| + |
PTPN9 | down-regulates 
dephosphorylation
|
INSR |
0.263 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-146668 |
Tyr1185 |
FGMTRDIyETDYYRK |
Homo sapiens |
|
| pmid |
sentence |
| 16679294 |
Ectopic expression of ptp-meg2 in cells inhibited insulin-induced phosphorylation of the insulin receptor, while rnai-mediated reduction of ptp-meg2 transcript levels enhanced insulin action |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-146672 |
Tyr1189 |
RDIYETDyYRKGGKG |
Homo sapiens |
|
| pmid |
sentence |
| 16679294 |
Ectopic expression of ptp-meg2 in cells inhibited insulin-induced phosphorylation of the insulin receptor, while rnai-mediated reduction of ptp-meg2 transcript levels enhanced insulin action |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-146676 |
Tyr1190 |
DIYETDYyRKGGKGL |
Homo sapiens |
|
| pmid |
sentence |
| 16679294 |
Ectopic expression of ptp-meg2 in cells inhibited insulin-induced phosphorylation of the insulin receptor, while rnai-mediated reduction of ptp-meg2 transcript levels enhanced insulin action |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-146680 |
Tyr999 |
YASSNPEyLSASDVF |
Homo sapiens |
|
| pmid |
sentence |
| 16679294 |
Ectopic expression of ptp-meg2 in cells inhibited insulin-induced phosphorylation of the insulin receptor, while rnai-mediated reduction of ptp-meg2 transcript levels enhanced insulin action |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| + |
PTPN9 | down-regulates
dephosphorylation
|
NSF |
0.423 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-128348 |
Tyr83 |
QEIEVSLyTFDKAKQ |
Homo sapiens |
|
| pmid |
sentence |
| 15322554 |
Our results suggest that the molecular mechanism by which ptp-meg2 promotes secretory vesicle fusion involves the local release of nsf from a tyrosine-phosphorylated, inactive state. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTPN9 | down-regulates activity
dephosphorylation
|
GHR |
0.319 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248505 |
|
|
Cricetulus griseus |
CHO Cell |
| pmid |
sentence |
| 12907755 |
Protein tyrosine phosphatases (PTPs) play key roles in switching off tyrosine phosphorylation cascades, such as initiated by cytokine receptors. We have used substrate-trapping mutants of a large set of PTPs to identify members of the PTP family that have substrate specificity for the phosphorylated human GH receptor (GHR) intracellular domain. Among 31 PTPs tested, T cell (TC)-PTP, PTP-beta, PTP1B, stomach cancer-associated PTP 1 (SAP-1), Pyst-2, Meg-2, and PTP-H1 showed specificity for phosphorylated GHR |
|
| Publications: |
1 |
Organism: |
Cricetulus Griseus |
| + |
PTPN9 | down-regulates
dephosphorylation
|
GHR |
0.319 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-104577 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12907755 |
Using ghr hyper-phosphorylated by elk kinase, we have identified tc-ptp, ptp- , pyst-2, sap1, meg-2, ptp1b, and ptph1 as having substrate specificity for this receptor. In addition, we have shown that these same ptps (or rather their nonmutated counterparts) can dephosphorylate the ghr. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
PTPN9
- 
- 