The Endogenous Ratio of Smad2 and Smad3 Influences the Cytostatic Function of Smad3

• DOI: 10.1091/mbc.e05-01-0054
• Publication Date: 2005-08-11T00:34:15Z
• Authors: Sang Gyun Kim; Hyun-Ah Kim; Hyun-Soon Jong; Jung-Hyun Park; Noe Kyeong Kim; Seung Hwan Hong; Tae-You Kim; Yung-Jue Bang
• Keywords: BETA (programming language); Smad2 Protein

Although Smad2 and Smad3, critical transcriptional mediators of transforming growth factor-beta (TGF-beta) signaling, are supposed to play a role in the TGF-beta cytostatic program, it remains unclear whether delivers signals through both Smads equally or either differentially. Here, we report that rely on Smad3-, but not Smad2-, dependent pathway intensity can be modulated by changing endogenous ratio Smad3 Smad2. Depleting RNA interference sufficiently interfered with actions various TGF-beta-sensitive cell lines, whereas raising relative Smad2, depleting markedly enhanced response. Consistently, activation its activity upon stimulation were facilitated Smad2-depleted cells controls. Most significantly, single event increasing this depletion was sufficient restore action resistant TGF-beta. These findings suggest new important determinant sensitivity signaling.