By Barry D. Nelkin
This publication examines what's identified concerning the molecular biology of a number of endocrine neoplasia, sort 2 (MEN2). Mutations and changes in gene expressions and sign transduction are positioned within the context in their results at the biology of the thyroid and adrenal cells which generate cancers in MEN2. hence, this quantity addresses the ret mutations, the results those mutations could have on sign transduction, and developmental and neurobiological features of the cells affected of MEN2, and offers the elemental researcher - in genetics, sign transduction, mobile transformation, developmental or neurobiology - with a greater knowing of the way the data generated via each one of those fields intercalates in the total biology of MEN2.
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Additional resources for Genetic Mechanisms in Multiple Endocrine Neoplasia Type 2
2. Schuchardt A, Srinivas S, Pachnis V, Constantini F. Isolation and characterization of a chicken homolog of the c-ret proto-oncogene. Oncogene 1994; 10:641-49. 3. Sugaya R, Ishimara S, Hosoya T. A Drosophila homology of hu- 34 Genetic Mechanisms in Multiple Endocrine Neoplasia Type 2 man proto-oncogene ret transiently expressed in embyronic neuronal precursor cells including neuroblasts and CNS cells. Mechanisms of Development 1994; 45:139-45. 4. Mulligan LM, Marsh DJ, Robinson BG et al. Genotype-phenotype correlation in MEN 2: Report of the International RET Mutation Consortium.
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CELLULAR EFFECTS OF RET SIGNALING Specificity of the ret transduction pathway Central to the understanding of signal transduction is the question of specificity of response to stimuli, such as ligand-mediated activation of receptor tyrosines kinases. This question is divided into two parts. First, by what mechanism do different cell types Intracellular Signaling by the ret Tyrosine Kinase 51 respond differently to activation of a specific receptor? Second, how can two receptors, using ostensibly similar signal transduction pathways, induce disparate responses in a single cell?