Darrin P. Smith

TL;DR: A degenerate peptide library is used to show that each of nine tyrosine kinases investigated has a unique optimal peptide substrate, and indicates that a point mutation in the RET receptor-type tyosine kinase, which causes multiple endocrine neoplasia type 2B, results in a shift in peptide substrates specificity.

TL;DR: It is shown that glial-cell-line-derived neurotrophic factor (GDNF)7, a distant member of the transforming growth factor(TGF)-β superfamily, signals through the Ret RTK, and that GDNF, in addition to its potential role in the differentiation and survival of central nervous system neurons8–12, has profound effects on kidney organogenesis and the development of the peripheral nervous system.

TL;DR: A missense mutation, resulting in the substitution of a threonine for a methionine at codon 918 in the tyrosine kinase catalytic domain, is reported in the germline of 26 of 28 apparently distinct families with MEN 2B.

TL;DR: A missense mutation in the intracellular tyrosine kinase domain of RET is reported in the germline of a family with FMTC that does not have a cysteine codon mutation, confirming that it is likely to be of pathological significance rather than a rare polymorphism.

TL;DR: Cyclosporin A was given to pigs receiving orthotopic cardiac allografts from donors mismatched at the major locus and median survival is greater than 68 days, with 4 animals still alive.