Mitogen-activated protein kinase (MAPK) signaling pathways are key mediators of eukaryotic transcriptional responses to extracellular signals. These pathways control gene expression in a number of ways including the phosphorylation and regulation of transcription factors, co-regulatory proteins and chromatin proteins. MAPK pathways therefore target multiple components of transcriptional complexes at gene promoters and can regulate DNA binding, protein stability, cellular localization, transactivation or repression, and nucleosome structure. Recent work has uncovered further complexities in the mechanisms by which MAPKs control gene expression including their roles as integral components of transcription factor complexes and their interplay with other post-translational modification pathways. In this review I discuss these advances with particular focus on how MAPK signals are integrated by transcription factor complexes to provide specific transcriptional responses and how this relates to cellular function.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.bbamcr.2006.11.011 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Endothelial CD38-induced endothelial-to-mesenchymal transition is a pivotal driver in pulmonary fibrosis.
Cell Mol Life Sci
December 2024
National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, Nanchang, 330031, China.
Idiopathic pulmonary fibrosis (IPF) is a prevalent interstitial lung disease with high mortality. CD38 is a main enzyme for intracellular nicotinamide adenine dinucleotide (NAD) degradation in mammals. It has been reported that CD38 participated in pulmonary fibrosis through promoting alveolar epithelial cells senescence.
View Article and Find Full Text PDFClinical features and molecular genetics of patients with RASopathies: expanding the phenotype with rare genes and novel variants.
Eur J Pediatr
December 2024
Department of Medical Genetics, Dr. Behçet Uz Children's Hospital, Izmir, Turkey.
Unlabelled: The RASopathies are a group of disorders resulting from a germline variant in the genes encoding the Ras/mitogen-activated protein kinase pathway. These disorders include Noonan syndrome (NS), cardiofaciocutaneous syndrome (CFC), Costello syndrome (CS), Legius syndrome (LS), and neurofibromatosis type 1 (NF1), and have overlapping clinical features due to RAS/MAPK dysfunction. In this study, we aimed to describe the clinical and molecular features of patients exhibiting phenotypic manifestations consistent with RASopathies.
View Article and Find Full Text PDF[PHPS1 enhances PD-L1 serine phosphorylation by regulating ROS/SHP-2/AMPK activity to promote apoptosis of oral squamous cell carcinoma cells].
Nan Fang Yi Ke Da Xue Xue Bao
December 2024
Department of Stomatology, Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, China.
Objectives: To investigate the mechanism of PHPS1 for promoting apoptosis of oral squamous cell carcinoma cells and the role of AMPK in regulating tumor angiogenesis under hypoxic conditions.
Methods: Human oral squamous cell carcinoma Ca9-22 cells cultured in hypoxic conditions (1% O) were inoculated subcutaneously in 16 nude mice, which were divided into control group and PHPS1 group (8) for treatment with 10% DMSO and 10% PHPS1 respectively. Tumor growth in the mice was monitored till 14 days after the treatment, and the xenografts were examined pathologically using HE staining.
Effect of imatinib on lipopolysaccharide‑induced acute lung injury and endothelial dysfunction through the P38 MAPK and NF-κB signaling pathways in vivo and in vitro.
Respir Physiol Neurobiol
December 2024
Department of Emergency Medicine, The Second Hospital of Tianjin Medical University, Tianjin 300211, China. Electronic address:
Background: The primary purpose of this study was to demonstrate the preventive effects of imatinib (IMA) on lipopolysaccharide (LPS)-induced inflammation in a mouse model of acute lung injury (ALI) and human umbilical vascular endothelial cells.
Methods: LPS stimulation for 24h induced ALI and cell inflammation. The pathological results of the lungs were evaluated using the wet/dry weight ratio, pulmonary vascular permeability measurements, and myeloperoxidase immunohistochemistry.
Efficacy of Combined Encorafenib and Binimetinib Treatment for Erdheim-Chester Disease Harboring Concurrent BRAF and KRAS Mutations: A Case Report.
Cancer Rep (Hoboken)
December 2024
Department of Hematology and Clinical Immunology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Background: Erdheim-Chester disease (ECD) is a rare form of non-Langerhans cell histiocytosis with diverse clinical manifestations, often associated with mutations in the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway. BRAF and KRAS mutations, which are driver mutations of oncogenes, participate in the same signaling pathway (MAPK/ERK pathway) and are usually mutually exclusive. We report a case of ECD with concurrent BRAF and KRAS mutations treated using BRAF and MEK inhibitors.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!