+ |
TSHB | form complex
binding
|
TSH |
0.667 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267047 |
|
|
Homo sapiens |
|
pmid |
sentence |
8196184 |
TSH is a heterodimer composed of common alpha subunit and unique beta subunit encoded by genes located on different chromosomes. It is known that the expression of these subunit genes is regulated in different mechanism by several extracellular factors. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Thyroid Gland |
Pathways: | Thyroid Hormone Metabolism |
+ |
TSHB | up-regulates quantity by expression
transcriptional regulation
|
SLC5A5 |
0.389 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251995 |
|
|
Homo sapiens |
|
pmid |
sentence |
14623893 |
I– uptake is stimulated by TSH, the master hormone for thyroid gland regulation. TSH stimulation results, at least in part, from the cAMP-mediated increase in NIS biosynthesis. TSH not only stimulates NIS transcription and biosynthesis but is also required for modulating the NIS phosphorylation pattern, maintaining its half-life, and retaining NIS at the thyrocyte plasma membrane |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Thyroid cancer, Thyroid Hormone Metabolism |
+ |
POU1F1 | up-regulates quantity by expression
transcriptional regulation
|
TSHB |
0.45 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267205 |
|
|
Homo sapiens |
|
pmid |
sentence |
10931853 |
CBP and Pit-1 acted synergistically in TRH stimulation of the TSH-β promoter. The human TSH-β promoter contains three well defined Pit-1 DNA-binding sites. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Thyroid Gland |
Pathways: | Thyroid Hormone Metabolism |
+ |
TSHB | up-regulates quantity by stabilization
|
SLC5A5 |
0.389 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251994 |
|
|
Homo sapiens |
|
pmid |
sentence |
14623893 |
Uptake is stimulated by TSH, the master hormone for thyroid gland regulation. TSH stimulation results, at least in part, from the cAMP-mediated increase in NIS biosynthesis. TSH not only stimulates NIS transcription and biosynthesis but is also required for modulating the NIS phosphorylation pattern, maintaining its half-life, and retaining NIS at the thyrocyte plasma membrane |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Thyroid cancer, Thyroid Hormone Metabolism |
+ |
TSHB | up-regulates
binding
|
TSHR |
0.711 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-88653 |
|
|
Homo sapiens |
|
pmid |
sentence |
12045258 |
Two novel human glycoprotein hormonelike genes, alpha2 (a2) and beta5 (b5), recently have been identified. Using a yeast two-hybrid assay, the two subunits were found as potential heterodimerization partners. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Thyroid Hormone Metabolism |
+ |
GATA2 | up-regulates quantity by expression
transcriptional regulation
|
TSHB |
0.4 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267253 |
|
|
Homo sapiens |
|
pmid |
sentence |
9305891 |
Pit-1, is necessary but not sufficient to allow basal transcription of the mTSHβ gene.The analysis of the mTSHβ gene described in this report provides evidence for the participation of a zinc finger factor, GATA-2, with a POU homeodomain partner, Pit-1, on a such a composite element.In summary, we have shown the requirement for at least two different classes of transcription factors to regulate mTSHβ gene expression. Both GATA-2 and Pit-1 can bind independently to the P1 region of the promoter, form a heteromeric complex with DNA, and functionally synergize to activate TSHβ promoter activity. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Hypophysis |
Pathways: | Thyroid Hormone Metabolism |
+ |
TGFB1 | down-regulates quantity by repression
transcriptional regulation
|
TSHB |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251991 |
|
|
Homo sapiens |
|
pmid |
sentence |
14623893 |
TGF-β inhibits thyroid-stimulated hormone (TSH)-induced NIS mRNA and protein levels in a dose-dependent manner. This effect takes place at the transcriptional level, as TGF-β inhibits TSH-induced transcription |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Thyroid cancer, Thyroid Hormone Metabolism |