• Publications
  • Influence
Mammalian mitogen-activated protein kinase signal transduction pathways activated by stress and inflammation.
TLDR
This review focuses on the biochemical components and regulation of mammalian stress-regulated mitogen-activated protein kinase (MAPK) pathways, and the nuclear factor-kappa B pathway, a second stress signaling paradigm. Expand
The stress-activated protein kinase subfamily of c-Jun kinases
TLDR
The kinase p54s are the principal c-Jun N-terminal kinases activated by cellular stress and tumour necrosis factor (TNF)-α, hence they are designated stress-activated protein kinases, or SAPKs. Expand
Requirement for ceramide-initiated SAPK/JNK signalling in stress-induced apoptosis
TLDR
It is reported that ceramide initiates apoptosis through the SAPK cascade and evidence is provided for a signalling mechanism that integrates cytokine- and stress-activated apoptosis. Expand
Mammalian MAPK signal transduction pathways activated by stress and inflammation: a 10-year update.
TLDR
The molecular components of the mammalian stress-regulated MAPK pathways and their regulation as described thus far are summarized and some of the in vivo functions of these pathways are reviewed. Expand
Phosphorylation of c-jun mediated by MAP kinases
TLDR
Evidence is presented that mitogen-activated protein-serine (MAP) kinases (pp54 and pp42/44) specifically phosphorylate these sites and that their phosphorylation positively regulates the transacting activity of c-jun. Expand
Raf-1 activates MAP kinase-kinase
TLDR
Results indicate that c-Raf-1 is an immediate upstream activator of MAPK-K in vivo, the first physiological substrate of the c-raf-l protooncogene product to be identified. Expand
Activation of stress-activated protein kinase by MEKK1 phosphorylation of its activator SEK1
TLDR
Induction of MEKK does not result in the activation of MAPK, but instead stimulates the stress-activated protein kinases (SAPKs)6–8 which are identical to a Jun amino-terminal kinase9,10 which in turn phosphorylates and activates SAPK. Expand
Sounding the Alarm: Protein Kinase Cascades Activated by Stress and Inflammation*
TLDR
Although architecturally homologous to the Ras/MAPK pathway, the SAPK and p38 pathways are not activated primarily by mitogens but by cellular stresses and inflammatory cytokines, which stimuli result in growth arrest, apoptosis, or activation of immune and reticuloendothelial cells. Expand
Protein kinase cascades activated by stress and inflammatory cytokines
TLDR
Two cascades activated preferentially by the inflammatory cytokines TNF‐α and IL‐1‐β, as well as by a wide variety of cellular stresses such as UV and ionizing radiation, hyperosmolarity, heat stress, oxidative stress, etc, are defined. Expand
Activation of Apoptosis Signal-Regulating Kinase 1 (ASK1) by Tumor Necrosis Factor Receptor-Associated Factor 2 Requires Prior Dissociation of the ASK1 Inhibitor Thioredoxin
TLDR
It is shown that TNF receptor (TNFR) associated factor 2 (TRAF2), an adapter protein that couples TNFRs to the SAPKs and p38s, can activate AsK1 in vivo and can interact in vivo with the amino- and carboxyl-terminal noncatalytic domains of the ASK1 polypeptide. Expand
...
1
2
3
4
5
...