Results 101 to 110 of about 22,016 (234)

Anti‐cancer drugs targeting the NADH‐binding site of VDAC rewire channel electrophysiology and partially suppress cation selectivity

The FEBS Journal, EarlyView.
VA molecules alter VDAC1 gating by increasing anion flow and reducing cation permeability. In cancer cells, which rely on ER‐mitochondria Ca2+ transfer and overexpress VDAC1, this imbalance triggers bioenergetic stress, ROS buildup, and mitochondrial collapse, leading to cell death.
Stefano Conti‐Nibali, Giuseppe Battiato, Salvatore Antonio Maria Cubisino, Cristina Arrigoni, Marco Lolicato, Simona Reina, Vito De Pinto   +6 more
wiley   +1 more source

Maternal and perinatal effects of vaginal delivery after caesarean section

Medicine Science, 2016
We aimed to determine the risk factors of vaginal delivery after caesarean section (VDAC) that may be effective on maternal and neonatal outcomes and compare the pregnancy outcomes of VDAC with the results of the previous caesarean delivery.
Sibel Ozler, Efser Oztas, Basak Gumus Guler, Aykan Yucel, Dilek Uygur   +4 more
doaj   +1 more source

Involvement of VDAC, Bax and ceramides in the efflux of AIF from mitochondria during curcumin-induced apoptosis. [PDF]

PLoS ONE, 2009
BACKGROUND: We previously identified curcumin as a potent inducer of fibroblast apoptosis, which could be used to treat hypertrophic scar formation. Here we investigated the underlying mechanism of this process.
Alwin Scharstuhl, Henricus A M Mutsaers, Sebastiaan W C Pennings, Frans G M Russel, Frank A D T G Wagener   +4 more
doaj   +1 more source

Cardiac-specific Conditional Knockout of the 18-kDa Mitochondrial Translocator Protein Protects from Pressure Overload Induced Heart Failure. [PDF]

, 2018
Heart failure (HF) is characterized by abnormal mitochondrial calcium (Ca2+) handling, energy failure and impaired mitophagy resulting in contractile dysfunction and myocyte death.
Bers, Donald M, Daugherty, Daniel J, Dedkova, Elena N, Deng, Wenbin, Frederich, Bert J, Lu, Xiyuan, Schaefer, Saul, Thai, Phung N   +7 more
core   +2 more sources

To Include Plasmalemmal VDAC/Porin Pays

Journal of Biological Chemistry, 2012
The paper of Teijido et al. (1) will hopefully stimulate closer contacts between structure people and physiologists in the voltage-dependent anion channel (VDAC) community. It refines the VDAC model of Marco Colombini and also refers to the accessibility of the VDAC N-terminal end at mitochondria or the outer surface of the plasmalemma.
openaire   +2 more sources

Calciprotein particle‐induced calcium overload triggers mitochondrial dysfunction in endothelial cells

The Journal of Physiology, EarlyView.
Abstract figure legend Calciprotein particles (CPPs) are small calcium‐ and phosphate‐containing nanoaggregates associated with the development of vascular disease (CVD) in chronic kidney disease (CKD). Previously, we have shown that CPPs induce endothelial cell (EC) dysfunction, possibly contributing to CVD in CKD, but the underlying molecular ...
Lian Feenstra, Laurent Chatre, Benoit Bernay, Julien Pontin, Mirjam F. Mastik, Azuwerus van Buiten, Dalibor Nakládal, Bastiaan S. Star, Jan‐Luuk Hillebrands, Guido Krenning   +9 more
wiley   +1 more source

Control of intestinal stem cell function and proliferation by mitochondrial pyruvate metabolism. [PDF]

, 2017
Most differentiated cells convert glucose to pyruvate in the cytosol through glycolysis, followed by pyruvate oxidation in the mitochondria. These processes are linked by the mitochondrial pyruvate carrier (MPC), which is required for efficient ...
A Ootani, A Ralston, A Roostaee, AG Muntean, Aimee Flores, B Ohlstein, B-Z Chen, C Moolenbeek, C Stringari, C Yang, CA Micchelli, CA Micchelli, Carl S. Thummel, CCP Aires, Christian S. Earl, Claire Bensard, D Dutta, D Karolchik, Dean Y. Li, DK Bricker, Don Delker, Dona R. Wisidagama, E Berger, F Cao, H Jiang, H Li, H Li, H Tateno, Heather R. Christofk, Helong Zhao, I Martínez-Reyes, J Benavides, J Wang, J Wang, James E. Cox, Jared Rutter, Jason Tanner, JC Schell, Jeffrey Mohlman, JL Golob, John C. Schell, JS Wu, K Birsoy, K Ito, K Nishino, K Weber, Kristofor A. Olson, KT Pate, KW McCool, LB Sullivan, Lei Jiang, Lise K. Sorensen, LK Boroughs, LR Edmunds, LR Gray, M Uhlen, M Uhlen, MA Keller, Mary P. Bronner, MB Gerstein, MJ Dailey, MJ Rodríguez-Colman, N Barker, N Buchon, NM Vacanti, O Warburg, PA Vigueira, Peng Wei, Priyanka Kanth, R Camarda, Ralph J. DeBerardinis, RB Flavell, Ren Miao, RW Daniels, S Beyaz, S Herzig, S Simmini, T Bender, T Sato, T Sato, T Sato, T Simsek, T. Cameron Waller, William E. Lowry, X Yin, X-M Wang, Y-Y Fan   +86 more
core   +1 more source

Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia‐reperfusion injury

The Journal of Physiology, EarlyView.
Abstract figure legend Heart attack causes ischaemia–reperfusion injury in cardiomyocytes. Mitochondria generate reactive oxygen species (ROS), leading to oxidative stress. High levels of mitochondrial calcium (Ca2+) activate the mitochondrial permeability transition pore (mPTP), and excess ROS levels can lower the Ca2+ required to activate the mPTP ...
Emily Rozich, Ulas Ozkurede, Shanmugasundaram Pakkiriswami, Ryan Gemilere, Samira M. Azarin, Julia C. Liu   +5 more
wiley   +1 more source

A novel mutation in NDUFB11 unveils a new clinical phenotype associated with lactic acidosis and sideroblastic anemia [PDF]

, 2017
NDUFB11, a component of mitochondrial complex I, is a relatively small integral membrane protein, belonging to the 'supernumerary' group of subunits, but proved to be absolutely essential for the assembly of an active complex I.
Bertini, Enrico, Bianchi, Marzia, Carrozzo, Rosalba, Christodoulou, John, Di Nottia, Michela, Diodato, Daria, Dionisi Vico, Carlo, Francisci, Silvia, Gelmetti, Vania, Guo, Yiran, Lucarelli, Barbarella, Martinelli, Diego, Montanari, Arianna, Niceta, Marcello, Piemonte, Fiorella, Riley, Lisa, Rizza, Teresa, Sorrentino, Francesco, Tartaglia, Marco, Torraco, Alessandra, Valente, Enza Maria, Verrigni, Daniela   +21 more
core   +2 more sources

The mitochondrial‐targeted antioxidant SkQ1 prevents skeletal muscle mitochondrial‐apoptotic but not necroptotic signalling during ovarian cancer

The Journal of Physiology, EarlyView.
Abstract figure legend An evaluation of the degree to which mitochondrial hydrogen peroxide emission (mH2O2)‐mediated apoptotic and necroptotic signalling contributes to skeletal muscle atrophy in an orthotopic epithelial ovarian cancer (EOC) model. To determine whether attenuating mH2O2 could prevent regulated cell death signalling and mitigate muscle
Shahrzad Khajehzadehshoushtar, Luca J. Delfinis, Fasih A. Rahman, Madison C. Garibotti, Shivam Gandhi, Aditya N. Brahmbhatt, Brooke A. Morris, Bianca Garlisi, Sylvia Lauks, Caroline Aitken, Leslie Ogilvie, Zhu‐Xu Zhang, Jeremy A. Simpson, Joe Quadrilatero, Jim Petrik, Christopher G. R. Perry   +15 more
wiley   +1 more source