|1.||Marshall, Vickie: 1 article (11/2015)|
|2.||Jain, Vaibhav: 1 article (11/2015)|
|3.||Krueger, Brian: 1 article (11/2015)|
|4.||Renne, Rolf: 1 article (11/2015)|
|5.||Choi, Hong Seok: 1 article (11/2015)|
|6.||Kim, Chang Hee: 1 article (11/2015)|
|7.||Whitby, Denise: 1 article (11/2015)|
|8.||Shisler, Joanna L: 1 article (11/2015)|
|9.||Tunca, Berrin: 1 article (07/2014)|
|10.||Bekar, Ahmet: 1 article (07/2014)|
07/01/2014 - "Analysis revealed a significant correlation between miR-455-3p expression and Smad2 protein levels as analyzed by immunohistochemistry in CSC (+) tumors (p = 0.002). "
01/01/2003 - "Smad2 protein was expressed by 99% (95% CI: 96-100%) of tumors. "
08/13/1999 - "Although Smad2 protein is significantly mutated in human cancers, there is no definitive evidence implicating Smad2 as a tumor-suppressor gene. "
01/01/2008 - "By down-regulating Smad2 protein expression, EBNA1 apparently disables TGF-beta signaling, which subsequently decreases transcription of the PTPRK tumor suppressor. "
05/01/2001 - "The ability of the Smad2.P445H to block the nuclear accumulation of wild-type Smad2 protein reveals a new mechanism for loss of sensitivity to the growth-inhibitory functions of TGF-beta in tumor development."
02/01/2007 - "Effect of the different phosphorylated Smad2 protein localizations on the invasive breast carcinoma phenotype."
01/01/2002 - "Expression of the mutant Smad2 protein in a TGFbeta sensitive carcinoma line induces resistance to this growth inhibitory factor and deregulates TGFbeta-responsive gene expression. "
|4.||Lung Neoplasms (Lung Cancer)
08/13/1999 - "Here we show that overexpression of the tumor-derived missense mutation Smad2.D450E, an unphosphorylable form of Smad2 found in colorectal and lung cancers, did not abolish the TGF-beta-mediated growth arrest, suggesting that resistance to the growth-inhibiting effects of TGF-beta exhibited by human tumors cannot be linked to the inactivation of Smad2 protein. "
01/01/2013 - "Given that KFs showed altered dependency on TGF-β for survival and proliferation, A.K-Ex-mediated reduction in Smad2 protein levels significantly inhibited the major characteristics of KFs such as cell growth, migration and collagen synthesis, suggesting that A.K-Ex exhibits possible therapeutic activity on keloids."
|1.||Transforming Growth Factor beta (TGF-beta)
|2.||Growth Differentiation Factor 9
|4.||growth inhibitory factor