Publications by authors named "T Uenaka"
Article Synopsis
- * In this study, researchers used mice models with varying levels of TROP2 expression to analyze the effects of a new ADC, TROP2-eribulin, focusing on its distribution and pharmacokinetics in tumor and lung tissues.
- * The findings indicated a higher concentration of released eribulin in tumors with high TROP2 expression and revealed that the uptake of TROP2-eribulin by alveolar macrophages in the lungs is linked to ILD, which could inform safer ADC development.
Article Synopsis
- Impaired glucose metabolism in the brain is a key feature of Alzheimer's disease, with recent studies showing that glial cell metabolism is disrupted.
- Inhibition of the enzyme IDO1, which converts tryptophan into kynurenine, can improve memory function in mouse models of Alzheimer's by restoring how astrocytes (a type of brain cell) metabolize.
- IDO1 inhibition not only enhances glucose metabolism in the brain but also boosts the production of lactate, which is beneficial for neurons, suggesting potential for IDO1 inhibitors, originally designed for cancer, to be used in Alzheimer's treatment.
Background: Several HER2-targeting antibody-drug conjugates (ADC) have gained market approval for the treatment of HER2-expressing metastasis. Promising responses have been reported with the new generation of ADCs in patients who do not respond well to other HER2-targeting therapeutics. However, these ADCs still face challenges of resistance and/or severe adverse effects associated with their particular payload toxins.
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- Impaired glucose metabolism in the brain is a key feature of Alzheimer's disease (AD), affecting the function of astrocytes, which support neurons.
- Inhibiting the enzyme IDO1 restores memory and neuronal function in preclinical models by enhancing astrocytic glucose metabolism and lactate production.
- Targeting IDO1 could offer new therapeutic strategies for AD, as its inhibition improves neuronal health by supporting glucose metabolism in the presence of amyloid and tau pathology.
Stress response pathways detect and alleviate adverse conditions to safeguard cell and tissue homeostasis, yet their prolonged activation induces apoptosis and disrupts organismal health. How stress responses are turned off at the right time and place remains poorly understood. Here we report a ubiquitin-dependent mechanism that silences the cellular response to mitochondrial protein import stress.
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