Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.4103/NRR.NRR-D-24-01220 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Mitochondria-derived vesicles: new players in the game of neurodegeneration.
Neural Regen Res
January 2025
Istituto per la Ricerca e l'Innovazione Biomedica, CNR, Via Ugo La Malfa, Palermo, Italy.
Lipophilicity Modulation of Fluorescent Probes for Imaging of Cellular Microvesicle Dynamics.
J Am Chem Soc
January 2025
School of Chemistry and Chemical Engineering, Institute of Physical Science and Information Technology, Information Materials and Intelligent Sensing Laboratory of Anhui Province, Key Laboratory of Structure and Functional Regulation of Hybrid Materials of Ministry of Education, Anhui University, Hefei, Anhui 230601, China.
Real-time monitoring of dynamic microvesicles (MVs), vesicles associated with living cells, is of great significance in deeply understanding their origin, transport, and function. However, specific labeling MVs poses a challenge due to the lack of unique biomarkers that differentiate them from other cellular compartments. Here, we present a strategy to selectively label MVs by evaluating a series of lipid layer-sensitive cationic indolium-coumarin fluorescent probes (designated as IC-C, with ranging from 1 to 18) that feature varying aliphatic side chains (CH).
View Article and Find Full Text PDFEndogenous interactomes of MFN1 and MFN2 provide novel insights into interorganelle communication and autophagy.
Autophagy
December 2024
Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Baldiri Reixac, Barcelona, Spain.
MFN1 (mitofusin 1) and MFN2 are key players in mitochondrial fusion, endoplasmic reticulum (ER)-mitochondria juxtaposition, and macroautophagy/autophagy. However, the mechanisms by which these proteins participate in these processes are poorly understood. Here, we studied the interactomes of these two proteins by using CRISPR-Cas9 technology to insert an HA-tag at the C terminus of MFN1 and MFN2, and thus generating HeLa cell lines that endogenously expressed MFN1-HA or MFN2-HA.
View Article and Find Full Text PDFHSP90 N-terminal inhibition promotes mitochondria-derived vesicles related metastasis by reducing TFEB transcription via decreased HSP90AA1-HCFC1 interaction in liver cancer.
Autophagy
November 2024
Department of Occupational Health and Occupational Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Cancer cells compensate with increasing mitochondria-derived vesicles (MDVs) to maintain mitochondrial homeostasis, when canonical MAP1LC3B/LC3B (microtubule associated protein 1 light chain 3 beta)-mediated mitophagy is lacking. MDVs promote the transport of mitochondrial components into extracellular vesicles (EVs) and induce tumor metastasis. Although HSP90 (heat shock protein 90) chaperones hundreds of client proteins and its inhibitors suppress tumors, HSP90 inhibitors-related chemotherapy is associated with unexpected metastasis.
View Article and Find Full Text PDFMitochondria break free: Mitochondria-derived vesicles in aging and associated conditions.
Ageing Res Rev
December 2024
Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy; Department of Medicine and Surgery, LUM University, Casamassima, Italy. Electronic address:
Mitophagy is the intracellular recycling system that disposes damaged/inefficient mitochondria and allows biogenesis of new organelles to ensure mitochondrial quality is optimized. Dysfunctional mitophagy has been implicated in human aging and diseases. Multiple evolutionarily selected, redundant mechanisms of mitophagy have been identified, but their specific roles in human health and their potential exploitation as therapeutic targets are unclear.
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!