#OXPHOS
🏗️ Why build respiratory machinery you don't need? #Yeast Bcs1p links complex III assembly to the mitochondrial ATP/ADP ratio, ensuring OXPHOS biogenesis scales with energy demand rather than running at constant levels

🧬 #YeastResearch 🧪 #SGD 🔬
www.yeastgenome.org/reference/S1...
November 2, 2026 at 7:22 PM
Research Spotlight💫: A promising approach to overcome OXPHOS-dependent resistance in AML: doi.org/10.1172/jci....

@gouthamnarla.bsky.social & team report on a PP2A-B56α-based strategy that overcomes treatment resistance in preclinical AML models by targeting cell metabolism. 🧪
@the-asci.org
November 2, 2026 at 1:01 AM
How do #incretin #obesitytherapies/ #GLP1 receptor agonists affect energy metabolism & #mitochondria function? Find out on the Mitoblog featuring Q&A with Nawfal Istfan
@harvardmed.bsky.social on his @obesitysociety.bsky.social publication
mitoworld.org/incretin-bas...
#mitoscientists #IBTs #OXPHOS
Incretin-Based Obesity Therapies - MitoWorld
Incretin-based obesity therapies (IBTs), such as GLP-1 receptor agonists, are very popular and highly effective for weight loss. However, how they affect muscle tissue is unclear. A research team, led...
mitoworld.org
November 3, 2026 at 8:51 PM
CRV Science Labs ⚗️
🧬 Exploring the Out-of-Africa L3-to-M/N Mitogenome Bottleneck: Decoupling D-Loop Hypermutability from OXPHOS Purifying Selection Across 18 Hominin Genomes — Analyzing 298.2 kb across 18 complete hominin mitochondrial…

https://crvscience.com/labs/discoveries/human-ooa-l3-mn-tier1
CRV Science Labs ⚗️ 🧬 Exploring the Out-of-Africa L3-to-M/N Mitogenome Bottleneck: Decoupling D-Loop Hypermutability from OXPHOS Purifying Selection Across 18 Hominin Genomes — Analyzing 298.2 kb across 18 complete hominin mitochondrial genomes (8 functional and structural cohorts) reveals an 11.4-…
crvscience.com
November 5, 2026 at 1:17 AM
Acetylation of NDUFA13 at K7 Senses OXPHOS Dysfunction to Disrupt Prohibitin Scaffolds and Drive Cristae Remodelling in Heart Failure https://www.biorxiv.org/content/10.64898/2026.10.26.761921v1
October 28, 2026 at 1:30 PM
Space-Flown Stem-Cell Organoids May Expose Hidden Drivers of Rare Childhood Diseases
Newswise — Earth-based hiPSC models have transformed disease research but remain limited by cellular immaturity, a strong reliance on glycolysis rather than oxidative phosphorylation (OXPHOS), and incomplete tissue architecture. Animal models often fail to recapitulate human phenotypes, and primary patient tissues are difficult to obtain, especially for rare pediatric conditions. Spaceflight exposes cells to microgravity and space radiation, stress conditions that may unmask or amplify disease-relevant vulnerabilities. Because these stressors converge on mitochondrial and cardiac pathways, they offer a biologically distinct context for studying rare metabolic and congenital disorders. Conventional culture also differs in oxygen tension. Based on these challenges, deeper investigation is needed into how patient-derived human induced pluripotent stem cells (hiPSCs) models respond to the space environment. A review published (DOI: 10.1093/pcmedi/pbag028) in Precision Clinical Medicine in 2026 by researchers affiliated with IRCCS Policlinico San Donato, the University of Milan, and Weill Cornell Medicine, with collaborators from multiple institutions, examines current space-based hiPSC studies and their relevance to mitochondrial diseases and congenital heart disorders (CHDs), and their potential to inform rare pediatric disease research. It summarizes reported effects on mitochondrial function, cytoskeletal organization, oxidative stress, calcium handling, and gene expression, and outlines experimental and mechanistic gaps that must...
www.newswise.com
November 3, 2026 at 3:28 PM
A promising approach to overcome OXPHOS-dependent resistance in AML: doi.org/10.1172/jci....

@gouthamnarla.bsky.social & team report on a PP2A-B56α-based strategy that overcomes treatment resistance in preclinical AML models by targeting cell metabolism.
@the-asci.org
October 27, 2026 at 4:08 PM
Acetylation of NDUFA13 at K7 Senses OXPHOS Dysfunction to Disrupt Prohibitin Scaffolds and Drive Cristae Remodelling in Heart Failure https://www.biorxiv.org/content/10.64898/2026.10.26.761921v1
October 28, 2026 at 1:30 PM
Spaceflight research opens new avenues for studying rare pediatric diseases
Earth-based hiPSC models have transformed disease research but remain limited by cellular immaturity, a strong reliance on glycolysis rather than oxidative phosphorylation (OXPHOS), and incomplete tissue architecture. Animal models often fail to recapitulate human phenotypes, and primary patient tissues are difficult to obtain, especially for rare pediatric conditions. Spaceflight exposes cells to microgravity and space radiation, stress conditions that may unmask or amplify disease-relevant vulnerabilities. Because these stressors converge on mitochondrial and cardiac pathways, they offer a biologically distinct context for studying rare metabolic and congenital disorders. Conventional culture also differs in oxygen tension. Based on these challenges, deeper investigation is needed into how patient-derived human induced pluripotent stem cells (hiPSCs) models respond to the space environment. A review published (DOI: 10.1093/pcmedi/pbag028) in Precision Clinical Medicine in 2026 by researchers affiliated with IRCCS Policlinico San Donato, the University of Milan, and Weill Cornell Medicine, with collaborators from multiple institutions, examines current space-based hiPSC studies and their relevance to mitochondrial diseases and congenital heart disorders (CHDs), and their potential to inform rare pediatric disease research. It summarizes reported effects on mitochondrial function, cytoskeletal organization, oxidative stress, calcium handling, and gene expression, and outlines experimental and mechanistic gaps that must be addressed...
www.news-medical.net
November 3, 2026 at 7:46 PM
Stabilization of the PP2A-B56α complex overcomes venetoclax-azacitidine resistance by impairing OXPHOS in AML: doi.org/10.1172/jci....
JCI Insight - Stabilization of the PP2A-B56α complex overcomes venetoclax-azacitidine resistance by impairing OXPHOS in AML
Research ArticleCell biologyHematology Open Access | 10.1172/jci.insight.205218
buff.ly
October 27, 2026 at 4:08 PM
A preprint using: OxPhos Rodent WB Ant (RRID:AB_2533835) from @thermofishersci.bsky.social was published.

SciScore made a table with this resource, see “Automated Services” module (download as csv, xml or #jats) #reproducibility #methodsmatter
www.biorxiv.org
October 27, 2026 at 12:00 PM
Invitamos a un nuevo Seminario institucional:

«Endo180 media la activación de OXPHOS inducida por el envejecimiento en cáncer de próstata».

Dra. Lucía Pastro, Docente G3 de la Unidad Académica de Genética. Facultad de Medicina, Udelar.

30/10, 11 h
Salón de Actos + Zoom

+info: mec.gub.uy/iibce
October 27, 2026 at 7:03 PM
(J Proteom) Distinct ROS-adaptive and OXPHOS-dependent cellular programs underlie Ewing sarcoma heterogeneity: Publication date: Available online 24 October 2026

Source: Journal of Proteomics

Author(s): Yogalakshmi Sabapathy, Jayavelu Subramani, Gopal Gopisetty #MassSpecRSS
Distinct ROS-adaptive and OXPHOS-dependent cellular programs underlie Ewing sarcoma heterogeneity
Publication date: Available online 24 October 2026 Source: Journal of Proteomics Author(s): Yogalakshmi Sabapathy, Jayavelu Subramani, Gopal Gopisetty
dlvr.it
October 25, 2026 at 2:07 PM
🧬 Excited to share our new study in @JCI_Insight!
We show that stabilizing PP2A-B56α overcome venetoclax–azacitidine resistance in acute myeloid leukemia by targeting mitochondrial metabolism.
Great collaboration with teams in Navarra and the University of Michigan!
insight.jci.org/articles/vie...
JCI Insight - Stabilization of the PP2A-B56α complex overcomes venetoclax-azacitidine resistance by impairing OXPHOS in AML
insight.jci.org
October 23, 2026 at 8:06 PM
TargetMITO is a rule-based model that generates synthetic mitochondrial targeting sequences with tightly controlled design parameters. In yeast, 33 of 50 tested sequences localised to mitochondria, and 42 of 50 rescued a COX4 deletion. Se more 👇
October 25, 2026 at 10:01 AM
Mice carrying the recurrent RMND1 p.(Asn238Ser) variant, the first in vivo model of RMND1 disease, show growth failure, early death and tissue-dependent OXPHOS defects. Heart proteomics revealed metabolic remodelling and altered mitoribosomal proteins.
October 20, 2026 at 6:21 PM
RMND1 is a mitoribosome assembly factor, so tissue-specific OXPHOS loss may just track translation demand. Did the heart proteomics show complex I/V loss proportional to the mitoribosome defect?
October 20, 2026 at 8:02 PM
🔬 Decoding NSCLC: Tumors exploit NDUFS2 (Complex I) for OXPHOS. Inhibiting it sparks a metabolic and energetic crisis & shuts down critical survival signaling (Akt-mTOR). This vital biomarker enables a "double-hit" target therapy. www.nature.com/articles/s41...
Targeting NDUFS2-mediated mitochondrial hyperfunction disrupts energy homeostasis and Akt-mTOR signaling in NSCLC - npj Precision Oncology
npj Precision Oncology - Targeting NDUFS2-mediated mitochondrial hyperfunction disrupts energy homeostasis and Akt-mTOR signaling in NSCLC
www.nature.com
October 19, 2026 at 6:18 PM
🧬New T2D molecular pathway: Muscle insulin resistance stems from Miro1 protein accumulation. Defective mitochondrial AKT-Miro1 interaction drives intramuscular mitochondrial network fragmentation. Targeting this axis restores GLUT4/OXPHOS, boosting glucoregulation www.nature.com/articles/s41...
Miro1 mediates skeletal muscle insulin resistance in type 2 diabetes - Nature Communications
Insulin resistance in skeletal muscle contributes to type 2 diabetes (T2D), but its causes remain unclear. We identify the mitochondrial protein Miro1 as a key regulator of muscle insulin sensiti...
www.nature.com
October 19, 2026 at 11:23 AM
Natascia Ventura, Lena Jentsch, Silvia Maglioni, Caleb Jerred, Tyler O'Hara, Eirini Mytilinaiou, Jimena Ruiz, Yulia Schaumkessel, Laura Schroeter, Jiwon Jung, Nikola Yotov, Johanna Hoffmann, Kai Kremers, Andrea Rossi, Andreas Reichert, Jennifer Watts, Konstantinos Palikaras, Suraiya Haroon, et al.
A novel multisystem approach uncovers conserved mitochondrial complex I disease phenotypes and suppressors
Mitochondriopathies are a large group of pathological conditions characterized by dysfunction of tissues and organs with high energy needs such as the brain, heart, and skeletal muscles, which highly rely on functional mitochondrial oxidative phosphorylation (OXPHOS). The vast majority of these disorders are ascribed to mutations in nuclear or mitochondrial encoded subunits of complex I (CI), the largest OXPHOS complex. In this study, we develop a multisystemic pipeline for CI-associated disease...
www.researchsquare.com
October 14, 2026 at 4:00 PM
PZL-26 targets LONP1 with nanomolar potency and on-target cellular activity, revealing OXPHOS and mitochondrial gene expression as key survival dependencies.
www.life-science-alliance.org/content/9/12...
October 9, 2026 at 3:04 PM
RRIDs were included in this in Nature Structural & Molecular Biology paper. RRIDs improve reproducibility in scientific research. #methodsmatter #OpenScience #STMpublishing
Stress adaptation of mitochondrial protein import by OMA1-mediated degradation of DNAJC15 - Nature Structural & Molecular Biology
Kroczek et al show that degradation of DNAJC15 by OMA1 and AFG3L2 under stress limits mitochondrial protein import and OXPHOS biogenesis. Non-imported proteins lead to the induction of the unfolded protein responses from the endoplasmic reticulum.
doi.org
October 9, 2026 at 7:03 AM
Rod photoreceptors have a dual dependency on both aerobic glycolysis and OXPHOS and diverge metabolically from other retinal neurons
Science Advances
www.science.org/doi/10.1126/...
Rod photoreceptors have a dual dependency on both aerobic glycolysis and OXPHOS and diverge metabolically from other retinal neurons
The retina metabolizes glucose into lactate, a hallmark of aerobic glycolysis known as the Warburg effect. Although evidence points to rod photoreceptors as the primary source of aerobic glycolysis, a...
www.science.org
October 8, 2026 at 7:25 AM
A preclinical #ScienceSignaling analysis of T helper 1 cells shows that shifting their metabolism from glycolysis to oxphos curtails their role in inflammatory bowel disease and identifies a potential therapeutic target for these conditions. https://scim.ag/4yzeCub
Metabolic reprogramming of pathogenic CD4+ T helper cells attenuates inflammatory bowel disease in mice
The kinase GSK3β drives the metabolism supporting the inflammatory function of pathogenic TH1 cells.
scim.ag
October 7, 2026 at 3:00 PM