The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

RET  -  ret proto-oncogene

Canis lupus familiaris

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of RET


High impact information on RET

  • Furthermore, the RET-transfected MDCK cells described in this report are a promising model for delineating RET signaling pathways in the renal epithelial cell lineage [3].
  • In this report, we have used the MDCK renal epithelial cell line to show that activation of the RET pathway results in increased cell motility, dissociation of cell adhesion, and the migration towards a localized source of GDNF [3].
  • Cellular responses to RET activation include the formation of lamellipodia, filopodia, and reorganization of the actin cytoskeleton [3].
  • In Madin-Darby canine kidney (MDCK) cells, the Janus mutation impairs the glial cell line-derived neurotrophic factor-induced effects of RET on cell migration, differentiation, and survival but simultaneously promotes rapid cell proliferation [1].
  • However, the Y1062F mutation, which abrogates the transforming activity of both activated RET isoforms in NIH3T3 cells, does not abolish scattering and branching morphogenesis of RET51, whereas impairs these biological effects of RET9 [4].

Anatomical context of RET

  • Activated RET induces different biological responses such as morphological transformation, neurite outgrowth, proliferation, cell migration and branching [4].
  • These mutations constitutively activate RET due to aberrant disulfide homodimerization and diminish the level of RET at the plasma membrane [1].
  • AFT and RET were determined using trains of rectangular current pulses (13 single pulses, 2 ms, 200 Hz) applied to the right atrial endocardium via bipolar platinum electrodes during the vulnerable period of atrial excitation, which was determined by scanning of the relative refractory period in steps of 10 ms [2].


  1. Biological effects of the dual phenotypic Janus mutation of ret cosegregating with both multiple endocrine neoplasia type 2 and Hirschsprung's disease. Arighi, E., Popsueva, A., Degl'Innocenti, D., Borrello, M.G., Carniti, C., Perälä, N.M., Pierotti, M.A., Sariola, H. Mol. Endocrinol. (2004) [Pubmed]
  2. Effects of the new vagolytic compound ciclotropium bromide on heart rate and atrial vulnerability. Heuer, H., Frenking, B., Thale, J., Gülker, H., Müller, U.S., Bender, F. Arzneimittel-Forschung. (1986) [Pubmed]
  3. The RET-glial cell-derived neurotrophic factor (GDNF) pathway stimulates migration and chemoattraction of epithelial cells. Tang, M.J., Worley, D., Sanicola, M., Dressler, G.R. J. Cell Biol. (1998) [Pubmed]
  4. Differential requirement of Tyr1062 multidocking site by RET isoforms to promote neural cell scattering and epithelial cell branching. Degl'Innocenti, D., Arighi, E., Popsueva, A., Sangregorio, R., Alberti, L., Rizzetti, M.G., Ferrario, C., Sariola, H., Pierotti, M.A., Borrello, M.G. Oncogene (2004) [Pubmed]
WikiGenes - Universities