Three Special Issues, so far, have been dedicated to overall MSC prospective biology, from cell regulation to tissue regeneration [...].
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10488037 | PMC |
| http://dx.doi.org/10.3390/ijms241713392 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Universal receptive system as a novel regulator of transcriptomic activity of Staphylococcus aureus.
Microb Cell Fact
January 2025
Human Microbiology Institute, New York, NY, 10014, USA.
Our previous studies revealed the existence of a Universal Receptive System that regulates interactions between cells and their environment. This system is composed of DNA- and RNA-based Teazeled receptors (TezRs) found on the surface of prokaryotic and eukaryotic cells, as well as integrases and recombinases. In the current study, we aimed to provide further insight into the regulatory role of TezR and its loss in Staphylococcus aureus gene transcription.
View Article and Find Full Text PDFYBX1 alleviates ferroptosis in osteoporosis via the ATF4/FSP1 axis in an mC manner.
J Orthop Surg Res
January 2025
Kunshan First People's Hospital Joint Surgery Department, 566 Qianjin East Road, Kunshan City, Suzhou, Jiangsu Province, 215399, China.
Background: Interactions between RNA-binding proteins and RNA regulate RNA transcription during osteoporosis. Ferroptosis, a programmed cell death caused by iron metabolism, plays a vital role in osteoporosis. However, the mechanisms by which RNA-binding proteins are involved in ferroptosis during osteoporosis remain unclear.
View Article and Find Full Text PDFKDM6A facilitates Xist upregulation at the onset of X inactivation.
Biol Sex Differ
January 2025
Department of Laboratory Medicine and Pathology, School of Medicine, University of Washington, Seattle, WA, 98195, USA.
Background: X chromosome inactivation (XCI) is a female-specific process in which one X chromosome is silenced to balance X-linked gene expression between the sexes. XCI is initiated in early development by upregulation of the lncRNA Xist on the future inactive X (Xi). A subset of X-linked genes escape silencing and thus have higher expression in females, suggesting female-specific functions.
View Article and Find Full Text PDFCross-species single-nucleus analysis reveals the potential role of whole-genome duplication in the evolution of maize flower development.
BMC Genomics
January 2025
Peking University Institute of Advanced Agricultural Sciences, Shandong Laboratory of Advanced Agriculture Sciences in Weifang, Weifang, Shandong, 261325, China.
Background: The evolution and development of flowers are biologically essential and of broad interest. Maize and sorghum have similar morphologies and phylogeny while harboring different inflorescence architecture. The difference in flower architecture between these two species is likely due to spatiotemporal gene expression regulation, and they are a good model for researching the evolution of flower development.
View Article and Find Full Text PDFEpigenetic modification regulates the ligamentum flavum hypertrophy through miR-335-3p/SERPINE2/β-catenin signaling pathway.
Cell Mol Biol Lett
January 2025
Department of Orthopaedics, Peking University Third Hospital, Peking University, No.49 NorthGarden Road, Haidian District, Beijing, 100191, Beijing, China.
Background: Epigenetic modifications have been proved to play important roles in the spinal degenerative diseases. As a type of noncoding RNA, the microRNA (miRNA) is a vital class of regulatory factor in the epigenetic modifications, while the role of miRNAs in the regulation of epigenetic modifications in ligamentum flavum hypertrophy (LFH) has not been fully investigated.
Methods: The miRNA sequencing analysis was used to explore the change of miRNA expression during the fibrosis of ligamentum flavum (LF) cells caused by the TGF-β1 (10 ng/ml).
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!