Recent studies have shown that IκB kinase α (IKKα) plays an important role in human skin cancer and acts as a major regulator for keratinocyte terminal differentiation and proliferation. IKKα deficiency or mutation is associated with human tumor development; thus, overexpression of IKKα could prevent tumor progression. However, findings suggest that IKKα is equally essential for many other epithelial-derived tumors. In the present study, we discussed the role of IKKα as a tumor suppressor in IKKα-mediated epithelial‑derived tumors and its activation pathway, which is different from the traditional NF-κB pathway. The present study provides theoretical basis for understanding the molecular mechanisms involved in IKKα-related tumors.
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http://dx.doi.org/10.3892/or.2015.4229 | DOI Listing |
Mech Dev
August 2011
Department of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
MicroRNAs (miRNAs) play important roles in regulating gene expression during numerous biological/pathological processes. Dicer encodes an RNase III endonuclease that is essential for generating most, if not all, functional miRNAs. In this work, we applied a conditional gene inactivation approach to examine the function of Dicer during neural crest cell (NCC) development.
View Article and Find Full Text PDFDev Biol
January 2006
Institute for Genetic Medicine, Keck School of Medicine, School of Dentistry, University of Southern California, 2250 Alcazar St., IGM240, Los Angeles, 90033, USA.
Previous studies have demonstrated that TGFbeta induces a smooth muscle fate in primary neural crest cells in culture. By crossing a conditional allele of the type II TGFbeta receptor with the neural crest-specific Wnt1cre transgene, we have addressed the in vivo requirement for TGFbeta signaling in smooth muscle specification and differentiation. We find that elimination of the TGFbeta receptor does not alter neural crest cell specification to a smooth muscle fate in the cranial or cardiac domains, and that a smooth muscle fate is not realized by trunk neural crest cells in either control or mutant embryos.
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