In asking what progress might occur in molecular modeling in the next 25 years it is worth asking what progress has been made in the last twenty-five. In doing so it is hard to be optimistic for the future of the field unless a greater commitment is made to basic science.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s10822-011-9520-3 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Aminoguanidine hemisulfate improves mitochondrial autophagy, oxidative stress, and muscle force in Duchenne muscular dystrophy via the AKT/FOXO1 pathway in mdx mice.
Skelet Muscle
January 2025
Department of Anesthesia and Critical Care, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Background: Duchenne muscular dystrophy (DMD) is a prevalent, fatal degenerative muscle disease with no effective treatments. Mdx mouse model of DMD exhibits impaired muscle performance, oxidative stress, and dysfunctional autophagy. Although antioxidant treatments may improve the mdx phenotype, the precise molecular mechanisms remain unclear.
View Article and Find Full Text PDFTargeting deubiquitinase USP7-mediated stabilization of XPO1 contributes to the anti-myeloma effects of selinexor.
J Transl Med
January 2025
Department of Hematology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Background: Targeting exportin1 (XPO1) with Selinexor (SEL) is a promising therapeutic strategy for patients with multiple myeloma (MM). However, intrinsic and acquired drug resistance constitute great challenges. SEL has been reported to promote the degradation of XPO1 protein in tumor cells.
View Article and Find Full Text PDFClinical-grade extracellular vesicles derived from umbilical cord mesenchymal stromal cells: preclinical development and first-in-human intra-articular validation as therapeutics for knee osteoarthritis.
J Nanobiotechnology
January 2025
Laboratorio de Medicina Nano-Regenerativa, Centro de Investigación e Innovación Biomédica (CiiB), Universidad de los Andes, Santiago, Chile.
Osteoarthritis (OA) is a joint disease characterized by articular cartilage degradation. Persistent low-grade inflammation defines OA pathogenesis, with crucial involvement of pro-inflammatory M1-like macrophages. While mesenchymal stromal cells (MSC) and their small extracellular vesicles (sEV) hold promise for OA treatment, achieving consistent clinical-grade sEV products remains a significant challenge.
View Article and Find Full Text PDFYTHDF1-mediated m6A modification of GBP4 promotes M1 macrophage polarization in acute lung injury.
Respir Res
January 2025
Department of Respiratory Intensive Care Unit, First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, P. R. China.
Background: Acute lung injury (ALI) is a severe condition with multifaceted causes, including inflammation and oxidative stress. This research investigates the influence of m6A (N6-methyladenosine) modification on GBP4, a protein pivotal for macrophage polarization, a critical immune response in ALI.
Methods: Utilizing a mouse model to induce ALI, the study analyzed GBP4 expression in alveolar macrophages.
Drug-target binding affinity prediction based on power graph and word2vec.
BMC Med Genomics
January 2025
School of Computer Science and Technology, Wuhan University of Science and Technology, Wuhan, 430065, Hubei, China.
Background: Drug and protein targets affect the physiological functions and metabolic effects of the body through bonding reactions, and accurate prediction of drug-protein target interactions is crucial for drug development. In order to shorten the drug development cycle and reduce costs, machine learning methods are gradually playing an important role in the field of drug-target interactions.
Results: Compared with other methods, regression-based drug target affinity is more representative of the binding ability.
Want 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!