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Articles by Michael Kinter
Interdependent roles of PKM2 in photoreceptors and RPE: implications for retinal degeneration
Abstract Pyruvate kinase M2 (PKM2) functions as both a glycolytic enzyme and a transcriptional co-activator that coordinates metabolism and cell survival. Here, we define the developmental timing, cellular distribution, and physiological role of PKM isoforms in the mouse retina. PKM2 expression begins at postnatal day 2, preceding PKM1, and is highly enriched in photoreceptors, whereas PKM1 predominates in retinal ganglion cells.
Mitochondria directly interact with the nuclear pore complex
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Abstract Mitochondria regulate cellular processes through direct and indirect interactions with other organelles. A well-studied example has been contact with the endoplasmic reticulum at mitochondrial-associated endoplasmic reticulum membranes1, which control pathways including redox and calcium homeostasis2,3. Recent studies have also reported direct mitochondria–nuclear membrane contacts in cancer cells and yeast that promote pro-survival signalling4,5.
By Ivan Menendez-Montes, Consuelo Marin-Vicente, Shibani Mukherjee, Mahmoud Ahmed, Manuel Gomez Verified, Manuel Gómez Verified, Chukwuemeka George Anene-Nzelu, Svenja Koslowski, Ashley D Solmonson, Tara Tassin, Shah Ali, Pedro Pessoa, Abdallah Elnwasany, Nicholas T. Lam, Suwannee Thet, Enrique Gil Calvo, Alisson C. Cardoso, Ana Pereira Verified, Feng Xiao, Ping Wang, Asim Mohamed, Hamed El-feky, Ahmed Elghamry, Gonzalo Gancedo-Alonso, Ching-Cheng Hsu, Aundrea K. Westfall, Ralph J. DeBerardinis, Roger Sik-Yin Foo, Michael Kinter, Steve Pressé, Chao Xing, Luke I. Szweda, Asaithamby Aroumougame, Fátima Sánchez-Cabo, José Antonio Enríquez, Miguel Torres Verified, Jesús Vázquez Verified, Hesham Sadek
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Nature
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Identification of a Key Regulator of Mitochondrial Metabolism, the Lrpprc Protein as a Novel Therapeutic Target in Sdha Overexpressing Ovarian Tumors
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Colonic Dysregulation of Major Metabolic Pathways in Experimental Ulcerative Colitis
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High‐fat diet increases electron transfer flavoprotein synthesis and lipid respiration in skeletal muscle during exercise training in female mice
1 INTRODUCTION High-fat diet (HFD) and exercise are robust stimuli to remodel the skeletal muscle mitochondria. Diets high in fat content have been shown to increase mitochondrial content (i.e., mitochondrial quantity) and respiratory capacity (Hancock et al., 2008; Leckey et al., 2018; Turner et al., 2007) with preferential regulation of fat oxidation.
Functional changes in the neural retina occur in the absence of mitochondrial dysfunction in a rodent model of diabetic retinopathy
Diabetic retinopathy is a neurovascular diabetes complication resulting in vision loss. A wealth of literature reports retinal molecular changes indicative of neural deficits, inflammation, and vascular leakage with chronic diabetes, but the mechanistic causes of disease initiation and progression are unknown. Microvascular mitochondrial DNA (mtDNA) damage leading to mitochondrial dysfunction has been proposed to drive vascular dysfunction in retinopathy.
Regulation of Pyruvate Dehydrogenase Kinase 4 in the Heart Through Degradation by the Lon Protease in Response to Mitochondrial Substrate Availability
Cardiac metabolic inflexibility is driven by robust up-regulation of pyruvate dehydrogenase kinase 4 (PDK4) and phosphorylation-dependent inhibition of pyruvate dehydrogenase (PDH) within a single day of feeding mice a high fat diet. In the current study, we have discovered that PDK4 is a short-lived protein (t1/2 ~1 h) and is specifically degraded by the mitochondrial protease, Lon.
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