Results 111 to 120 of about 542,977 (297)

TAp73 promotes anti-senescence-anabolism not proliferation

open access: yes, 2014
TAp73, a member of the p53 family, has been traditionally considered a tumor suppressor gene, but a recent report has claimed that it can promote cellular proliferation.
Maria Valeria Catani (7651889)   +5 more
core   +3 more sources

Autophagy and mitophagy in pancreatic β‐cell homeostasis and their involvement in diabetes pathophysiology

open access: yesFEBS Letters, EarlyView.
This review focuses on the role of autophagy and mitophagy in maintaining pancreatic β‐cell function and homeostasis. We discuss how genetic defects affecting these pathways contribute to the development of type 1, type 2, monogenic, and gestational diabetes. We further explore their potential as therapeutic targets. Created in BioRender.
Yunkyeong Lee   +2 more
wiley   +1 more source

Cellular senescence: from homeostasis to pathological implications and therapeutic strategies

open access: yesFrontiers in Immunology
Cellular aging is a multifactorial and intricately regulated physiological process with profound implications. The interaction between cellular senescence and cancer is complex and multifaceted, senescence can both promote and inhibit tumor progression ...
Chunhong Li   +5 more
doaj   +1 more source

Partial depletion of plasminogen activator inhibitor‐1 decreases subcutaneous fat cell hypertrophy and liver cholesterol in high‐fat‐fed female mice

open access: yesFEBS Letters, EarlyView.
Obesity raises blood levels of PAI‐1, a protein linked to metabolic dysfunction‐associated steatotic liver disease in people with obesity. In female mice fed a high‐fat diet, partially lowering PAI‐1 led to smaller subcutaneous fat cells and lower liver cholesterol, without changing body weight or insulin sensitivity.
Claudia E. Ramirez Bustamante   +10 more
wiley   +1 more source

Emerging experimental and computational methods for studying redox‐regulated structural transitions

open access: yesFEBS Letters, EarlyView.
Redox reactions can reshape proteins and alter how they behave in cells, with important consequences for health and disease. This review explores emerging experimental and computational approaches for discovering these redox‐sensitive protein switches, revealing their structural effects, and predicting their behavior, opening new opportunities to ...
Tasneem Rass   +2 more
wiley   +1 more source

PseudoCell: A Multivalued Logical Regulatory Network to Investigate Premature Senescence Dynamics and Heterogeneity

open access: yesAging Medicine
Purpose Premature cellular senescence is a pivotal process in aging and age‐related diseases, triggered by various stressors. However, this is not a homogeneous phenotype, but a heterogeneous cellular state composed of multiple senescence programs with ...
Vinícius Pierdoná   +6 more
doaj   +1 more source

The Regulation of Cellular Senescence in Cancer

open access: yesBiomolecules
Cellular senescence is a stable state of cell cycle arrest caused by telomere shortening or various stresses. After senescence, cells cease dividing and exhibit many age-related characteristics. Unlike the halted proliferation of senescence cells, cancer
Xianhong Zhang   +6 more
doaj   +1 more source

Translophagy—A potential link between autophagy impairment and translational errors

open access: yesFEBS Letters, EarlyView.
Neurodegenerative diseases are characterised by the accumulation of abnormal proteins and protein aggregates, but their origin often remains unknown. We propose that selective autophagy removes damaged protein‐making machinery, preventing errors during protein synthesis.
Mykola V. Korolchuk   +11 more
wiley   +1 more source

seneR: An R package for comprehensive senescence assessment and its application in type 2 diabetes and osteoarthritis

open access: yesComputational and Structural Biotechnology Journal
Background: Cellular senescence is a key driver of aging and chronic diseases. However, accurately identifying senescent cells is challenging due to limitations of conventional biomarkers and senescence heterogeneity.
Yi Zhang   +6 more
doaj   +1 more source

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