In alcoholised rats, proliferation of satellite cells consistently decreased as well as the number of myonuclei, while phosphorylation of p90RSK became reduced. The mechano-growth factor abministration increased the proliferate activity of the myogenic precursors and restored the myonuclei pool. Phosphorylation of p90RSK increased too.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
RSK1 and RSK2 as therapeutic targets: an up-to-date snapshot of emerging data.
Expert Opin Ther Targets
December 2024
Department of Biomedical Engineering, Vanderbilt University, Nashville, TN, USA.
Introduction: The four members of the p90 ribosomal S6 kinase (RSK) family are serine/threonine protein kinases, which are phosphorylated and activated by ERK1/2. RSK1/2/3 are further phosphorylated by PDK1. Receiving inputs from two major signaling pathways places RSK as a key signaling node in numerous pathologies.
View Article and Find Full Text PDFThe MAPK/ERK signaling pathway involved in Raddeanin A induces apoptosis via the mitochondrial pathway and G2 phase arrest in multiple myeloma.
Sci Rep
November 2024
School of Basic Medicine, Chengdu Medical College, Chengdu, 610500, China.
Article Synopsis
- Multiple myeloma (MM) is a type of blood cancer marked by excessive production of plasma cells that release antibodies, and current research on treatments like Raddeanin A (RA) focuses mainly on solid tumors, leaving a gap in understanding its effects on MM specifically.
- RA, derived from Anemone raddeana regel, shows promising anti-tumor effects, and this study explores how it may inhibit MM cell growth through network pharmacology and experimental methods, revealing significant interactions with the MAPK signaling pathway.
- Experimental results demonstrate that RA effectively slows MM cell proliferation, induces apoptosis, alters mitochondrial function, and impacts the expression of key proteins involved in cell growth and survival, suggesting a powerful potential for RA as a treatment for multiple my
Treatment of a mutant KRAS lung cancer cell line with polyisoprenylated cysteinyl amide inhibitors activates the MAPK pathway, inhibits cell migration and induces apoptosis.
PLoS One
October 2024
Institute of Public Health, Florida A&M University College of Pharmacy Pharmaceutical Sciences, Tallahassee, FL, United States of America.
Article Synopsis
- - KRAS mutations are prevalent in lung adenocarcinoma among Black Americans, leading to the exploration of Polyisoprenylated Cysteinyl amide Inhibitors (PCAIs) as potential therapies to disrupt hyperactive G-protein signaling caused by mutated RAS proteins.
- - Among 17 PCAIs tested, NSL-YHJ-2-27 and NSL-YHJ-2-46 demonstrated significant potency in affecting KRAS-mutated lung cancer cells, with EC50 values of 2.7 μM and 3.3 μM, and notable changes in MAPK pathway enzyme phosphorylation.
- - Treatment with these PCAIs led to decreased levels of key G-proteins linked to cell migration
Punicalagin as a novel selective aryl hydrocarbon receptor (AhR) modulator upregulates AhR expression through the PDK1/p90RSK/AP-1 pathway to promote the anti-inflammatory response and bactericidal activity of macrophages.
Cell Commun Signal
October 2024
State Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Article Synopsis
- * Punicalagin (PUN), an extract from pomegranate peel, was discovered to increase AhR expression and activate its signaling pathways, which play a role in inflammatory macrophages.
- * PUN's effects depended on specific kinase pathways and contributed to reducing inflammation and enhancing macrophage survival against bacterial infections.
Targeting the p90RSK/MDM2/p53 Pathway Is Effective in Blocking Tumors with Oncogenic Up-Regulation of the MAPK Pathway Such as Melanoma and Lung Cancer.
Cells
September 2024
Institute of Endocrinology and Experimental Oncology (IEOS), National Research Council (CNR), Via S. Pansini 5, 80131 Naples, Italy.
In most human tumors, the MAPK pathway is constitutively activated. Since p90RSK is downstream of MAPK, it is often hyperactive and capable of phosphorylating oncogenic substrates. We have previously shown that p90RSK phosphorylates MDM2 at S166, promoting p53 degradation in follicular thyroid carcinomas.
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!