p38? and p38d kinases regulate the Toll-like receptor 4 (TLR4)-induced cytokine production by controlling ERK1/2 protein kinase pathway activation.
AuthorsRisco A, del Fresno C, Mambol A, Alsina-Beauchamp D, MacKenzie KF, Yang HT, Barber DF, Morcelle C, Arthur JS, Ley SC, Ardavin C, Cuenda A,
JournalProc Natl Acad Sci U S A
PubMed ID22733747
On the basis mainly of pharmacological experiments, the p38a MAP kinase isoform has been established as an important regulator of immune and inflammatory responses. However, the role of the related p38? and p38d kinases has remained unclear. Here, we show that deletion of p38? and p38d impaired the innate immune ... More
Basic fibroblast growth factor-induced cell death is effected through sustained activation of p38MAPK and up-regulation of the death receptor p75NTR.
AuthorsWilliamson AJ, Dibling BC, Boyne JR, Selby P, Burchill SA,
JournalJ Biol Chem
PubMed ID15310753
'Basic fibroblast growth factor (bFGF) induces cell death in cells of the Ewing''s sarcoma family of tumors in vivo and in vitro. In this study we demonstrate that this is dependent on the rapid and sustained activation of p38(MAPK), in contrast to the transient activation of p38(MAPK) associated with bFGF-induced ... More
BIRB796 inhibits all p38 MAPK isoforms in vitro and in vivo.
AuthorsKuma Y, Sabio G, Bain J, Shpiro N, Márquez R, Cuenda A,
JournalJ Biol Chem
PubMed ID15755732
The compound BIRB796 inhibits the stress-activated protein kinases p38alpha and p38beta and is undergoing clinical trials for the treatment of inflammatory diseases. Here we report that BIRB796 also inhibits the activity and the activation of SAPK3/p38gamma. This occurs at higher concentrations of BIRB796 than those that inhibit p38alpha and p38beta ... More
Overexpression of mitogen-activated protein kinase kinase 6 in the heart improves functional recovery from ischemia in vitro and protects against myocardial infarction in vivo.
AuthorsMartindale JJ, Wall JA, Martinez-Longoria DM, Aryal P, Rockman HA, Guo Y, Bolli R, Glembotski CC,
JournalJ Biol Chem
PubMed ID15492008
The mitogen-activated protein kinases (MAPK) have been the subject of many studies to identify signaling pathways that promote cell survival or death. In cultured cardiac myocytes, p38 MAPK promotes cell survival or death depending on whether it is activated by mitogen-activated protein kinase kinase 6 (MKK6) or MKK3, respectively. The ... More
Cooperation of p38 and extracellular signal-regulated kinase mitogen-activated protein kinase pathways during granulocyte colony-stimulating factor-induced hemopoietic cell proliferation.
AuthorsRausch O, Marshall CJ,
JournalJ Biol Chem
PubMed ID9933603
Hemopoietic cytokines such as interleukin-3 and granulocyte colony-stimulating factor (G-CSF) are potent activators of hemopoietic cell growth and strongly induce activation of extracellular signal-regulated kinase (ERK), c-Jun-N-terminal kinase (JNK), and p38 mitogen-activated protein (MAP) kinases. However, the role of these kinases is unclear. Using specific chemical inhibitors for MEK and ... More
Stress kinase phosphorylation is increased in pacing-induced heart failure in rabbits.
AuthorsSchulz R, Aker S, Belosjorow S, Konietzka I, Rauen U, Heusch G,
JournalAm J Physiol Heart Circ Physiol
PubMed ID12842818
In hearts with chronic left ventricular (LV) systolic dysfunction secondary to hypertension or myocardial infarction, MAPK phosphorylation and/or activity are increased. Whether other settings of LV dysfunction not associated with ischemia-reperfusion are also characterized by increased MAPK phosphorylation or activity is unknown. After 3 wk of rapid LV pacing (400 ... More