Zobrazeno 1 - 10
of 48
pro vyhledávání: '"Pablo M Peixoto"'
Publikováno v:
Frontiers in Oncology, Vol 5 (2015)
Cancer transformation involves reprograming of mitochondrial function to avert cell death mechanisms, monopolize energy metabolism, accelerate mitotic proliferation, and promote metastasis. Mitochondrial ion channels are emerging as promising therape
Externí odkaz:
https://doaj.org/article/5f32fb8dc66e4aeca4660c69262c9bee
Autor:
Jason Karch, Jennifer Q Kwong, Adam R Burr, Michelle A Sargent, John W Elrod, Pablo M Peixoto, Sonia Martinez-Caballero, Hanna Osinska, Emily H-Y Cheng, Jeffrey Robbins, Kathleen W Kinnally, Jeffery D Molkentin
Publikováno v:
eLife, Vol 2 (2013)
A critical event in ischemia-based cell death is the opening of the mitochondrial permeability transition pore (MPTP). However, the molecular identity of the components of the MPTP remains unknown. Here, we determined that the Bcl-2 family members Ba
Externí odkaz:
https://doaj.org/article/05dd5d4356784fc28183de961bc98086
EMC1 Is Required for the Sarcoplasmic Reticulum and Mitochondrial Functions in the Drosophila Muscle
Autor:
Carlos Antonio Couto-Lima, Maiaro Cabral Rosa Machado, Lucas Anhezini, Marcos Túlio Oliveira, Roberto Augusto da Silva Molina, Rodrigo Ribeiro da Silva, Gabriel Sarti Lopes, Vitor Trinca, David Fernando Colón, Pablo M. Peixoto, Nadia Monesi, Luciane Carla Alberici, Ricardo Guelerman P. Ramos, Enilza Maria Espreafico
Publikováno v:
Biomolecules, Vol 14, Iss 10, p 1258 (2024)
EMC1 is part of the endoplasmic reticulum (ER) membrane protein complex, whose functions include the insertion of transmembrane proteins into the ER membrane, ER–mitochondria contact, and lipid exchange. Here, we show that the Drosophila melanogast
Externí odkaz:
https://doaj.org/article/ed6aa207d631414394a42949806293a8
Publikováno v:
Biophysical Journal. 122:95a
Autor:
Irina Stavrovskaya, Erna Mitaishvilli, Bethany Kristi Morin, Aria Walls, Grace Terry, Pablo M. Peixoto
Publikováno v:
Biophysical Journal. 121:508a
Autor:
Jason Karch, Jeffery D. Molkentin, Michael J. Bround, Nadina Latchman, Naohiro Terada, Hadi Khalil, Pablo M. Peixoto, Michelle A. Sargent
Publikováno v:
Science Advances
Genetic deletion of Ant1/2/4 and Ppif in mice inhibits the mitochondrial permeability transition pore.
The mitochondrial permeability transition pore (MPTP) has resisted molecular identification. The original model of the MPTP that proposed the
The mitochondrial permeability transition pore (MPTP) has resisted molecular identification. The original model of the MPTP that proposed the
Publikováno v:
The FASEB Journal. 34:1-1
Autor:
Pablo M. Peixoto, Stephen Madamba, Ludovic Debure, Silvia Fossati, Maria E. Solesio, Mony J. de Leon, Thomas Wisniewski, Evgeny Pavlov
Publikováno v:
Aging Cell
Summary Mounting evidence suggests that mitochondrial dysfunction plays a causal role in the etiology and progression of Alzheimer's disease (AD). We recently showed that the carbonic anhydrase inhibitor (CAI) methazolamide (MTZ) prevents amyloid β
Autor:
Giovanni Manfredi, Federica Valsecchi, Meri Gerges, Csaba Konrad, Gloria M. Palomo, Pablo M. Peixoto, Kirsten Bredvik, John Ravits, Leonard Petrucelli, Anatoly A. Starkov, Hibiki Kawamata
Publikováno v:
Molecular Neurodegeneration, Vol 12, Iss 1, Pp 1-15 (2017)
Molecular Neurodegeneration
Molecular Neurodegeneration
Background Mitochondrial dysfunction has been linked to the pathogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Functional studies of mitochondrial bioenergetics have focused mostly on superoxide dismutas
Publikováno v:
Molecular Basis for Mitochondrial Signaling ISBN: 9783319555379
Mitochondrial biogenesis and function, since the eukaryotic merger millions of years ago to now, relies on protein import channels across its membranes. This chapter reviews the current literature on the import pathways, how they are regulated, and h
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::f231ccb513711aad6e7fa8ce477e7443
https://doi.org/10.1007/978-3-319-55539-3_12
https://doi.org/10.1007/978-3-319-55539-3_12