Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.neuron.2017.04.028 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
RSPO3 Promotes Proliferation and Self-Renewal of Limbal Epithelial Stem Cells Through a WNT/β-Catenin-Independent Signaling Pathway.
Invest Ophthalmol Vis Sci
January 2025
Department of Ophthalmology, Eye, Ear, Nose, and Throat Hospital of Fudan University, Shanghai, China.
Article Synopsis
- RSPO3 is a specific protein that amplifies the WNT signaling pathway and plays a role in maintaining the function of adult stem cells, particularly limbal epithelial stem cells (LESCs) at the limbus.
- The study found that only RSPO3 is consistently expressed in the human limbus, where it enhances the proliferation and self-renewal of LESCs in a dose-dependent manner, independent of the traditional WNT/β-catenin signaling pathway.
- These findings suggest that RSPO3 could be a potential therapeutic target for improving wound healing in corneal injuries and addressing limbal stem cell deficiencies.
Differential functional role of Orai1 variants in constitutive Ca entry and calcification in luminal breast cancer cells.
J Biol Chem
October 2024
Department of Physiology (Cellular Physiology Research Group), Institute of Molecular Pathology Biomarkers (IMPB), University of Extremadura, Caceres, Spain. Electronic address:
Article Synopsis
- Resting cytosolic Ca concentration is crucial for regulating cellular functions, with luminal breast cancer cells relying on Orai1 and SPCA2 to sustain Ca entry, leading to mammary microcalcifications as a prognostic marker.
- Two isoforms of Orai1 exist, with only the full-length Orai1α capable of supporting SPCA2-mediated Ca entry in Orai1-KO MCF7 cells, indicating its specific importance in these processes.
- The N-terminal 38 amino acids of Orai1α are key for its interaction with SPCA2, and Orai1α's ability to restore microcalcification formation suggests it could be a potential target for preventing complications in luminal breast cancer.
Nucleosomal DNA unwinding pathway through canonical and non-canonical histone disassembly.
Commun Biol
September 2024
Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan.
Article Synopsis
- The study focuses on H2A.B, a unique variant of the H2A histone, which plays important roles in processes like sperm and embryo development as well as cancer formation, pointing to its distinct transcriptional regulation compared to standard H2A.
- Researchers used solid-state nanopores to analyze how DNA unwinds from nucleosomes, discovering that H2A.B requires less voltage to completely unwind DNA and does so more rapidly than canonical H2A nucleosomes.
- The findings highlight that H2A.B facilitates a smoother DNA unwinding process due to quicker disassembly of the histone complex, suggesting a novel method for examining DNA-protein interactions and the dynamics of nucleosomes.
Engineered Cas9 variants bypass Keap1-mediated degradation in human cells and enhance epigenome editing efficiency.
Nucleic Acids Res
October 2024
Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Article Synopsis
- Cas9 is a powerful genome-editing tool used in biomedical research, but its interaction with mammalian cells and regulatory mechanisms is not well understood.
- Researchers identified Keap1 as an E3 ligase in mammals that targets Cas9 and its variants for degradation through a specific signal, impacting their effectiveness.
- By creating Cas9 mutants that avoid Keap1 recognition, the study shows improved gene editing capabilities and less disruption of Keap1's normal function, offering potential for more efficient gene regulation.
Transcriptome analysis of cardiac endothelial cells after myocardial infarction reveals temporal changes and long-term deficits.
Sci Rep
May 2024
Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Endothelial cells (ECs) have essential roles in cardiac tissue repair after myocardial infarction (MI). To establish stage-specific and long-term effects of the ischemic injury on cardiac ECs, we analyzed their transcriptome at landmark time points after MI in mice. We found that early EC response at Day 2 post-MI centered on metabolic changes, acquisition of proinflammatory phenotypes, initiation of the S phase of cell cycle, and activation of stress-response pathways, followed by progression to mitosis (M/G2 phase) and acquisition of proangiogenic and mesenchymal properties during scar formation at Day 7.
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!