pubmed-article:10430610 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10430610 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:10430610 | lifeskim:mentions | umls-concept:C0587901 | lld:lifeskim |
pubmed-article:10430610 | lifeskim:mentions | umls-concept:C1522496 | lld:lifeskim |
pubmed-article:10430610 | lifeskim:mentions | umls-concept:C0521425 | lld:lifeskim |
pubmed-article:10430610 | lifeskim:mentions | umls-concept:C0242469 | lld:lifeskim |
pubmed-article:10430610 | lifeskim:mentions | umls-concept:C0597298 | lld:lifeskim |
pubmed-article:10430610 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:10430610 | pubmed:dateCreated | 1999-8-17 | lld:pubmed |
pubmed-article:10430610 | pubmed:abstractText | Thyroid hormone receptors (TRs) modulate various physiological functions in many organ systems. The TR alpha and TR beta isoforms are products of 2 distinct genes, and the beta 1 and beta 2 isoforms are splice variants of the same gene. Whereas TR alpha 1 and TR beta 1 are widely expressed, expression of the TR beta 2 isoform is mainly limited to the pituitary, triiodothyronine-responsive TRH neurons, the developing inner ear, and the retina. Mice with targeted disruption of the entire TR beta locus (TR beta-null) exhibit elevated thyroid hormone levels as a result of abnormal central regulation of thyrotropin, and also develop profound hearing loss. To clarify the contribution of the TR beta 2 isoform to the function of the endocrine and auditory systems in vivo, we have generated mice with targeted disruption of the TR beta 2 isoform. TR beta 2-null mice have preserved expression of the TR alpha and TR beta 1 isoforms. They develop a similar degree of central resistance to thyroid hormone as TR beta-null mice, indicating the important role of TR beta 2 in the regulation of the hypothalamic-pituitary-thyroid axis. Growth hormone gene expression is marginally reduced. In contrast, TR beta 2-null mice exhibit no evidence of hearing impairment, indicating that TR beta 1 and TR beta 2 subserve divergent roles in the regulation of auditory function. | lld:pubmed |
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pubmed-article:10430610 | pubmed:language | eng | lld:pubmed |
pubmed-article:10430610 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10430610 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:10430610 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10430610 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:10430610 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10430610 | pubmed:month | Aug | lld:pubmed |
pubmed-article:10430610 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:10430610 | pubmed:author | pubmed-author:LibermanM CMC | lld:pubmed |
pubmed-article:10430610 | pubmed:author | pubmed-author:LowellBB | lld:pubmed |
pubmed-article:10430610 | pubmed:author | pubmed-author:ZakariaMM | lld:pubmed |
pubmed-article:10430610 | pubmed:author | pubmed-author:MoureAA | lld:pubmed |
pubmed-article:10430610 | pubmed:author | pubmed-author:RadovickSS | lld:pubmed |
pubmed-article:10430610 | pubmed:author | pubmed-author:AbelE DED | lld:pubmed |
pubmed-article:10430610 | pubmed:author | pubmed-author:KaulbachHH | lld:pubmed |
pubmed-article:10430610 | pubmed:author | pubmed-author:WondisfordFF | lld:pubmed |
pubmed-article:10430610 | pubmed:author | pubmed-author:BoersM EME | lld:pubmed |
pubmed-article:10430610 | pubmed:author | pubmed-author:Pazos-MouraCC | lld:pubmed |
pubmed-article:10430610 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10430610 | pubmed:volume | 104 | lld:pubmed |
pubmed-article:10430610 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10430610 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10430610 | pubmed:pagination | 291-300 | lld:pubmed |
pubmed-article:10430610 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:10430610 | pubmed:year | 1999 | lld:pubmed |