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Recent advances in our understanding of seven transmembrane receptor signaling show that it is possible to design ligands with "functional selectivity," acting as agonists on certain signaling pathways while antagonizing others.
Specifically, animals deficient in AMPK signaling show a hypersensitivity to starvation conditions, altered activity levels, and differential lipid quantities and distributions.
Drugs that can inhibit the production of VEGF or block its receptor signaling show significant inhibition of tumor growth [ 8- 10].
Our recordings from animals with manipulated hormone levels and hormone signaling show that sexually dimorphic patterns of MeA function in adult mice are estrogen dependent.
Clinical studies in severely obese humans with two different forms of defective leptin signaling show that these observations are relevant to human physiology and pathophysiology.
Thus, αv integrin and TGF-β signaling show extensive interplay and αv integrin may be an effector and mediator of TGF-β signaling responses [ 21, 22].
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Molecular signaling showed abnormalities in cyclin proteins and cell-cycle progression upon Pkd1 knockdown.
Parallel signaling shows cross talk at several points and network branches in many directions.
Several genes that are involved in ABA synthesis, response, metabolism, receptors or signaling showed differential expression.
STAT3 signaling showed only a slight increase in response to treatment with everolimus.
Mice lacking EphA/ephrinA signalling show defects in axonal mapping at the SC and the thalamus.
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