Poster Abstract

Winter 2013 Biomedical Seminar Series

January 18, 2013

Regulation of signal transduction by mono- and deubiquitylation
Dr. Stuart Newfeld, Department of Cellular and Molecular Biosciences
Arizona State University

Brief abstract: Polyubiquitylation of signal transducers leading to degradation is a well-established mechanism for turning off signaling pathways. Monoubiquitylation also turns off signaling but does not lead to protein degradation. Deubiquitylation can reactivate an affected signal transducer restoring pathway function. Cycling of protein mono- and deubiquitylation is a highly efficient "off-on switch" regulating signal transduction pathways.


Relevant references:

Stinchfield, M., Takaesu, N., Quijano, J., Castillo, A., Tiusanen, N., Shimmi, O., Enzo, E., Dupont, S. Piccolo, S. & Newfeld, S.J. (2012) Fat facets deubiquitylation of Medea/Smad4 modulates interpretation of a Dpp morphogen gradient. Development 139:2721-2729

Dupont, S., Inui, M. & Newfeld, S.J. (2012) Regulation of TGF-beta signal transduction by mono- and deubiquitylation of Smads. FEBS Letters 586:1913-1920.

Dupont, S., Mamidi, A., Cordenonsi, M., Montagner, M., Zacchigna, L., Adorno, M., Martello, G., Stinchfield, M., Soligo, S., Morsut, L., Inui, M., Moro, S., Argenton, F., Newfeld, S.J. & Piccolo, S. (2009) FAM/USP9x, a deubiquitinating enzyme essential for TGF-bets signaling, controls Smad4 monoubiquitination. Cell 136:123-135.

Konikoff, C., Wisotzkey, R. & Newfeld, S.J. (2008) Lysine conservation and context in TGF-beta and Wnt signaling suggests new targets and general themes for post-translational modification. J Mol Evol 67:323-333.

Newfeld lab website:

School of Life Sciences website: ASU IMSD

Training Program website:

back to seminars