| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10800606 | Biochimica et Biophysica Acta (BBA) - General Subjects | 2013 | 9 Pages |
Abstract
⺠Mutations of thyroid hormone receptors (TRs) are associated with human cancers. ⺠Loss of TR normal functions by deletion or mutations contributes to cancer development. ⺠Mice harboring a homozygous mutation of TRβ spontaneously develop thyroid cancer. ⺠Nuclear and extra-nuclear actions of a TRβ mutant mediate thyroid carcinogenesis. ⺠Mouse models of thyroid cancer allow uncovering novel molecular targets for treatment.
Keywords
RTHsteroid receptor co-activatorRXRαRetinoid X Receptor αECMPIP3TRSTREsthyroid hormone response elementsPPTgSrc kinasePIP2TSHSMRTPPARγSRCFAKNCOR1mTORPAX8Silencing mediator of retinoid and thyroid hormone receptorsPeroxisome proliferator responsive elementMMPPI3KMAPKPhosphatidylinositol-3,4,5-TriphosphateSKYPPREloss of heterozygosityepithelial mesenchymal transitionβ-cateninTriiodothyronineEMTThyroid cancerbasement membranephosphatase and tensin homologue deleted from chromosome 10Phosphatidylinositol 3-kinasephosphatidylinositol 3 kinasephosphatidylinositol-4,5-biphosphateLOHmatrix metalloproteinaseMouse modelResistance to thyroid hormonemammalian target of rapamycinSrc homologythyroid stimulating hormonemitogen-activated protein kinasePtenfocal adhesion kinaseperoxisome proliferator-activated receptor γ
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Authors
Won Gu Kim, Sheue-yann Cheng,