Fibroblast growth factor induces dephosphorylation and inactivation of the NPR2 guanylyl cyclase, thus decreasing cyclic GMP production in growth plate chondrocytes and contributing to FGF-dependent decreases in bone growth.
A protein interaction screen revealed desmosomes as a scaffold for the COP9 de-neddylating complex, to promote epidermal differentiation by governing the balance of Nedd8 and Ubiquitin modifications on Epidermal Growth Factor Receptor.
A mechanistic basis is provided for the regulative ability of the mammalian embryo offering a long-sought explanation for coordinating cell behaviors at the population level ensuring robustness in developmental outcome.
The iRhom2 protein, a catalytically inactive relative of rhomboid proteases, controls inflammation and growth factor signalling by acting as an essential multifunctional regulatory subunit of the cell surface shedding protease TACE (ADAM17).
The first reconstitution of an unconventional secretory mechanism uncovered the molecular mechanism by which Fibroblast Growth Factor 2 is secreted from mammalian cells.
Ligand binding to the ectodomain of the insulin-like growth factor receptor destabilises an autoinhibitory inter-subunit interaction, which allows the transmembrane domains to associate and the intracellular regions to autophosphorylate.
Although central nervous system (CNS) regeneration has been considered to be controlled by CNS microenvironment, CNS injury causes leading to leakage of circulating factors into CNS, which promotes CNS regeneration.
Cells package active receptors in endosomes at fairly constant amounts and can determine different cell-fate decisions by regulating the number and lifetime of receptor packages.
