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B. Bellei, E. Flori, E. Izzo, V. Maresca and M. Picardo, “GSK3beta Inhibition Promotes Melanogenesis in Mouse B16 Melanoma Cells and Normal Human Melanocytes,” Cellular Signaling, Vol. 20, No. 10, 2008, pp. 1750-1761. doi:10.1016/j.cellsig.2008.06.001

has been cited by the following article:

• TITLE: Distinct Subcellular Localization of GSK-3β in Melanocytic Nevi: Implications in Melanocyte Senescence

  AUTHORS: Jonathan L. Curry, Carlos A. Torres-Cabala, Carla L. Warneke, Peter Zhang, Victor G. Prieto

  KEYWORDS: GSK-3β; Nevi; Melanoma; Senescence

  JOURNAL NAME: Open Journal of Pathology, Vol.2 No.4, October 31, 2012

  ABSTRACT: Melanocytic nevi are a transient in vivo proliferation of melanocytes that after time undergo cellular senescence. Most nevi harbor B-Raf mutations, which appear to activate cellular mechanisms of senescence in melanocytes. Glycogen synthase kinase 3β (GSK-3β), a critical downstream effector of the AKT signaling pathway, is involved in the development of melanoma and has been associated with senescence in melanocytes. Our immunohistochemical and immunofluorescence studies revealed distinct, perinuclear, dot-like reactivity of GSK-3β in melanocytic nevi. Furthermore, our tissue microarray analysis demonstrated significant perinuclear dot-like sublocalization of GSK-3β in melanocytic nevi compared with the amount of GSK-3β observed in melanoma (P β in human nevi may contribute to senescence in melanocytes.