Results 81 to 90 of about 3,157,910 (364)
p53 directly regulates the glycosidase FUCA1 to promote chemotherapy-induced cell death [PDF]
, 2016 p53 is a central factor in tumor suppression as exemplified by its frequent loss in human cancer. p53 exerts its tumor suppressive effects in multiple ways, but the ability to invoke the eradication of damaged cells by programmed cell death is considered
Baudot, Alice D. +5 more
core +2 more sources
Social context prevents heat hormetic effects against mutagens during fish development
FEBS Letters, EarlyView.This study shows that sublethal heat stress protects fish embryos against ultraviolet radiation, a concept known as ‘hormesis’. However, chemical stress transmission between fish embryos negates this protective effect. By providing evidence for the mechanistic molecular basis of heat stress hormesis and interindividual stress communication, this study ...
Lauric Feugere +5 more
wiley +1 more source
A non-linear mathematical model of cell turnover, differentiation and tumorigenesis in the intestinal crypt [PDF]
Journal of Theoretical Biology (2007) 244(3):367-377, 2013 We present a development of a model of the relationship between cells in three compartments of the intestinal crypt: stem cells, semi-differentiated cells and fully differentiated cells. Stem and semi-differentiated cells may divide to self-renew, undergo programmed death or progress to semi-differentiated and fully differentiated cells respectively ...
arxiv +1 more source
External and internal triggers of cell death in yeast [PDF]
, 2016 In recent years, yeast was confirmed as a useful eukaryotic model system to decipher the complex mechanisms and networks occurring in higher eukaryotes, particularly in mammalian cells, in physiological as well in pathological conditions.
FALCONE, Claudio, MAZZONI, Cristina
core +2 more sources
FEBS Letters, EarlyView.Spot‐14 and Spot‐14R play distinct roles in regulating metabolism in brown and beige adipocytes. While both influence lipid and glucose pathways, Spot‐14 uniquely controls thermogenic gene expression. This dual regulation balances energy storage and heat production, highlighting potential therapeutic targets for obesity and metabolic disorders. Spot 14
Lidia Itzel Castro‐Rodríguez +3 more
wiley +1 more source
Persistent random walk of cells involving anomalous effects and random death [PDF]
, 2014 The purpose of this paper is to implement a random death process into a persistent random walk model which produces subballistic superdiffusion (L\'{e}vy walk). We develop a Markovian model of cell motility with the extra residence variable $\tau .$ The model involves a switching mechanism for cell velocity with dependence of switching rates on $\tau $.
arxiv +1 more source
Autophosphorylation at serine 166 regulates RIP kinase 1-mediated cell death and inflammation [PDF]
, 2020 Receptor interacting protein kinase 1 (RIPK1) regulates cell death and inflammatory responses downstream of TNFR1 and other receptors, and has been implicated in the pathogenesis of inflammatory and degenerative diseases.
Bertrand, Mathieu +11 more
core +1 more source
Journal of Cell Death, 2019 Although much is known regarding intestinal stem cell (ISC) self-renewal and differentiation, the specific mechanisms used for their elimination is unclear. We recently discovered that the pro-apoptotic protein ARTS, a Septin4 isoform, interacts with X-linked inhibitor of apoptosis (XIAP) in the ISC niche to regulate stem cell survival during ...
Elle Koren, Yaron Fuchs
openaire +2 more sources
FEBS Letters, EarlyView.Heart failure with preserved ejection fraction (HFpEF) accounts for half of the heart failure cases. It is characterised by microvascular dysfunction, associated with reduced pericyte coverage and diminished STAT3 expression in pericytes. Loss of STAT3 impairs pericyte adhesion, promotes senescence, and activates a pro‐fibrotic gene program.
Leah Rebecca Vanicek +15 more
wiley +1 more source
Impact of aging : sporadic, and genetic risk factors on vulnerability to apoptosis in Alzheimer's disease [PDF]
, 2003 The identification of specific genetic (presenilin-1 [PS1] and amyloid precursor protein [APP] mutations) and environmental factors responsible for Alzheimer's disease (AD) has revealed evidence for a shared pathway of neuronal death.
Czech, Christian +11 more
core +1 more source