EC Number   |
Disease |
PubMed ID |
Title of Publication |
Category |
Confidence Level |
|---|
   2.1.1.244 | Breast Neoplasms |
25909287 |
Loss of the N-terminal methyltransferase NRMT1 increases sensitivity to DNA damage and promotes mammary oncogenesis. |
causal interaction
therapeutic application
unassigned |
4
1
0 |
| 2.1.1.244 | Breast Neoplasms |
26543161 |
Structural basis for substrate recognition by the human N-terminal methyltransferase 1. |
therapeutic application
unassigned |
1
0 |
| 2.1.1.244 | Breast Neoplasms |
28556566 |
Select human cancer mutants of NRMT1 alter its catalytic activity and decrease N-terminal trimethylation. |
causal interaction
diagnostic usage
ongoing research
therapeutic application |
1
3
2
1 |
| 2.1.1.244 | Carcinogenesis |
25909287 |
Loss of the N-terminal methyltransferase NRMT1 increases sensitivity to DNA damage and promotes mammary oncogenesis. |
causal interaction
therapeutic application
unassigned |
4
1
0 |
| 2.1.1.244 | Carcinogenesis |
28556566 |
Select human cancer mutants of NRMT1 alter its catalytic activity and decrease N-terminal trimethylation. |
causal interaction
diagnostic usage
ongoing research
therapeutic application |
1
3
2
1 |
| 2.1.1.244 | Carcinogenesis |
30612740 |
METTL13 Methylation of eEF1A Increases Translational Output to Promote Tumorigenesis. |
causal interaction
diagnostic usage
ongoing research
therapeutic application |
4
4
2
2 |
| 2.1.1.244 | Carcinogenesis |
30635279 |
KRAS-Driven Cancers Are Dependent on METTL13-Mediated eEF1A Methylation. |
unassigned |
0 |
| 2.1.1.244 | Carcinogenesis |
34437210 |
KRAS-Driven Cancers Are Dependent on METTL13-Mediated eEF1A Methylation. |
unassigned |
0 |
| 2.1.1.244 | Carcinoma |
26763933 |
METTL13 is downregulated in bladder carcinoma and suppresses cell proliferation, migration and invasion. |
causal interaction
diagnostic usage
ongoing research
therapeutic application |
4
4
4
3 |
| 2.1.1.244 | Carcinoma |
33985542 |
METTL13 inhibits progression of clear cell renal cell carcinoma with repression on PI3K/AKT/mTOR/HIF-1? pathway and c-Myc expression. |
causal interaction
ongoing research
therapeutic application
unassigned |
1
4
1
0 |
