| + |
Ionizing radiation | up-regulates 
|
ELE1-RET |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251984 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23128507 |
In PTC, genomic rearrangements juxtapose the RET tyrosine kinase domain to unrelated genes, thereby creating dominantly transforming oncogenes, denominated RET/PTC. The RET/PTC rearrangements are the 2nd most common genetic alteration described in PTC and observed in ∼13–43% of cases, mostly in pediatric cancers or in individuals exposed to ionizing radiation from nuclear accidents |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Thyroid cancer |
| + |
ELE1-RET | up-regulates activity 
binding
|
SHC1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251985 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16946010 |
RET/PTC is tumorigenic in thyroid follicular cells; it transforms thyroid cells in culture and gives rise to thyroid carcinomas in transgenic mice. effects of RET/PTC activation require signaling along the MAPK pathway and, more specifically, the presence of the functional BRAF kinase. all breakpoints in the RET gene occur within intron 11, leaving intact the TK domain of the receptor and enabling the RET/PTC oncoprotein to bind SHC via Y1062 and activate the RAS-RAF-MAPK cascade |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Thyroid cancer |
3.0
ELE1-RET