Results 51 to 60 of about 1,037,185 (302)

Age-related increase of oxidative stress-induced apoptosis in mice prevention by Ginkgo biloba extract (EGb761) [PDF]

open access: yes, 2006
Enhanced apoptosis and elevated levels of reactive oxygen species (ROS) play a major role in aging. In addition, several neurodegenerative diseases are associated with increased oxidative stress and apoptosis in neuronal tissue.
Schindowski, Katharina   +4 more
core  

Exposure to the complement C5b-9 complex sensitizes 661W photoreceptor cells to both apoptosis and necroptosis. [PDF]

open access: yes, 2015
The loss of photoreceptors is the defining characteristic of many retinal degenerative diseases, but the mechanisms that regulate photoreceptor cell death are not fully understood.
Dimitrios Stampoulis   +11 more
core   +1 more source

Unique circulating miRNAome signatures captured with distinct molecular states in Lynch syndrome and sporadic colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Circulating microRNA profiles distinguish nonmalignant Lynch syndrome from cancer‐associated Lynch syndrome, sporadic colorectal cancer, and healthy controls. Age‐stratified analysis reveals disease‐specific regulatory states, and a six‐miRNA panel shows concordant separation in an independent colorectal tissue cohort.
Ramadhani Salum Chambuso   +5 more
wiley   +1 more source

A hyperfunctional NCX3-proteolytic fragment generated by Abeta1-42 delays caspase-12 activation and neuronal death in mice [PDF]

open access: yes, 2011
Abeta1-42, the peptide involved in the pathogenesis of Alzheimer’s disease, causes a dysregulation of intracellular Ca2+ homeostasis. However, all the mechanisms involved in this process remain unknown. Here, we reported that A1-42 induced an increase in
D'Avanzo, Carla
core   +1 more source

Methylene Blue Reduces Neuronal Apoptosis and Improves Blood-Brain Barrier Integrity After Traumatic Brain Injury

open access: yesFrontiers in Neurology, 2019
Objective: To investigate whether methylene blue (MB) treatment can reverse neuronal mitochondrial dysfunction caused by oxygen glucose deprivation/reoxygenation (OGD) injury and then investigate whether MB treatment can reduce neuronal apoptosis and ...
Jun Shen   +16 more
doaj   +1 more source

Proneurotrophins, Seizures, and Neuronal Apoptosis [PDF]

open access: yesThe Neuroscientist, 2010
Neurons respond to numerous factors in their environment that influence their survival and function during development and in the mature brain. Among these factors, the neurotrophins have been shown to support neuronal survival and function, acting primarily through the Trk family of receptor tyrosine kinases.
openaire   +2 more sources

Cooperative calcium and zinc signaling underlies oxidant-induced neuronal injury [PDF]

open access: yes, 2013
Intracellular zinc release triggered by oxidative injury leads to cellular K+ efflux and neuronal apoptosis. Low intracellular K+ enables protease and nuclease activation during cell death processes. Our laboratory has demonstrated that the reduction in
McCord, Meghan
core  

The multifaceted roles of lysosomes in cancer

open access: yesMolecular Oncology, EarlyView.
Lysosomes support cancer cell adaptation by integrating macromolecule degradation and nutrient recycling with nutrient sensing, inter‐organelle communication and immune regulation. These interconnected functions can promote tumour growth, stress tolerance and therapy resistance, while also creating context‐dependent vulnerabilities that may be ...
Jia Li, Kevin M. Ryan
wiley   +1 more source

Loss of AMBRA1 activates MAPK and angiogenesis signaling pathways in melanoma cells

open access: yesFEBS Open Bio, EarlyView.
Loss of AMBRA1 in melanoma cells activates multiple oncogenic pathways associated with tumor progression. Transcriptomic and protein network analyses revealed that AMBRA1 depletion enhances MAPK/ERK signaling, angiogenesis, TGF‐β/EMT signaling, and Wnt/axon guidance pathways.
Milad Ibrahim   +4 more
wiley   +1 more source

Mitochondrial Depolarization Is Not Required for Neuronal Apoptosis [PDF]

open access: yesThe Journal of Neuroscience, 1999
Mitochondria are sites of cellular energy production but may also influence life and death decisions by initiating or inhibiting cell death. Mitochondrial depolarization and the subsequent release of pro-apoptotic factors have been suggested to be required for the activation of a cell death program in some forms of neuronal apoptosis.
A J, Krohn, T, Wahlbrink, J H, Prehn
openaire   +2 more sources

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