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A novel high-throughput method for measuring many weak protein-peptide affinities simultaneously reveals how calcineurin, a human phosphatase essential for the immune response, recognizes its peptide substrates.

The progenitor cells that form articular cartilage express a gene for a protein called NFATc1, which stops articular chondrocytes from developing too early in the joint.

miR-335-3p, which targets FOS and inhibits its activation of NFATC1 signaling, is an important regulator for osteoclast function and responsible for the psychological stress-induced osteoporosis.

Gene knockout in cell lines and mice reveal that store-operated calcium entry is synergistically mediated by Orai1 and Orai3 channel proteins in B cells and is important for signaling to the nucleus and metabolic activity in response to antigenic stimulation.

Eugenol has the potential as a novel exercise mimetic, and TRPV1 may represent a promising target for the development of exercise mimetics.

Caffeine modulates the genetic risk for cardiovascular disease through changes in target gene expression, likely due to regulation of transcription factor binding.

Calcium-calcineurin signaling cascade drives the acquisition of both the phenotype of the most self-reactive naive CD4 T cells and their enhanced cell-intrinsic ability to commit into induced regulatory T cells upon activation.

ORAI1 ion channel lipid modification is required for a proper immune synapse formation and T cell activation.

Notch ligands Jag1 and Dll4 and their effector Ephb2 are required in sinus venosus endocardium for primitive coronary vasculature formation and later for arterial differentiation and maturation of coronary endothelium.

T-cell receptor signaling actively regulates gating of the nuclear pore complex (NPC) in T cells by inducing translocation of protein kinase C-θ to the NPC to promote the sumoylation of RanGAP1.