%0 Journal Article
%T Thyroid hormone receptor actions on transcription in amphibia: The roles of histone modification and chromatin disruption
%A Yun-Bo Shi
%A Kazuo Matsuura
%A Kenta Fujimoto
%A Luan Wen
%A Liezhen Fu
%J Cell & Bioscience
%D 2012
%I BioMed Central
%R 10.1186/2045-3701-2-42
%X Thyroid hormone (T3) affects numerous biological processes in vertebrates and thyroid diseases are arguably the most prevalent group of metabolic disorders in the world [1-3]. In the adult mammals such as humans, T3 deficiency leads to reduced metabolic rate while both hyperthyroidism and hypothyroidism result in abnormal function of diverse organs and tissues [4-6].T3 plays a critical role for vertebrate development. T3 deficiency during human development leads to a number of developmental defects, including the formation of a goiter, i.e., a lump in the neck due to enlarged thyroid gland, and cretinism, which is manifested with severe mental deficiency and short stature [7,8]. Similar requirement for T3 is also observed in other vertebrates. The most dramatic T3-regulated developmental process is anuran metamorphosis, when an aquatic tadpole is transformed into a terrestrial frog, as first demonstrated a century ago [9-11]. This process resembles the postembryonic, or perinatal development in mammals when plasma T3 levels also peak [12].T3 can exert its effects at both the genomic level through nuclear T3 receptors (TRs) and the non-genomic levels. The non-genomic effects of T3 involve the binding of T3 to diverse cellular proteins. Among them include the cell surface integrin ¦ÁV¦Â3, better known as a receptor for the extracellular matrix, and a number of cytosolic proteins, which have additional, often enzymatic functions [13-19]. In addition, while TRs are predominantly localized in the nucleus even in the absence of T3, some are present in the cytoplasm. Interestingly, cytosolic TR¦Â can form a complex with the signaling kinase MAPK, which may be responsible for the rapid activation of MAPK by T3 [19], and unliganded TR¦Â can interact with phosphatidylinosital 3 kinase (PI3K) to activate this signaling pathway [20,21], suggesting that cytoplasmic TR may mediate some non-genomic effect of T3.The genomic action of T3, i.e., transcriptional regulation through TR, is
%K Transcriptional coactivator
%K Corepressor
%K Thyroid hormone receptor
%K Stem cell
%K Apoptosis
%K Metamorphosis
%K Xenopus laevis and tropicalis
%K Histone methylation
%K Histone acetylation
%K Nucleosome removal
%U http://www.cellandbioscience.com/content/2/1/42