Results 101 to 110 of about 4,393,966 (332)
An isoform of 14‐3‐3 protein regulates transbilayer lipid movement at the plasma membrane
Loss of 14‐3‐3ζ in CHO cells confers resistance to exogenous phosphatidylserine (PS) and impairs endocytosis‐independent inward flip‐flop of fluorescent PS at the plasma membrane. RNAi‐mediated knockdown reproduces this defect, while no additive effect is seen in ATP11C‐deficient cells.
Akiko Yamaji‐Hasegawa +3 more
wiley +1 more source
Neural mechanisms of social learning in the female mouse [PDF]
Social interactions are often powerful drivers of learning. In female mice, mating creates a long-lasting sensory memory for the pheromones of the stud male that alters neuroendocrine responses to his chemosignals for many weeks.
Abraham +79 more
core +1 more source
GDNF‐RET signaling drives pulmonary neuroendocrine cell hyperplasia and allergic airway inflammation
A neuroimmune interaction centered on the PNEC‐ILC2 axis in an asthma model. PNEC‐derived CGRP activates nearby ILC2s, which then release cytokines, including IL‐5 and IL‐13. These cytokines promote eosinophil and macrophage infiltration. Subsequently, GDNF produced by these cells induces PNEC hyperplasia via the GDNF receptors, RET and GFRα1 ...
Tasuku Kawano +3 more
wiley +1 more source
Critical excitation-inhibition balance in dense neural networks [PDF]
The "edge of chaos" phase transition in artificial neural networks is of renewed interest in light of recent evidence for criticality in brain dynamics. Statistical mechanics traditionally studied this transition with connectivity $k$ as the control parameter and an exactly balanced excitation-inhibition ratio.
Baumgarten, Lorenz, Bornholdt, Stefan
openaire +3 more sources
ERRFI1, a neural crest (NC)‐associated gene, was upregulated in melanoma and negatively correlated with the expression of melanocytic differentiation markers and the susceptibility of melanoma cells toward BRAF inhibitors (BRAFi). Knocking down ERRFI1 significantly increased the sensitivity of melanoma cells to BRAFi.
Nina Wang +8 more
wiley +1 more source
Neural delays shape selectivity to interaural intensity differences in the lateral superior olive [PDF]
Neurons in the lateral superior olive (LSO) respond selectively to interaural intensity differences (IIDs), one of the chief cues used to localize sounds in space.
Grothe, Benedikt +4 more
core +1 more source
Potential therapeutic targeting of BKCa channels in glioblastoma treatment
This review summarizes current insights into the role of BKCa and mitoBKCa channels in glioblastoma biology, their potential classification as oncochannels, and the emerging pharmacological strategies targeting these channels, emphasizing the translational challenges in developing BKCa‐directed therapies for glioblastoma treatment.
Kamila Maliszewska‐Olejniczak +4 more
wiley +1 more source
Existence and Stability of Standing Pulses in Neural Networks : I Existence
We consider the existence of standing pulse solutions of a neural network integro-differential equation. These pulses are bistable with the zero state and may be an analogue for short term memory in the brain.
Aliprantis Charalambos +16 more
core +3 more sources
Exploiting metabolic adaptations to overcome dabrafenib treatment resistance in melanoma cells
We show that dabrafenib‐resistant melanoma cells undergo mitochondrial remodeling, leading to elevated respiration and ROS production balanced by stronger antioxidant defenses. This altered redox state promotes survival despite mitochondrial damage but renders resistant cells highly vulnerable to ROS‐inducing compounds such as PEITC, highlighting redox
Silvia Eller +17 more
wiley +1 more source
Etoposide induces DNA damage, activating p53‐dependent apoptosis via caspase‐3/7, which cleaves PARP1. Dammarenediol II enhances this apoptotic pathway by suppressing O‐GlcNAc transferase activity, further decreasing O‐GlcNAcylation. The reduction in O‐GlcNAc levels boosts p53‐driven apoptosis and influences the Akt/GSK3β/mTOR signaling pathway ...
Jaehoon Lee +8 more
wiley +1 more source

