Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

p38 Mitogen activated protein kinases (p38MAPK) are a group of evolutionary conserved protein kinases which are central for cell adaptation to environmental changes as well as for immune response, inflammation, tissue regeneration and tumour formation. The interest in this group of protein kinases has grown continually since their discovery. Recent studies using new genetic and pharmacological tools are providing helpful information on the function of these stress-activated protein kinases and show that they have an acute impact on the development of prevalent diseases related to inflammation, diabetes, neurodegeneration, and cancer. In this Special Issue we present novel advances and review the knowledge on the identification of p38MAPK substrates, functions, and regulation; mechanisms underlying the role of p38MAPK in malignant transformation and other pathologies; and therapeutic opportunities associated with regulation of p38MAPK activity.

arginine methylation --- erythroid differentiation --- MKK3 --- phosphorylation, PRMT1 --- p38 MAPK --- cocaine --- conditioned place preference --- reward --- stress --- anxiety --- depression --- nucleus accumbens --- social interaction --- k opioid receptors --- p38α --- Rab5 --- endosome --- Alzheimer’s --- Lewy Bodies --- amyloid-β --- tau --- α-synuclein --- p38-MAPK α inhibitor --- Alzheimer’s disease --- synaptic plasticity --- neuroinflammation --- β-amyloid --- Tau --- Kv4.2 --- seizure --- temporal lobe epilepsy --- hippocampus --- neuronal firing and excitability --- p38MAPK --- nuclear translocation --- β-like importins --- inflammation --- cancer --- skeletal muscle --- energy metabolism --- signal transduction --- exercise --- type 2 diabetes --- p38 mitogen-activated protein kinase --- bleomycin-induced pulmonary fibrosis --- idiopathic pulmonary fibrosis --- RNA sequencing --- alveolar epithelial type II cells --- MAPK --- p38 --- physiology --- metabolism --- signaling --- hypoxia --- arrhythmia --- MAPK11 --- p38β --- n/a --- Alzheimer's --- Alzheimer's disease

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Mitogen-activated protein kinases (MAPK) are a large family of enzymes that function as signal transducers to regulate a diverse range of physiological responses. However, signaling via extracellular signal-regulated kinase (ERK), c-Jun amino terminal kinase (JNK), and p38 MAPK also underpin many disease processes. This Special Issue provides new insights into how MAPK signaling contributes to specific pathological processes across a range of conditions, including disorders of lung development, type 2 diabetes, proliferative skin diseases, cardiovascular diseases, and neurological diseases.

Research & information: general --- Biology, life sciences --- Rabdosia inflexa --- inflammation --- gastric ulcer --- cytokines --- MAPK --- NF-κB --- extracellular signal-regulated kinases 1/2 --- hyperoxia --- bronchopulmonary dysplasia --- HPAECs --- angiogenesis --- cell cycle --- SIRT1 --- oxidative stress --- psoriasis --- antimicrobial peptide --- cecropin A --- tight junction protein --- MEK/ERK signaling --- porcine intestinal epithelial cell --- extracellular signal-regulated kinase 5 (ERK5) --- Kv4.2 --- PC12 cells --- infantile myofibromatosis --- receptor tyrosine kinases --- platelet-derived growth factor receptor --- protein kinase inhibitors --- sunitinib --- erlotinib --- FR180204 --- U0126 --- targeted therapy --- apoptosis --- ERK1/2 --- JNKs --- mitochondrial dysfunction --- neurodegeneration --- neuro-inflammation --- p38 MAPKs --- Parkinson's disease --- mitogen-activated protein kinases (MAPKs) --- MAPK kinetics --- osteoclast differentiation --- bone remodeling --- DAPK --- ERK --- p38 --- JNK --- mitogen-activated protein kinase pathway (MAPK pathway) --- protein tyrosine phosphatase interacting protein 51 (PTPIP51) --- protein-protein interaction (PPI) --- cancer signaling --- SR --- CR --- Compatibility --- T2DM --- metabolic profiling --- MAPK/PI3K/Akt signaling pathway --- reactive oxygen species --- PTPN6 --- SRC --- DOK4 --- MKK4 --- MKK7 --- p53 --- DUSP1 --- SIRT2 --- atherosclerosis --- aortic valve sclerosis --- aortic valve stenosis --- naphthalimide-metal complex conjugates --- N-heterocyclic carbene --- mitochondria --- ROS --- p38 MAPK --- cancer --- FGF-induced signaling --- FRS2 --- phosphorylation --- downregulation --- Rabdosia inflexa --- inflammation --- gastric ulcer --- cytokines --- MAPK --- NF-κB --- extracellular signal-regulated kinases 1/2 --- hyperoxia --- bronchopulmonary dysplasia --- HPAECs --- angiogenesis --- cell cycle --- SIRT1 --- oxidative stress --- psoriasis --- antimicrobial peptide --- cecropin A --- tight junction protein --- MEK/ERK signaling --- porcine intestinal epithelial cell --- extracellular signal-regulated kinase 5 (ERK5) --- Kv4.2 --- PC12 cells --- infantile myofibromatosis --- receptor tyrosine kinases --- platelet-derived growth factor receptor --- protein kinase inhibitors --- sunitinib --- erlotinib --- FR180204 --- U0126 --- targeted therapy --- apoptosis --- ERK1/2 --- JNKs --- mitochondrial dysfunction --- neurodegeneration --- neuro-inflammation --- p38 MAPKs --- Parkinson's disease --- mitogen-activated protein kinases (MAPKs) --- MAPK kinetics --- osteoclast differentiation --- bone remodeling --- DAPK --- ERK --- p38 --- JNK --- mitogen-activated protein kinase pathway (MAPK pathway) --- protein tyrosine phosphatase interacting protein 51 (PTPIP51) --- protein-protein interaction (PPI) --- cancer signaling --- SR --- CR --- Compatibility --- T2DM --- metabolic profiling --- MAPK/PI3K/Akt signaling pathway --- reactive oxygen species --- PTPN6 --- SRC --- DOK4 --- MKK4 --- MKK7 --- p53 --- DUSP1 --- SIRT2 --- atherosclerosis --- aortic valve sclerosis --- aortic valve stenosis --- naphthalimide-metal complex conjugates --- N-heterocyclic carbene --- mitochondria --- ROS --- p38 MAPK --- cancer --- FGF-induced signaling --- FRS2 --- phosphorylation --- downregulation