Acts as a transcriptional coactivator for NOTCH proteins. Has been shown to amplify NOTCH-induced transcription of HES1. Potentiates activation by NOTCH3 and NOTCH4 more efficiently than MAML1 or MAML3. {ECO:0000269|PubMed:12370315, ECO:0000269|PubMed:12386158, ECO:0000269|PubMed:12539049}.
In 14 of 15 cancers, the evidence for MAML2 comes mainly from mutations found in tumours
Each row is a cancer, strongest overall evidence first. The two dots show how strong the inherited (germline) and tumour-mutation (somatic) evidence is; the line between them is the gap.
Inherited (germline) variantsMutations in tumours (somatic)
Scores run from 0 (no evidence) to 1 (strongest). A missing dot at 0 means Open Targets holds no evidence of that kind. Source: Open Targets Platform, fetched live.
Tractability
No positive tractability buckets.
gnomAD loss of function constraint: o/e 0.22891999781131744 (upper bound 0.32688000798225403). Low values mean loss of function is poorly tolerated, a safety flag for inhibition.
Who runs trials of these drugs
No named investigators on registry trials of MAML2's approved or late-stage drugs in the last three years.
No terminated, withdrawn or suspended trials of MAML2's drugs are registered
All 0 drugs and clinical candidates as a table
Each drug, stage and indication links to its Open Targets record, where the trials and approvals behind it are listed. Salt forms (for example a mesylate) are listed as Open Targets records them, as separate entries.