Experiments

Searchable full-text extractions: founding hypothesis, core claims, experimental setups, key results and statistics — pulled out of each paper as structure. Search a cell line, an assay or an entity (e.g. HUH7) and find every paper that worked with it. This corpus stands on its own: most entries carry no reproduction assessment (yet).

• Heritable ER stress impairs mitochondrial metabolism and maintenance of hematopoietic stem cells after low-dose irradiation.

  PMID 41675062 · PMC12886522 · iScience · 2026 · 8 claims · 8 setups

  Full-text index only

  Proliferating 20 mGy-irradiated HSC exhibit oxidative stress and altered metabolism with increased mitochondrial ROS and mitochondrial Ca2+ overload compared to non-irradiated HSC

  cd45.1 hsc hspc-enriched bone flow carbonylation

• Metabolic Adaptation of CD8⁺ T Cells Limits the Efficacy of Fatty Acid Oxidation Inhibition in Type 1 Diabetes.

  PMID 41800251 · PMC12965062 · International journal of biological sciences · 2026 · 8 claims · 8 setups

  Full-text index only

  TMZ enhances mitochondrial membrane potential and suppresses fatty acid oxidation (FAO) in human T cells

  peripheral endoc-βh5 nod pancreatic mitochondrial extracellular glucose-stimulated

• Purinergic adipocyte-macrophage crosstalk promotes degeneration of thermogenic brown adipose tissue.

  PMID 41261284 · PMC12715258 · EMBO reports · 2025 · 8 claims · 8 setups

  Has reproduction · 78

  Imbalanced sympathetic/thermogenic activation (via UCP1 deficiency or pharmacological futile thermogenesis) causes BAT inflammation, fibrosis and degeneration

  bat wild-type brown histology qrt-pcr norepinephrine

• The ubiquitin ligase KLHL6 drives resistance to CD8(+) T cell dysfunction.

  PMID 41535474 · PMC12979199 · Nature · 2026 · 8 claims · 8 setups

  Full-text index only

  KLHL6 is a dual-negative regulator of both T cell exhaustion and mitochondrial dysfunction

  cd8+ cas9+ sgklhl6-transduced klhl6 bulk pooled flow

• Activation instead of blocking mesolimbic dopaminergic reward circuitry is a preferred modality in the long term treatment of reward deficiency syndrome (RDS): a commentary.

  PMID 19014506 · PMC2615745 · Theoretical biology & medical modelling · 2008 · 8 claims · 6 setups

  Full-text index only

  A biphasic treatment approach—acute DA receptor blocking followed by long-term DA release/activation at the NAc—is needed to treat RDS without inducing abnormal mood or craving.

  kidney alcohol-preferring obese rodents receptor dna-directed meta-analysis