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Northwestern University researchers have identified structural features in engineered cell receptors that correlate with variations in receptor function. Computational protein structure prediction ...
enabling Notch to be specifically activated in AVC and OFT by regional increased shear stress. The strong shear stress altered the membrane lipid microdomain structure of endocardial cells, which ...
Touch receptors are a subtype of sensory neuron ... The vibrissa follicle is a blood-filled encapsulated mechano-transducer, the structure of which has been difficult to resolve.
Weng and his team reveal that out of hundreds of animal species, amphibians, specifically frogs, have the highest number of bitter taste receptors, known as TAS2Rs. While humans have 25 TAS2Rs ...
An interesting form of crosstalk exists between the Notch receptor and the Epidermal Growth Factor Receptor Tyrosine Kinase family, which consists of HER-1, -2, -3, and -4. Overexpression of HER ...
Division of Chemical Biology and Medicinal Chemistry, Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, North Carolina 27599-7365, United States ...
Estrogen is neuroprotective and exerts its functions through estrogen receptors. Loss of estrogen at menopause has been proposed as a risk factor in Alzheimer’s disease (AD) and a contributing factor ...
In this section, we discuss the main components and steps of the Notch signaling cascade. We will avoid excessive details on the molecular structure of the Notch receptor and ligands that are not ...
The Notch signalling pathway plays fundamental roles in diverse developmental processes in metazoans, where it is important in driving cell fate and directing differentiation of various cell types.
Figure 1. Signal transduction mechanism of EGFR (epidermal growth factor receptor) transactivation by angiotensin II (AngII) in vascular smooth muscle cells leading to vascular remodeling. Please note ...
Taken together, all these results suggest that Hes1 functions downstream to Notch signaling for the suppression of AML development in mice.
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