| + |
SLC5A5 | up-regulates quantity 
relocalization
|
iodide |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266960 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 28192058 |
Active iodide (I-) transport in both the thyroid and some extrathyroidal tissues is mediated by the Na+/I- symporter (NIS). In the thyroid, NIS-mediated I- uptake plays a pivotal role in thyroid hormone (TH) biosynthesis. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| Pathways: | Thyroid cancer, Thyroid Hormone Metabolism |
| + |
PAX8 | up-regulates quantity by expression
transcriptional regulation
|
SLC5A5 |
0.425 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251990 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14623893 |
Pax8 has an essential role in thyroid organogenesis and differentiation, being the main mediator of thyroid gene transcription, including the NIS gene. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Thyroid Hormone Metabolism |
| + |
monobenzyl phthalate | up-regulates quantity by expression 
transcriptional regulation
|
SLC5A5 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268743 |
|
|
Rattus norvegicus |
PCCL-3 Cell |
| pmid |
sentence |
| 16257484 |
DIDP, BBP and DOP stimulate NIS mRNA expression. Here, hNIS promoter construct (N3) was up-regulated 2.5-fold by DIDP, 2.6-fold by BBP and 2.4-fold by DOP in the presence of TSH. Likewise, these phthalates also enhanced rNIS endogenous mRNA expression, which increased ca. 2-fold after 48 h of treatment compared with the expression level generated by TSH only. At 72 h, mRNA content was unchanged. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
SLC5A5 | up-regulates activity
chemical activation
|
iodide |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251996 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14623893 |
Iodide is an essential element in thyroid physiology as a critical component of thyroxine and triiodothyronine molecules and a key regulator of thyroid gland function. The first step in iodide metabolism is represented by thyroid trapping, which is achieved by an active, energy-dependent transport process across the basolateral plasma membrane of the thyrocytes. The protein responsible for this process, the sodium/iodide symporter (NIS),1 is an intrinsic plasma membrane protein that mediates active transport of I- in the thyroid, lactating mammary gland, stomach, and salivary glands |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Thyroid cancer, Thyroid Hormone Metabolism |
| + |
TSHB | up-regulates quantity by expression
transcriptional regulation
|
SLC5A5 |
0.395 |
| 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 |
| + |
SLC5A5 | up-regulates quantity
relocalization
|
sodium(1+) |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266961 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 28192058 |
Active iodide (I-) transport in both the thyroid and some extrathyroidal tissues is mediated by the Na+/I- symporter (NIS). In the thyroid, NIS-mediated I- uptake plays a pivotal role in thyroid hormone (TH) biosynthesis. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| Pathways: | Thyroid Hormone Metabolism |
| + |
Diisodecyl phthalate | up-regulates quantity by expression
transcriptional regulation
|
SLC5A5 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268742 |
|
|
Rattus norvegicus |
PCCL-3 Cell |
| pmid |
sentence |
| 16257484 |
DIDP, BBP and DOP stimulate NIS mRNA expression. Here, hNIS promoter construct (N3) was up-regulated 2.5-fold by DIDP, 2.6-fold by BBP and 2.4-fold by DOP in the presence of TSH. Likewise, these phthalates also enhanced rNIS endogenous mRNA expression, which increased ca. 2-fold after 48 h of treatment compared with the expression level generated by TSH only. At 72 h, mRNA content was unchanged. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
APEX1 | up-regulates quantity by expression
transcriptional regulation
|
SLC5A5 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261564 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 14630715 |
These data demonstrate a role for APE/Ref-1 protein in the transcriptional regulation of NIS gene expression by itself and in cooperation with PAX8. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TSHB | up-regulates quantity by stabilization
|
SLC5A5 |
0.395 |
| 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 |
| + |
TGFB1 | down-regulates quantity by repression 
transcriptional regulation
|
SLC5A5 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259912 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14623893 |
The sodium/iodide symporter mediates the active transport of iodide in thyroid follicular cells. A number of agents regulate NIS expression; among these, TGF-β is a potent inhibitor of both iodide uptake and NIS gene expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Thyroid cancer, Thyroid Hormone Metabolism |
| + |
CREB1 | up-regulates quantity by expression
transcriptional regulation
|
SLC5A5 |
0.273 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267137 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 34751390 |
CREB recognized and bound to the promoter of SLC5A5 to facilitate its transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Thyroid Gland |
| Pathways: | Thyroid Hormone Metabolism |
| + |
bis(2-ethylhexyl) phthalate | up-regulates quantity by expression
transcriptional regulation
|
SLC5A5 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268744 |
|
|
Rattus norvegicus |
PCCL-3 Cell |
| pmid |
sentence |
| 16257484 |
DIDP, BBP and DOP stimulate NIS mRNA expression. Here, hNIS promoter construct (N3) was up-regulated 2.5-fold by DIDP, 2.6-fold by BBP and 2.4-fold by DOP in the presence of TSH. Likewise, these phthalates also enhanced rNIS endogenous mRNA expression, which increased ca. 2-fold after 48 h of treatment compared with the expression level generated by TSH only. At 72 h, mRNA content was unchanged. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
BRAF | down-regulates quantity by repression 
transcriptional regulation
|
SLC5A5 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251989 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19861538 |
The BRAFV600E oncogene induces transforming growth factor beta secretion leading to sodium iodide symporter repression and increased malignancy in thyroid cancer. BRAF induces TGFβ secretion leading to NIS repression in a MEK-ERK–independent manner but cooperating with the MEK-ERK pathway to induce strong tumor invasion, two major traits acquired during PTC progression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Thyroid cancer |
3.0
SLC5A5
- 
- 