Thomas M. DeChiara

TL;DR: Two genes encode ubiquitin ligases that are potential drug targets for the treatment of muscle atrophy, and mice deficient in either MAFbx orMuRF1 were found to be resistant to atrophy.

TL;DR: It is indicated that MuSK responds to a critical nerve-derived signal (agrin), and in turn activates signaling cascades responsible for all aspects of synapse formation, including organization of the postsynaptic membrane, synapse-specific transcription, and presynaptic differentiation.

TL;DR: The results strongly suggest an autocrine role for BDNF in mediating the survival of a subpopulation of adult DRG neurons, which could be rescued by exogenous BDNF or neurotrophin-3, but not by other growth factors.

TL;DR: The development of a high-throughput and largely automated process that uses targeting vectors based on bacterial artificial chromosomes (BACs) that permits genetic alteration with nucleotide precision, is not limited by the size of desired deletions, does not depend on isogenicity or on positive–negative selection, and can precisely replace the gene of interest with a reporter that allows for high-resolution localization of target-gene expression.

TL;DR: It is demonstrated that agrin acts via a receptor complex that includes MuSK as well as a myotube-specific accessory component, which is a receptor tyrosine kinase localized to the motor endplate.