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Dr. Shoshanna Zucker

Research Assistant Professor
Cooke 629
phone: (716) 645-2363 ext: 155
email: snzucker@buffalo.edu

Research Summary

My research is focused on the development of a novel 3D model to study melanoma tumor progression. This model will enable the quantification of outward radial growth as compared to invasive vertical growth.  Furthermore, changes in the expression or functionality of different proteins will allow for the identification of specific roles for these proteins in melanoma growth and invasive potential.  We are currently studying the role of gap junction proteins in these processes through the use of dominant negative connexins.  We are also studying changes in chromosome organization during melanoma progression with the ultimate goal of identifying markers associated with tumor metastasis

Selected Publications

• Zucker, S.N., Polusani, S.R., and Nicholson, B.J. "Mechanism of Cx26 induced increased migration of HeLa cells" (in preparation).

• Chandrasekhar, A., Zucker, S.N., and Nicholson, B.J. "Comprehensive mechanism of growth suppression by connexin26 in HeLa cells" (in preparation).

• Beahm, D.L., Oshima, A., Gaietta, G.M., Hand, G.M. Smock, A.E. Zucker, S.N., Toloue, M.M., Chandrasekhar, A., Nicholson, B.J., and  Sosinsky, G.E. (2006) Mutation of a conserved threonine in the third transmembrane helix of alpha- and beta-connexins creates a dominant-negative closed gap junction channel. J Biol Chem.;281(12):7994-8009.

• Chandrasekhar, A., Merritt, M., Huh, S.J., Nicholson, B.J., and Zucker, S.N. (2004) Connexin expression and cell coupling fail to reverse the v-src transformed growth characteristics of a Cx43-/-cell line.  Cell Commun Adhes (2-4):103-19.

• Zucker, S.N. & Nicholson, B.J. (2002) Mutagenic approaches to modifying gap junction phenotype. Curr. Drug Targets.  3(1):  441-453.