Journal:

Article Title: How does cAMP/Protein kinase A signaling lead to tumors in the adrenal cortex and other tissues?

doi: 10.1016/j.mce.2010.11.018

Figure Lengend Snippet: Schematic representation of Wnt signaling pathway activation in R1α deficient tumor cells. Wnt signaling enrichment was demonstrated in human and mouse tumors associated with cAMP/PKA activation. Up-regulation of WNT3, WNT3A, WNT7 and WISP2 induces the activation of the β-catenin-dependent signaling (canonical pathway). Binding of Wnt ligands to the frizzled, LRP5, and LRP6 receptors inhibits the degradation of β-catenin cytoplasmic complex and leads to nuclear accumulation of β-catenin. CTNNB1 mutations in adrenal tumors also promote β-catenin stabilization. miR-449 is one of the highest down-regulated microRNAs in PPNAD and regulates WISP2 expression. WNT, Wingless-type MMTV integration site family; DKK, Dickkopf; WISP2, WNT1-inducible signaling pathway protein 2; LRP5, low-density lipoprotein receptor-related protein 5; DVL, Dishevelled; APC, activated protein C; GSK3β, glycogen synthase kinase 3 beta; LEF/TCF, lymphoid enhancer factor/T-cell factor; PKA, protein kinase A; PPNAD, primary pigmented nodular adrenocortical disease.

Article Snippet: Up-regulation of Wnt3, Wnt3a, Wnt7a, Wnt8a and Wnt8b was also identified in bone tumors from Prkar1a +/- Prkaca +/- mice ( Tsang et al., 2010 ).

Techniques: Activation Assay, Binding Assay, Expressing