| + |
PTGES2 | up-regulates quantity 
chemical modification
|
prostaglandin E2(1-) |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269766 |
|
|
in vitro |
|
| pmid |
sentence |
| 10922363 |
Importantly, this enzyme is capable of converting COX-1-, but not COX-2-, derived PGH2 to PGE2 efficiently. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
prostaglandin E2(1-) | up-regulates activity
chemical activation
|
PTGER2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257570 |
|
|
Homo sapiens |
HEK-293A Cell |
| pmid |
sentence |
| 31160049 |
Here we systematically quantified ligand-induced interactions between 148 GPCRs and all 11 unique G alpha subunit C-termini. For each receptor, we probed chimeric G alpha subunit activation via a transforming growth factor-alpha (TGF alpha) shedding response in HEK293 cells lacking endogenous Gq/11- and G12/13- signaling. | We defined positive coupling if any member of the subfamily scored LogRAi ≥ -1 and negative coupling if all of the members scored LogRAi < -1 (Figure 3A-B). ROC analysis gives AUC = 0.78 (Figure S4A) when considering high-confidence known coupling data and suggested a threshold of LogRAi ≥ -1.0 for defining true couplings. | The score associated to this interaction has a LogRAi ≥ -1.0. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTGS2 | up-regulates quantity
chemical modification
|
prostaglandin E2(1-) |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255684 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16540375 |
Arachidonic acid is transformed into PGE2 via cyclooxygenase (COX) enzymes and terminal prostaglandin E synthases (PGES) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML |
| + |
prostaglandin E2(1-) | up-regulates activity
chemical activation
|
PTGER4 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257572 |
|
|
Homo sapiens |
HEK-293A Cell |
| pmid |
sentence |
| 31160049 |
Here we systematically quantified ligand-induced interactions between 148 GPCRs and all 11 unique G alpha subunit C-termini. For each receptor, we probed chimeric G alpha subunit activation via a transforming growth factor-alpha (TGF alpha) shedding response in HEK293 cells lacking endogenous Gq/11- and G12/13- signaling. | We defined positive coupling if any member of the subfamily scored LogRAi ≥ -1 and negative coupling if all of the members scored LogRAi < -1 (Figure 3A-B). ROC analysis gives AUC = 0.78 (Figure S4A) when considering high-confidence known coupling data and suggested a threshold of LogRAi ≥ -1.0 for defining true couplings. | The score associated to this interaction has a LogRAi ≥ -1.0. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
prostaglandin E2(1-) | up-regulates activity
chemical activation
|
PTGER1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257569 |
|
|
Homo sapiens |
HEK-293A Cell |
| pmid |
sentence |
| 31160049 |
Here we systematically quantified ligand-induced interactions between 148 GPCRs and all 11 unique G alpha subunit C-termini. For each receptor, we probed chimeric G alpha subunit activation via a transforming growth factor-alpha (TGF alpha) shedding response in HEK293 cells lacking endogenous Gq/11- and G12/13- signaling. | We defined positive coupling if any member of the subfamily scored LogRAi ≥ -1 and negative coupling if all of the members scored LogRAi < -1 (Figure 3A-B). ROC analysis gives AUC = 0.78 (Figure S4A) when considering high-confidence known coupling data and suggested a threshold of LogRAi ≥ -1.0 for defining true couplings. | The score associated to this interaction has a LogRAi ≥ -1.0. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
prostaglandin E2(1-) | up-regulates activity
chemical activation
|
PTGER3 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257571 |
|
|
Homo sapiens |
HEK-293A Cell |
| pmid |
sentence |
| 31160049 |
Here we systematically quantified ligand-induced interactions between 148 GPCRs and all 11 unique G alpha subunit C-termini. For each receptor, we probed chimeric G alpha subunit activation via a transforming growth factor-alpha (TGF alpha) shedding response in HEK293 cells lacking endogenous Gq/11- and G12/13- signaling. | We defined positive coupling if any member of the subfamily scored LogRAi ≥ -1 and negative coupling if all of the members scored LogRAi < -1 (Figure 3A-B). ROC analysis gives AUC = 0.78 (Figure S4A) when considering high-confidence known coupling data and suggested a threshold of LogRAi ≥ -1.0 for defining true couplings. | The score associated to this interaction has a LogRAi ≥ -1.0. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
prostaglandin E2(1-) | up-regulates 
|
CTNNB1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255685 |
|
|
Homo sapiens |
Hematopoietic Stem Cell |
| pmid |
sentence |
| 23645839 |
Prostaglandin E2 (PGE2), 1 of the major metabolites downstream of both COX-1 and COX-2, has been shown to activate β-catenin–dependent signaling in hematopoietic stem cells (HSCs) and promote HSC expansion |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML |
| + |
prostaglandin H2(1-) | up-regulates quantity
precursor of
|
prostaglandin E2(1-) |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269765 |
|
|
in vitro |
|
| pmid |
sentence |
| 10922363 |
Importantly, this enzyme is capable of converting COX-1-, but not COX-2-, derived PGH2 to PGE2 efficiently. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
prostaglandin E2(1-) | up-regulates quantity
precursor of
|
prostaglandin H2(1-) |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269767 |
|
|
in vitro |
|
| pmid |
sentence |
| 10922363 |
Importantly, this enzyme is capable of converting COX-1-, but not COX-2-, derived PGH2 to PGE2 efficiently. |
|
| Publications: |
1 |
Organism: |
In Vitro |
3.0
prostaglandin E2(1-)