolet (UV) radiation-caused skin diseases has not been investigated. As UV-induced oxidative stress has been implicated in several skin diseases, we assessed the role of obesity on UVB-induced oxidative stress in genetically obese Lep ob /Lep ob (leptin-deficient) mice. Here, we report that chronic exposure to UVB (120 mJ/cm 2 ) resulted in greater oxidative stress in the skin of obese mice in terms of higher levels of H 2 O 2 and NO production, photo-oxidative damage of lipids and proteins, and greater depletion of antioxidant defense enzymes, like, glutathione, glutathione peroxidase and catalase. As UV-induced oxidative stress mediates activation of MAPK and NF-κB signaling pathways, we determined the effect of UVB on these pathways in obese mice. Exposure of obese mice to UVB resulted in phosphorylation of ERK1/2, JNK and p38 proteins of the MAPK family. Compared to wild-type mice, the obese mice exhibited higher levels of phosphorylation of these proteins, greater activation of NF-κB/p65, and higher levels of circulating proinflammatory cytokines, including TNF-α, IL-1-β and IL-6, on UVB irradiation. Together, our study suggests for the first time that obesity in mice is associated with greater susceptibility to UVBinduced oxidative stress, and therefore may be a risk factor for skin diseases associated with UVBinduced oxidative stress.

show abstract

Section: Discussionmentioning

confidence: 99%

Obesity increases the risk of UV radiation-induced oxidative stress and activation of MAPK and NF-κB signaling

Katiyar

Meeran

2007

Free Radical Biology and Medicine

View full text Add to dashboard Cite

show abstract

“…The role of the ERK1/2 and PI3-K/Akt signaling pathways in controlling apoptosis is well known [reviewed in 39,40], and it has been shown that ERK1/2 or PI3-K/Akt activation can confer resistance to ligands of the TNF superfamily [41,42]. Moreover, it has been reported that cells constitutively expressing HSV-2 R1 exhibit activation of the ERK1/2 signaling pathway [43] and that such activation could be involved in HSV-2 R1 antiapoptotic activity [22].…”

Section: Erk1/2 and Aktmentioning

confidence: 99%

The ribonucleotide reductase R1 subunits of herpes simplex virus types 1 and 2 protect cells against TNFα- and FasL-induced apoptosis by interacting with caspase-8

et al. 2010

View full text Add to dashboard Cite

We previously reported that HSV-2 R1, the R1 subunit (ICP10; UL39) of herpes simplex virus type-2 ribonucleotide reductase, protects cells against apoptosis induced by the death receptor (DR) ligands tumor necrosis factor-alpha-(TNFa) and Fas ligand (FasL) by interrupting DR-mediated signaling at, or upstream of, caspase-8 activation. Further investigation of the molecular mechanism underlying HSV-2 R1 protection showed that extracellularregulated kinase 1/2 (ERK1/2), phosphatidylinositol 3-kinase (PI3-K)/Akt, NF-jB and JNK survival pathways do not play a major role in this antiapoptotic function. Interaction studies revealed that HSV-2 R1 interacted constitutively with caspase-8. The HSV-2 R1 deletion mutant R1(1-834)-GFP and Epstein-Barr virus (EBV) R1, which did not protect against apoptosis induced by DR ligands, did not interact with caspase-8, indicating that interaction is required for protection. HSV-2 R1 impaired caspase-8 activation induced by caspase-8 over-expression, suggesting that interaction between the two proteins prevents caspase-8 dimerization/activation. HSV-2 R1 bound to caspase-8 directly through its prodomain but did not interact with either its caspase domain or Fas-associated death domain protein (FADD). Interaction between HSV-2 R1 and caspase-8 disrupted FADD-caspase-8 binding. We further demonstrated that individually expressed HSV-1 R1 (ICP6) shares, with HSV-2 R1, the ability to bind caspase-8 and to protect cells against DR-induced apoptosis. Finally, as the long-lived Fas protein remained stable during the early period of infection, experiments with the HSV-1 UL39 deletion mutant ICP6D showed that HSV-1 R1 could be essential for the protection of HSV-1-infected cells against FasL.Keywords FasL Á ICP6 Á ICP10 Á Viral inhibitor of apoptosis Á Caspase-8Electronic supplementary material The online version of this article

show abstract

“…Among these are mitogen-activated protein kinases (MAPKs), which represent a central converge point regulating cellular behaviour. The three most-characterized MAPK pathways are the extracellular signal regulated kinases (ERKs), the c-Jun N-terminal kinases (JNKs) and the p38s (Kyriakis and Avruch, 2001;Wang, 2007).…”

Section: Introductionmentioning

confidence: 99%

Distinct regulation of B-type natriuretic peptide transcription by p38 MAPK isoforms

Koivisto

Kaikkonen

Tokola

et al. 2011

Molecular and Cellular Endocrinology

View full text Add to dashboard Cite

Persistent controversy underlies the functional roles of specific p38 MAPK isoforms in cardiac biology and regulation of hypertrophy-associated genes. Here we show that adenoviral gene transfer of p38β but not p38α increased B-type natriuretic peptide (BNP) mRNA levels in vitro as well as atrial natriuretic peptide mRNA levels both in vitro and in vivo. Overexpression of p38α, in turn, augmented the expression fibrosis-related genes connective tissue growth factor, basic fibroblast growth factor and matrix metalloproteinase-9 both in vitro and in vivo. p38β-induced BNP transcription was diminished by mutation of GATA-4 binding site, whereas overexpression of MKK6b, an upstream regulator of p38α and p38β, activated BNP transcription through both GATA-4 and AP-1. Overexpression of MKK3, upstream regulator of p38α, induced BNP transcription independently from AP-1 and GATA-4. These data provide new evidence for diversity in downstream targets and functional roles of p38 pathway kinases in regulation of hypertrophy-associated cardiac genes.

show abstract

Mammalian Mitogen-Activated Protein Kinase Signal Transduction Pathways Activated by Stress and Inflammation

Cited by 3,047 publications

References 365 publications

Obesity increases the risk of UV radiation-induced oxidative stress and activation of MAPK and NF-κB signaling

Obesity increases the risk of UV radiation-induced oxidative stress and activation of MAPK and NF-κB signaling

The ribonucleotide reductase R1 subunits of herpes simplex virus types 1 and 2 protect cells against TNFα- and FasL-induced apoptosis by interacting with caspase-8

Distinct regulation of B-type natriuretic peptide transcription by p38 MAPK isoforms

Contact Info

Product

Resources

About