scholarly journals Loss of tyrosine phosphorylation at Y406 abrogates the tumor suppressor functions of the thyroid hormone receptor β

2016 ◽  
Vol 56 (2) ◽  
pp. 489-498 ◽  
Author(s):  
Jeong Won Park ◽  
Li Zhao ◽  
Mark C. Willingham ◽  
Sheue-yann Cheng
Endocrinology ◽  
2010 ◽  
Vol 151 (11) ◽  
pp. 5528-5536 ◽  
Author(s):  
Celine J. Guigon ◽  
Dong Wook Kim ◽  
Xuguang Zhu ◽  
Li Zhao ◽  
Sheue-yann Cheng

2007 ◽  
Vol 192 (1) ◽  
pp. 83-86 ◽  
Author(s):  
Ana Sofia Rocha ◽  
Ricardo Marques ◽  
Inês Bento ◽  
Ricardo Soares ◽  
João Magalhães ◽  
...  

Thyroid cancer constitutes the most frequent endocrine neoplasia. Targeted expression of rearranged during transfection (RET)/papillary thyroid carcinoma (PTC) and V600E V-raf murine sarcoma viral oncogene homolog B1 (BRAF) to the thyroid glands of transgenic mice results in tumours similar to those of human PTC, providing evidence for the involvement of these oncogenes in PTC. Kato et al. developed a mouse model that mimics the full spectrum of the human follicular form of thyroid cancer (FTC). FTC rapidly develops in these mice through introduction of the thyroid hormone receptor β (THRB)PV mutant on the background of the inactivated THRB wt locus. Our aim was to verify if, in the context of human follicular thyroid carcinogenesis, THRB acted as a tumour suppressor gene. We screened for mutations of the THRB gene in the hot-spot region, spanning exons 7–10, in 51 thyroid tumours and six thyroid cancer cell lines by PCR and direct sequencing. We did not find mutations in any of the tumours or cell lines analysed. Our findings suggest that, in contrast to the findings on the THRB-mutant transgenic mice, THRB gene mutations are not a relevant mechanism for human thyroid carcinogenesis.


Thyroid ◽  
1997 ◽  
Vol 7 (5) ◽  
pp. 771-773 ◽  
Author(s):  
TOMOHISA NAGASHIMA ◽  
HIDEKI YAGI ◽  
KANJI NAGASHIMA ◽  
AKIHIRO SAKURAI ◽  
KAZUMICHI ONIGATA ◽  
...  

Oncotarget ◽  
2015 ◽  
Vol 6 (10) ◽  
pp. 8115-8131 ◽  
Author(s):  
Jeong Won Park ◽  
Li Zhao ◽  
Mark Willingham ◽  
Sheue-yann Cheng

Endocrinology ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 1136-1142 ◽  
Author(s):  
Carmen Grijota-Martínez ◽  
Eric Samarut ◽  
Thomas S. Scanlan ◽  
Beatriz Morte ◽  
Juan Bernal

Thyroid hormone analogs with selective actions through specific thyroid hormone receptor (TR) subtypes are of great interest. They might offer the possibility of mimicking physiological actions of thyroid hormone with receptor subtype or tissue specificity with therapeutic aims. They are also pharmacological tools to dissect biochemical pathways mediated by specific receptor subtypes, in a complementary way to mouse genetic modifications. In this work, we studied the in vivo activity in developing rats of two thyroid hormone agonists, the TRβ-selective GC-24 and the TRα-selective CO23. Our principal goal was to check whether these compounds were active in the rat brain. Analog activity was assessed by measuring the expression of thyroid hormone target genes in liver, heart, and brain, after administration to hypothyroid rats. GC-24 was very selective for TRβ and lacked activity on the brain. On the other hand, CO23 was active in liver, heart, and brain on genes regulated by either TRα or TRβ. This compound, previously shown to be TRα-selective in tadpoles, displayed no selectivity in the rat in vivo.


1997 ◽  
Vol 272 (20) ◽  
pp. 13060-13065 ◽  
Author(s):  
Trevor N. Collingwood ◽  
Alison Butler ◽  
Yukiko Tone ◽  
Rory J. Clifton-Bligh ◽  
Malcolm G. Parker ◽  
...  

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