Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/978-3-540-47783-9_16 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Regulation of autophagy and cellular signaling through non-histone protein methylation.
Int J Biol Macromol
December 2024
Hubei Key Laboratory of Diabetes and Angiopathy, School of Pharmacy, Hubei University of Science and Technology, Xianning 437000, China; School of Basic Medical Sciences, Xianning Medical College, Hubei University of Science and Technology, Xianning 437000, China. Electronic address:
Autophagy is a highly conserved catabolic pathway that is precisely regulated and plays a significant role in maintaining cellular metabolic balance and intracellular homeostasis. Abnormal autophagy is directly linked to the development of various diseases, particularly immune disorders, neurodegenerative conditions, and tumors. The precise regulation of proteins is crucial for proper cellular function, and post-translational modifications (PTMs) are key epigenetic mechanisms in the regulation of numerous biological processes.
View Article and Find Full Text PDFATAD2 and TWIST1 Interaction Promotes MYC Activation in Colorectal Carcinoma.
Biochemistry
December 2024
Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, West Bengal 741246, India.
ATPase family AAA domain-containing protein 2 (ATAD2) is significantly up-regulated in many cancer types and contributes to poor patient outcomes. ATAD2 exhibits a multidomain architecture comprising an N-terminal acidic domain, two AAA+ ATPase domains, a bromodomain, and a C-terminal domain. The AAA+ ATPase domain facilitates protein oligomerization and ATP binding, while the bromodomain recognizes acetylated lysine in histones and nonhistone proteins.
View Article and Find Full Text PDFProgress in Lactate Metabolism and Its Regulation via Small Molecule Drugs.
Molecules
November 2024
School of Pharmacy, Hunan University of Chinese Medicine, Changsha 410208, China.
Lactate, once viewed as a byproduct of glycolysis and a metabolic "waste", is now recognized as an energy-providing substrate and a signaling molecule that modulates cellular functions under pathological conditions. The discovery of histone lactylation in 2019 marked a paradigm shift, with subsequent studies revealing that lactate can undergo lactylation with both histone and non-histone proteins, implicating it in the pathogenesis of various diseases, including cancer, liver fibrosis, sepsis, ischemic stroke, and acute kidney injury. Aberrant lactate metabolism is associated with disease onset, and its levels can predict disease outcomes.
View Article and Find Full Text PDFHit Identification and Functional Validation of Novel Dual Inhibitors of HDAC8 and Tubulin Identified by Combining Docking and Molecular Dynamics Simulations.
Antioxidants (Basel)
November 2024
Department of Health Sciences, University Magna Græcia, 88100 Catanzaro, Italy.
Chromatin organization, which is under the control of histone deacetylases (HDACs), is frequently deregulated in cancer cells. Amongst HDACs, HDAC8 plays an oncogenic role in different neoplasias by acting on both histone and non-histone substrates. Promising anti-cancer strategies have exploited dual-targeting drugs that inhibit both HDAC8 and tubulin.
View Article and Find Full Text PDFLactate and lysine lactylation of histone regulate transcription in cancer.
Heliyon
November 2024
Department of Thoracic Surgery and Institute of Thoracic Oncology, West China Hospital, Frontiers Science Center for Disease-related Molecular Network Sichuan University, Chengdu, 610097, China.
Histone lysine modifications were well-established epigenetic markers, with many types identified and extensively studied. The discovery of histone lysine lactylation had revealed a new form of epigenetic modification. The intensification of this modification was associated with glycolysis and elevated intracellular lactate levels, both of which were closely linked to cellular metabolism.
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!