Results 71 to 80 of about 698,916 (379)

Autophagy in cancer and protein conformational disorders

FEBS Letters, EarlyView.
Autophagy plays a crucial role in numerous biological processes, including protein and organelle quality control, development, immunity, and metabolism. Hence, dysregulation or mutations in autophagy‐related genes have been implicated in a wide range of human diseases.
Sergio Attanasio
wiley   +1 more source

Tafazzin Mutation Affecting Cardiolipin Leads to Increased Mitochondrial Superoxide Anions and Mitophagy Inhibition in Barth Syndrome

Cells, 2020
Tafazzin is a phospholipid transacylase that catalyzes the remodeling of cardiolipin, a mitochondrial phospholipid required for oxidative phosphorylation.
Patrice X. Petit, Hector Ardilla-Osorio, Lucile Penalvia, Nathan E. Rainey   +3 more
doaj   +1 more source

The thioredoxin‐like and one glutaredoxin domain are required to rescue the iron‐starvation phenotype of HeLa GLRX3 knock out cells

FEBS Letters, EarlyView.
Glutaredoxin (Grx) 3 proteins contain a thioredoxin domain and one to three class II Grx domains. These proteins play a crucial role in iron homeostasis in eukaryotic cells. In human Grx3, at least one of the two Grx domains, together with the thioredoxin domain, is essential for its function in iron metabolism.
Laura Magdalena Jordt, Manuela Gellert, Finja Zelms, Sander Bekeschus, Christopher Horst Lillig   +4 more
wiley   +1 more source

Isolation and analysis of fractions enriched in WrappER-associated mitochondria from mouse liver

STAR Protocols, 2021
Summary: The endoplasmic reticulum (ER) plays a central role in lipid homeostasis, but the role of individual ER subdomains in lipid biology has not been elucidated.
Nicolò Ilacqua, Irene Anastasia, Luca Pellegrini   +2 more
doaj  

MEGADOCK-Web-Mito: human mitochondrial protein-protein interaction prediction database [PDF]

arXiv, 2021
Mitochondrial diseases are largely caused by dysfunction in mitochondrial proteins. However, annotations of human mitochondrial proteins are scattered across various public databases and individual studies. To facilitate research aimed at elucidating mitochondrial functions, we constructed the MEGADOCK-Web-Mito database as a protein-protein interaction
arxiv  

Apoptosis and Mitochondria

, 2005
Peer ...
Fernández-Checa, José C., García-Ruiz, Carmen   +1 more
openaire   +4 more sources

Inhibition of acyl‐CoA synthetase long‐chain isozymes decreases multiple myeloma cell proliferation and causes mitochondrial dysfunction

Molecular Oncology, EarlyView.
Triacsin C inhibition of the acyl‐CoA synthetase long chain (ACSL) family decreases multiple myeloma cell survival, proliferation, mitochondrial respiration, and membrane potential. Made with Biorender.com. Multiple myeloma (MM) is an incurable cancer of plasma cells with a 5‐year survival rate of 59%.
Connor S. Murphy, Heather Fairfield, Victoria E. DeMambro, Samaa Fadel, Carlos A. Gartner, Michelle Karam, Christian Potts, Princess Rodriguez, Ya‐Wei Qiang, Habib Hamidi, Xiangnan Guan, Calvin P. H. Vary, Michaela R. Reagan   +12 more
wiley   +1 more source

Transfer of mitochondria from astrocytes to neurons after stroke

Nature, 2016
Neurons can release damaged mitochondria and transfer them to astrocytes for disposal and recycling. This ability to exchange mitochondria may represent a potential mode of cell-to-cell signalling in the central nervous system.
K. Hayakawa, E. Esposito, Xiaohua Wang, Y. Terasaki, Yi Liu, Changhong Xing, X. Ji, E. Lo   +7 more
semanticscholar   +1 more source

Decoding SARS-CoV-2 hijacking of host mitochondria in COVID-19 pathogenesis

American Journal of Physiology - Cell Physiology, 2020
Because of the ongoing pandemic around the world, the mechanisms underlying the SARS-CoV-2-induced COVID-19 are subject to intense investigation. Based on available data for the SARS-CoV-1 virus, we suggest how CoV-2 localization of RNA transcripts in ...
Keshav K. Singh, G. Chaubey, J. Chen, P. Suravajhala   +3 more
semanticscholar   +1 more source

Etoposide‐induced cancer cell death: roles of mitochondrial VDAC1 and calpain, and resistance mechanisms

Molecular Oncology, EarlyView.
The complex mode of action of the topoisomerase II inhibitor etoposide in triggering apoptosis involves several mechanisms: overexpression of the mitochondrial protein VDAC1, leading to its oligomerization and formation of a large channel that mediates the release of pro‐apoptotic protein; and overexpression of the apoptosis regulators p53, Bax, and ...
Aditya Karunanithi Nivedita, Varda Shoshan‐Barmatz   +1 more
wiley   +1 more source