Results 191 to 200 of about 114,148 (343)

Conversion of Transplanted Mature Hepatocytes into Afp+ Reprogrammed Cells for Liver Regeneration After Injury

open access: yesAdvanced Science, EarlyView.
Donor‐derived tdTomato+ mature hepatocytes were FACS‐isolated and transplanted into Fah−/− host mice. During regeneration, these cells convert into proliferative, unipotent Afp+ rHeps. Their plasticity is governed by a PPARγ/AFP‐dependent metabolic switch, segregating into pro‐proliferative Afplow and pro‐survival Afphigh subpopulations.
Ting Fang   +12 more
wiley   +1 more source

Glutamine‐utilizing transaminases are a metabolic vulnerability of TAZ/YAP‐activated cancer cells

open access: yesEMBO Reports, 2018
Chih-Sheng Yang   +5 more
semanticscholar   +1 more source

Regulation of Branched Chain Amino Acid Transaminase Formation During the Growth of Pseudomonas fluorescens UK-1. [PDF]

open access: bronze, 1972
M. Puukka   +4 more
openalex   +1 more source

Development of an Amine Transaminase-Lipase Cascade for Chiral Amide Synthesis under Flow Conditions

open access: green, 2023
Antía Pintor   +4 more
openalex   +1 more source

Smart Nanoparticles Disrupting Energy Supply through Triple Mechanisms to Kill Tumors via Dual Disruption of Mitochondria and Lysosomes

open access: yesAdvanced Science, EarlyView.
This study introduces a biomimetic nanoplatform (MTCA@C) designed for precise cancer therapy. It targets mitochondria to induce dysfunction through photodynamic activation, while concurrently blocking mitophagy via lysosomal alkalinization. The platform further triggers methuosis, resulting in tumor cell death through vacuolization and energy pathway ...
Xiao Xu   +6 more
wiley   +1 more source

Ibrutinib-Associated Liver Injury in a Patient with Chronic Lymphocytic Leukemia: Clinical Course and Therapeutic Approach. [PDF]

open access: yesHematol Rep
Frolli A   +7 more
europepmc   +1 more source

Integrin β3 Orchestrates Hepatic Steatosis via a Novel CD36‐Dependent Lipid Uptake Complex

open access: yesAdvanced Science, EarlyView.
In MASH, ITGB3 recruits LYN and drives its ubiquitin‐proteasomal degradation via phosphorylation. This relieves DHHC5 inhibition, enabling ITGB3/DHHC5/CD36 complex assembly to enhance CD36 palmitoylation and fatty acid uptake, thereby exacerbating disease. Targeting ITGB3 blocks this pathogenic axis and ameliorates MASH.
Ying Zhang   +13 more
wiley   +1 more source

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