Results 41 to 50 of about 60,467 (293)

Crif1 deficiency reduces adipose OXPHOS capacity and triggers inflammation and insulin resistance in mice. [PDF]

PLoS Genetics, 2013
Impaired mitochondrial oxidative phosphorylation (OXPHOS) has been proposed as an etiological mechanism underlying insulin resistance. However, the initiating organ of OXPHOS dysfunction during the development of systemic insulin resistance has yet to be
Min Jeong Ryu, Soung Jung Kim, Yong Kyung Kim, Min Jeong Choi, Surendar Tadi, Min Hee Lee, Seong Eun Lee, Hyo Kyun Chung, Saet Byel Jung, Hyun-Jin Kim, Young Suk Jo, Koon Soon Kim, Sang-Hee Lee, Jin Man Kim, Gi Ryang Kweon, Ki Cheol Park, Jung Uee Lee, Young Yun Kong, Chul-Ho Lee, Jongkyeong Chung, Minho Shong   +20 more
doaj   +1 more source

In vitro characterization of mitochondrial function and structure in rat and human cells with a deficiency of the NADH:ubiquinone oxidoreductase Ndufc2 subunit [PDF]

, 2017
Ndufc2, a subunit of the NADH:ubiquinone oxidoreductase, plays a key role in the assembly and activity of complex I within the mitochondrial OXPHOS chain. Its deficiency has been shown to be involved in diabetes, cancer and stroke.
1000 Genomes Project Consortium, Andrea Micaloni, Aron M Geurts, Baltan, Baltan, Baltan, Carta, Chin, Cristina Scrofani, De Smaele, Franca Bianchi, Galmozzi, Gershoni, Hackenbrock, Hackenbrock, Igci, Koopman, Leonard, Leone, Maria Rosaria Torrisi, Massimo Volpe, Maurizio Forte, Mimaki, Olsson, Putignani, Raffa, Roberta Coluccia, Rossignol, Rubattu, Rubattu, Sabatino Valente, Salvatore Raffa, Scalettar, Sebastiano Sciarretta, Shi, Smeitink, Speranza Rubattu, Turrens, Willems   +38 more
core   +1 more source

The phasor-FLIM fingerprints reveal shifts from OXPHOS to enhanced glycolysis in Huntington Disease. [PDF]

, 2016
Huntington disease (HD) is an autosomal neurodegenerative disorder caused by the expansion of Polyglutamine (polyQ) in exon 1 of the Huntingtin protein. Glutamine repeats below 36 are considered normal while repeats above 40 lead to HD.
Digman, Michelle A, Marsh, J Lawrence, Sameni, Sara, Syed, Adeela   +3 more
core   +1 more source

The Molecular Mechanisms behind Advanced Breast Cancer Metabolism: Warburg Effect, OXPHOS, and Calcium

Frontiers in Bioscience-Landmark
Altered metabolism represents a fundamental difference between cancer cells and normal cells. Cancer cells have a unique ability to reprogram their metabolism by deviating their reliance from primarily oxidative phosphorylation (OXPHOS) to glycolysis, in
Erna Mitaishvili, Hanna Feinsod, Zachary David, Jessica Shpigel, Chelsea Fernandez, Moira Sauane, Columba de la Parra   +6 more
doaj   +1 more source

Rcf1 and Rcf2, Members of the Hypoxia-induced Gene 1 Protein Family, Are Critical Components of the Mitochondrial Cytochrome bc1-cytochrome Oxidase Supercomplex [PDF]

, 2012
We report that Rcf1 (formerly Aim31), a member of the conserved hypoxia-induced gene 1 (Hig1) protein family, represents a novel component of the yeast cytochrome bc1-cytochrome c oxidase (COX) supercomplex.
Furness, Andrew, Garlich, Joshua, Robb-McGrath, Micaela, Strogolova, Vera, Stuart, Rosemary A.   +4 more
core   +2 more sources

Impaired OXPHOS Complex III in Breast Cancer

PLoS ONE, 2011
We measured the mitochondrial oxidative phosphorylation (mtOXPHOS) activities of all five complexes and determined the activity and gene expression in detail of the Complex III subunits in human breast cancer cell lines and primary tumors. Our analysis revealed dramatic differences in activity of complex III between normal and aggressive metastatic ...
Kjerstin M Owens, Mariola Kulawiec, Mohamad Mokhtar Desouki, Ayyasamy Vanniarajan, Keshav K Singh   +4 more
openaire   +4 more sources

The regulation of OXPHOS by extramitochondrial calcium

Biochimica et Biophysica Acta (BBA) - Bioenergetics, 2010
Despite extensive research, the regulation of mitochondrial function is still not understood completely. Ample evidence shows that cytosolic Ca2+ has a strategic task in co-ordinating the cellular work load and the regeneration of ATP by mitochondria. Currently, the paradigmatic view is that Cacyt2+ taken up by the Ca2+ uniporter activates the matrix ...
Gellerich, Frank N., Gizatullina, Zemfira, Trumbeckaite, Sonata, Nguyen, Huu P., Pallas, Thilo, Arandarcikaite, Odeta, Vielhaber, Stephan, Seppet, Enn, Striggow, Frank   +8 more
openaire   +2 more sources

Class IIa HDACs forced degradation allows resensitization of oxaliplatin‐resistant FBXW7‐mutated colorectal cancer

Molecular Oncology, EarlyView.
HDAC4 is degraded by the E3 ligase FBXW7. In colorectal cancer, FBXW7 mutations prevent HDAC4 degradation, leading to oxaliplatin resistance. Forced degradation of HDAC4 using a PROTAC compound restores drug sensitivity by resetting the super‐enhancer landscape, reprogramming the epigenetic state of FBXW7‐mutated cells to resemble oxaliplatin ...
Vanessa Tolotto, Nicolò Gualandi, Ylenia Cortolezzis, Raffaella Picco, Monica Colitti, Francesca D'Este, Mariachiara Gani, Wayne W. Hancock, Giovanni Terrosu, Cristina Degrassi, Francesca Agostini, Claudio Brancolini, Luigi E. Xodo, Eros Di Giorgio   +13 more
wiley   +1 more source

Regulated mitochondrial DNA replication during oocyte maturation is essential for successful porcine embryonic development. [PDF]

, 2006
Cellular ATP is mainly generated through mitochondrial oxidative phosphorylation, which is dependent on mitochondrial DNA (mtDNA). We have previously demonstrated the importance of oocyte mtDNA for porcine and human fertilization.
Alexander, Jan, Altieri, Andrea, Barregård, Lars, Bignami, Margherita, Brüschweiler, Beat, Ceccatelli, Sandra, Cottrill, Bruce, Dall'Asta, Chiara, Dinovi, Michael, Edler, Lutz, EFSA Panel on Contaminants in the Food Chain (CONTAM), Eriksen, Gunnar Sundstøl, Grasl-Kraupp, Bettina, Hogstrand, Christer, Hoogenboom, Laurentius (Ron), Knutsen, Helle Katrine, Nebbia, Carlo Stefano, Oswald, Isabelle P., Petersen, Annette, Roldán-Torres, Ruth, Rose, Martin, Roudot, Alain-Claude, Schwerdtle, Tanja, Taranu, Ionelia, Vleminckx, Christiane, Vollmer, Günter, Wallace, Heather   +26 more
core   +6 more sources

Exploiting metabolic adaptations to overcome dabrafenib treatment resistance in melanoma cells

Molecular Oncology, EarlyView.
We show that dabrafenib‐resistant melanoma cells undergo mitochondrial remodeling, leading to elevated respiration and ROS production balanced by stronger antioxidant defenses. This altered redox state promotes survival despite mitochondrial damage but renders resistant cells highly vulnerable to ROS‐inducing compounds such as PEITC, highlighting redox
Silvia Eller, Susanne Ebner, Carmen Haselrieder, Julia K. Günther, Astrid Drasche, Sophie Strich, Chiara Volani, Andrea Medici, Aleksandar Nikolajevic, Alex Deltedesco, Johannes E. Sigmund, Michael J. Blumer, Martin Hermann, Johanna Vanacker, Gerald Brandacher, Eduard Stefan, Omar Torres‐Quesada, Jakob Troppmair   +17 more
wiley   +1 more source