Non-mammalian models of multiple endocrine neoplasia type 2
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Figure 1
(A, C and D) Targeting a fluorescent probe specifically to the thyroid (thyroglobulin-TdTomato) highlighted the zebrafish follicular cells. Thyroid structure was disrupted by co-targeting human BRAF(V600E). Reproduced, under the terms of the original CC BY licence, from Anelli et al. (2017). Panel B shows a sagittal section of adult thyroid follicles, which are associated with the ventral aorta and gills. Reproduced, with permission, from Bourque & Houvras (2011).
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Figure 2
In contrast to control larval wing epithelia (panels A, C), activating SRC activity via CSK knockdown (B, D) led loss of apical junctions (P120-catenin, green), EMT and basal migration of transformed cells. Red: nuclear-localized RFP. E: schematic of panel D. Panel E reprinted from Developmental Cell, volume 10, Vidal M, Larson DE & Cagan RL, Csk-deficient boundary cells are eliminated from normal Drosophila epithelia by exclusion, migration, and apoptosis, pages 33–44, Copyright (2006), with permission from Elsevier.
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Figure 3
(A) Oncogenic RET isoforms. ICD, intracellular domain. (B) In contrast to controls, cells expressing KIF5B-RET (green) expressed phosphorylated EGFR as they underwent EMT and migrated basally. Bottom panel shows a closeup of invadopodia-like processes expressing phosphorylated EGFR (red) and phosphorylated SRC (not shown). Panel B reproduced, under the terms of the original CC BYNCND licence, from Das & Cagan (2017).
- © 2018 Society for Endocrinology