Affinage

MAML1

Mastermind-like protein 1 · UniProt Q92585

Length
1016 aa
Mass
108.1 kDa
Annotated
2026-06-10
54 papers in source corpus 25 papers cited in narrative 25 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MAML1 is a nuclear transcriptional coactivator that serves as the obligate third subunit of the canonical Notch transcriptional complex, binding the ankyrin repeat domain of all four mammalian Notch receptors and assembling a ternary DNA-binding complex with the Notch intracellular domain and CSL/RBP-Jκ to amplify Notch target-gene transcription such as HES1 (PMID:11101851, PMID:15019995); addition of Notch ICD and MAML1 does not alter CSL's intrinsic DNA-binding preference, indicating MAML1 works as an activation module rather than a specificity factor (PMID:21124806). In vivo MAML1 is required for receptor- and context-specific Notch outputs, including Notch2-dependent marginal zone B-cell development (PMID:17699740), and it acts redundantly with MAML3 such that combined loss produces pan-Notch developmental lethality (PMID:22069191). Mechanistically, MAML1 couples Notch to chromatin through p300: an N-terminal proline motif recruits p300, MAML1 potentiates p300 autoacetylation and HAT activity, and the MAML1/p300 complex acetylates histone H3/H4 tails and the Notch1 ICD itself, the latter reducing Notch1 ubiquitination (PMID:17300219, PMID:19304754, PMID:22100894). For enhancer-driven Notch targets, MAML1 contributes a recruitment activity beyond p300 HAT delivery, mapping to an essential central region (residues ~151–350) (PMID:32179552). Beyond Notch, MAML1 functions as an independent coactivator for MEF2C-driven myogenesis (PMID:16510869), p53 (PMID:17317671), NF-κB/RelA (PMID:20231278), EGR1 (PMID:23029358), Runx2-dependent chondrocyte and bone maturation (PMID:23326237), Gli/Shh signaling in cerebellar development (PMID:28726779), and STAT3 in hepatocellular carcinoma (PMID:41345959), and it is required for YAP/TAZ nuclear localization and activity (PMID:32482852). MAML1 activity is heavily regulated by post-translational modification: SUMOylation at Lys217/Lys299 (via UBC9/PIAS1, reversed by SENP1) recruits HDAC7 to repress it (PMID:20203086), GSK3β binding represses its activity (PMID:19740771), and PKN2-mediated phosphorylation at Ser314 destabilizes the liquid-liquid phase-separated nuclear condensates required for efficient Notch1 ICD engagement and transcriptional output (PMID:42246060). MAML1 also acts post-translationally to inhibit the E3 ligase Itch by promoting Itch K63-linked self-ubiquitylation, thereby stabilizing Notch1 and Gli1 (PMID:41272291). Charge-altering variants in a MAML1 intrinsically disordered region that abolish phase separation are associated with congenital heart disease (PMID:42246060), and cutaneous papillomavirus E6 oncoproteins repress MAML1 by binding its C-terminal LXXLL motif (PMID:22249263).

Mechanistic history

Synthesis pass · year-by-year structured walk · 25 steps
  1. 2000 High

    Established the founding mechanistic identity of MAML1 as the missing coactivator that converts the CSL/Notch ICD DNA-binding platform into an active transcription complex.

    Evidence Co-IP, reporter assays, and nuclear localization imaging defining ternary complex with Notch ICD and RBP-Jκ in mammalian cells

    PMID:11101851

    Open questions at the time
    • Did not resolve how the ternary complex recruits the general transcription machinery
    • No structural detail of the MAML1–ankyrin interface
  2. 2004 High

    Confirmed functional conservation of the Notch coactivator role in the murine ortholog, enabling in vivo genetic dissection.

    Evidence Co-IP, reporter assays, and localization of murine Maml1

    PMID:15019995

    Open questions at the time
    • Did not address receptor-specific or tissue-specific requirements
  3. 2006 High

    Showed MAML1 is not Notch-exclusive but a shared, limiting coactivator partitioned between MEF2C and Notch, linking it to myogenic differentiation.

    Evidence Co-IP, RNAi, overexpression in C2C12, and Maml1-KO mouse

    PMID:16510869

    Open questions at the time
    • Quantitative basis of competitive partitioning between MEF2C and Notch unresolved
  4. 2006 Medium

    Placed MAML1 downstream of Notch1 in controlling endothelial proliferation via MAPK and PI3K/Akt suppression.

    Evidence Dominant-negative MAML1 and pathway inhibitor proliferation assays in endothelial cells

    PMID:16571776

    Open questions at the time
    • Dominant-negative approach only; no direct binding to pathway components
    • Single lab, single study
  5. 2007 High

    Demonstrated a Notch-independent coactivator function for p53, broadening MAML1 from a Notch-specific factor to a multi-pathway hub.

    Evidence Co-IP, ChIP, gain/loss-of-function reporter assays, and C. elegans epistasis

    PMID:17317671

    Open questions at the time
    • Mechanism of p53 stabilization not fully defined
  6. 2007 High

    Defined the biochemical link between MAML1 and chromatin by mapping p300 recruitment and showing the complex acetylates histones and MAML1 itself.

    Evidence In vitro acetylation, mutagenesis of lysine/proline residues, chromatin HAT assay

    PMID:17300219

    Open questions at the time
    • Functional consequence of MAML1 autoacetylation at target genes not resolved
  7. 2007 High

    Showed receptor-specific in vivo requirement, establishing MAML1 as essential for Notch2-driven marginal zone B-cell development.

    Evidence Maml1-KO mouse and hematopoietic chimeras with B/T-cell phenotyping

    PMID:17699740

    Open questions at the time
    • Molecular basis of receptor selectivity unexplained
  8. 2009 High

    Showed MAML1 actively stimulates p300 enzymatic output, not merely recruits it, coupling coactivation to nuclear body translocation.

    Evidence In vitro HAT and autoacetylation assays plus nuclear body imaging

    PMID:19304754

    Open questions at the time
    • Nature and composition of the nuclear bodies undefined at this stage
  9. 2009 Medium

    Identified GSK3β as a direct repressor of MAML1 activity, adding a kinase-based regulatory layer.

    Evidence Co-IP, reporter assays, GSK3 inhibitor treatment, nuclear body imaging

    PMID:19740771

    Open questions at the time
    • GSK3β phosphorylation site on MAML1 not mapped
    • Single lab
  10. 2010 High

    Defined a complete SUMOylation regulatory circuit that represses MAML1 via HDAC7 recruitment.

    Evidence In vitro SUMOylation, acceptor-site mutagenesis, HDAC7 Co-IP, reporter assays

    PMID:20203086

    Open questions at the time
    • Signals controlling the SUMOylation/de-SUMOylation balance in vivo unknown
  11. 2010 High

    Extended MAML1 coactivation to NF-κB/RelA and linked its loss to hepatocyte survival in vivo.

    Evidence Co-IP, NF-κB reporter assays, Maml1-KO MEFs and mice, TNFα cytotoxicity

    PMID:20231278

    Open questions at the time
    • Mechanism of IκBα degradation promotion not detailed
  12. 2010 Medium

    Clarified that MAML1 activates transcription without reprogramming CSL DNA-binding specificity.

    Evidence Protein-binding microarrays with purified CSL, ICN, and MAML1

    PMID:21124806

    Open questions at the time
    • In vitro array context; chromatin-level effects on site selection not tested
  13. 2011 High

    Demonstrated genetic redundancy with MAML3 for global Notch-dependent development.

    Evidence Single- and double-KO mice with developmental and molecular phenotyping

    PMID:22069191

    Open questions at the time
    • Determinants of paralog specificity vs. redundancy across tissues unresolved
  14. 2011 Medium

    Connected MAML1/p300 acetylation directly to Notch1 ICD stability and identified CDK8 as an opposing regulator.

    Evidence Cellular and in vitro acetylation/ubiquitination assays plus CDK8 overexpression

    PMID:22100894

    Open questions at the time
    • Causal chain between ICD acetylation and reduced ubiquitination partly inferred
    • Single lab
  15. 2012 High

    Identified a viral repression mechanism via E6 binding to the MAML1 C-terminal LXXLL motif.

    Evidence Proteomic pulldown, Co-IP, reporter assays, motif mapping across multiple E6 proteins

    PMID:22249263

    Open questions at the time
    • Structural detail of the E6–LXXLL interaction not resolved
  16. 2012 Medium

    Added EGR1 as a MAML1 partner with feed-forward activation of EGR1 and p300 promoters.

    Evidence Co-IP, reporter assays, acetylation assay in HEK cells

    PMID:23029358

    Open questions at the time
    • In vivo relevance of the EGR1 circuit not tested
    • Single lab
  17. 2013 High

    Established a Notch-independent role for MAML1 in Runx2-driven skeletal maturation through domain mapping and KO phenotype.

    Evidence Reporter assays with deletion mutants, Maml1-KO mouse embryos, ALP assays

    PMID:23326237

    Open questions at the time
    • Whether p300 acetylation underlies Runx2 coactivation not addressed
  18. 2013 Medium

    Revealed a competitive antagonism mechanism in which Snail displaces MAML1 from the Notch complex.

    Evidence Co-IP, reporter assays, competition binding assay

    PMID:23454378

    Open questions at the time
    • Physiological contexts of Snail competition not defined
    • Single lab
  19. 2015 Medium

    Showed MAML1 can bridge p53 into the Notch complex to repress Notch transcription, illustrating cross-pathway regulation through a shared coactivator.

    Evidence Co-IP, far-Western, ChIP, dominant-negative MAML1 in MCF-7 cells

    PMID:26033683

    Open questions at the time
    • Generalizability beyond MCF-7 cells untested
    • Single lab
  20. 2017 High

    Established MAML1 as a Gli/Shh coactivator essential for cerebellar GCP proliferation and development.

    Evidence Co-IP, reporter assays, RNAi, Maml1-KO MEFs and GCPs

    PMID:28726779

    Open questions at the time
    • Whether Gli coactivation uses the same p300 mechanism not resolved
  21. 2020 High

    Identified an unexpected requirement for MAML1 (and MAML2) in YAP/TAZ nuclear localization, expanding its role into Hippo pathway output.

    Evidence Overexpression/knockdown with localization imaging, domain mutagenesis, Co-IP, in vivo tumor models

    PMID:32482852

    Open questions at the time
    • Mechanism by which MAML1 promotes YAP/TAZ import not fully defined
  22. 2020 High

    Mapped an essential central region and showed MAML1 provides recruitment activity distinct from p300 HAT delivery for enhancer-driven Notch targets.

    Evidence CRISPR KO with add-back variants, HAT-domain fusion rescue, H3K27ac ChIP

    PMID:32179552

    Open questions at the time
    • Identity of the additional enhancer recruitment factor not determined
  23. 2025 High

    Uncovered a post-translational, non-transcriptional function in which MAML1 inhibits Itch to stabilize Notch1 and Gli1.

    Evidence Co-IP, K63-linkage ubiquitylation assay, PPQY motif mutagenesis, Maml1-KO and tumor models

    PMID:41272291

    Open questions at the time
    • How MAML1 selects Itch among HECT ligases not addressed
  24. 2025 Medium

    Defined a YAP-MAML1-STAT3 axis driving hepatocellular carcinoma via p300-dependent STAT3 acetylation.

    Evidence Co-IP, acetylation assay, STAT3 inhibitor rescue, YAP-promoter ChIP, knockdown/overexpression

    PMID:41345959

    Open questions at the time
    • Direct vs. indirect MAML1–STAT3 contact not fully resolved
    • Single lab
  25. 2026 High

    Showed MAML1 forms liquid-liquid phase-separated condensates required for Notch1 ICD engagement, with PKN2 phosphorylation at Ser314 and CHD-associated IDR variants disrupting condensates and Notch output.

    Evidence Knock-in and endocardium-specific KO mice, human heart organoids, in vitro LLPS assays, mass spectrometry, condensate microscopy

    PMID:42246060

    Open questions at the time
    • Whether condensate formation governs MAML1's non-Notch functions unknown
    • Composition of MAML1 condensates beyond Notch components undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how MAML1 integrates its many independent coactivator partnerships and its post-translational Itch-regulatory role into coordinated cellular decisions, and whether phase separation underlies coactivation of pathways beyond Notch.
  • No unifying model linking competitive partner partitioning, PTM regulation, and condensate behavior
  • Structural basis of the diverse partner interfaces unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 6 GO:0140096 catalytic activity, acting on a protein 3 GO:0003677 DNA binding 2 GO:0098772 molecular function regulator activity 2
Localization
GO:0005654 nucleoplasm 3 GO:0005634 nucleus 2
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-162582 Signal Transduction 3 R-HSA-4839726 Chromatin organization 2
Partners
EP300GLI1ITCHMEF2CNOTCH1RBPJTP53YAP1
Complex memberships
MAML1/p300 coactivator complexNotch/CSL/MAML1 ternary transcription complex

Evidence

Reading pass · 25 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 MAML1 binds to the ankyrin repeat domain of all four mammalian NOTCH receptors, forms a ternary DNA-binding complex with the Notch intracellular domain (ICN) and RBP-Jκ (CSL), and amplifies NOTCH-induced transcription of HES1. MAML1 localizes to nuclear bodies. Co-immunoprecipitation, transcriptional reporter assays, nuclear localization imaging Nature genetics High 11101851
2004 Murine Maml1 encodes a nuclear protein that binds the ankyrin repeat domain of Notch receptors, forms a ternary complex with ICN and CSL, and enhances Notch-induced transcription of HES-1, confirming it as the functional murine ortholog of human MAML1. Co-immunoprecipitation, transcriptional reporter assays, nuclear localization Gene High 15019995
2006 MAML1 interacts physically with MEF2C and functions as a potent co-transcriptional regulator for MEF2C-driven muscle-specific genes. MAML1 is required for MyoD-induced myogenic differentiation, and activation of Notch signaling recruits MAML1 away from MEF2C to the Notch transcriptional complex, thereby blocking pro-myogenic effects. Co-immunoprecipitation, RNAi knockdown, overexpression in C2C12 cells, Maml1-knockout mouse model Genes & development High 16510869
2006 MAML1 is required downstream of Notch1 activation to suppress endothelial cell proliferation; a dominant-negative MAML1 mutant antagonizes Notch1-mediated suppression of the MAPK and PI3K/Akt pathways. Dominant-negative MAML1 overexpression, pathway inhibitor assays, proliferation assays in endothelial cells FASEB journal Medium 16571776
2007 MAML1 physically interacts with p53 via its N-terminal region binding to the p53 DNA-binding domain, associates with native p53-response element promoters by ChIP, stabilizes p53 protein, enhances p53 phosphorylation/acetylation upon DNA damage, and functions as a transcriptional coactivator for p53 independently of its Notch coactivator role. Co-immunoprecipitation, chromatin immunoprecipitation (ChIP), overexpression/RNAi, p53-reporter assays, C. elegans genetic epistasis (lag-3 RNAi) The Journal of biological chemistry High 17317671
2007 p300 acetylates MAML1 at conserved N-terminal lysine residues; a proline repeat motif (PXPAAPAP) in the MAML1 N-terminus mediates direct interaction with p300 and enhances MAML1 transcriptional activity. The MAML1 N-terminal domain also directly interacts with histones, and the p300-MAML1 complex acetylates histone H3 and H4 tails in chromatin. In vitro acetylation assay, co-immunoprecipitation, mutagenesis of lysine/proline residues, chromatin HAT assay The Biochemical journal High 17300219
2007 Maml1 deficiency specifically impairs Notch2-dependent marginal zone B-cell development while minimally affecting T-cell development, demonstrating that MAML1 is required for Notch2 signaling in a receptor-specific context in vivo. Maml1-knockout mouse, hematopoietic chimeras, B-cell and T-cell developmental analysis Blood High 17699740
2009 MAML1 potentiates p300 autoacetylation and directly enhances p300 HAT activity, coinciding with translocation of MAML1, p300, and acetylated histones to nuclear bodies. In vitro HAT assay, autoacetylation assay, nuclear body imaging Nucleic acids research High 19304754
2009 Active GSK3β directly interacts with the MAML1 N-terminus and decreases MAML1 transcriptional activity. MAML1 translocates GSK3β to nuclear bodies (requires full-length MAML1). GSK3 inhibition further enhances MAML1-dependent histone acetylation. Co-immunoprecipitation, transcriptional reporter assays, nuclear body imaging, GSK3 inhibitor treatment Nucleic acids research Medium 19740771
2010 MAML1 is SUMOylated at Lys217 and Lys299 by UBC9 (E2 enzyme); PIAS1 (E3 ligase) stimulates SUMOylation; SENP1 reverses it. SUMOylation represses MAML1 transcriptional activity by enhancing its interaction with HDAC7. Mutation of both lysines abolishes SUMOylation and strongly increases MAML1-activated transcription. In vitro SUMOylation assay, site-directed mutagenesis, co-immunoprecipitation (HDAC7 interaction), transcriptional reporter assays FASEB journal High 20203086
2010 MAML1 co-activates the NF-κB subunit RelA (p65) and promotes degradation of IκBα, thereby modulating NF-κB signaling. Maml1-deficient MEFs show impaired TNFα-induced NF-κB responses, and Maml1-null mice exhibit spontaneous hepatocyte apoptosis in vivo. Co-immunoprecipitation, NF-κB reporter assays, Maml1-KO MEFs and mice, TNFα cytotoxicity assays The Journal of biological chemistry High 20231278
2010 Addition of NOTCH intracellular domains and MAML1 to CSL does not detectably alter the DNA binding site preferences of CSL, supporting the conclusion that MAML1 promotes transcriptional activation without changing CSL's preferred DNA binding specificity. Protein-binding microarrays (PBMs) with purified CSL, ICN, and MAML1 proteins PloS one Medium 21124806
2011 MamL1 and MamL3 are collectively essential for Notch signaling in vivo: MamL1/MamL3 double-null mice die during early organogenesis with classic pan-Notch defects, while single nulls are viable, demonstrating functional redundancy between MamL1 and MamL3 in Notch-dependent developmental processes. MamL1 and MamL3 single- and double-knockout mouse generation, embryological and molecular phenotyping (lunatic fringe expression) Development High 22069191
2011 MAML1-mediated potentiation of p300 autoacetylation enhances p300-dependent acetylation of the Notch1 intracellular domain at conserved C-terminal NLS lysines. This MAML1/p300-dependent acetylation of Notch1 ICD decreases Notch1 ICD ubiquitination. CDK8 inhibits Notch acetylation and Notch transcription enhanced by p300. Cell-based and in vitro acetylation assays, co-immunoprecipitation, ubiquitination assays, CDK8 overexpression Biochemical and biophysical research communications Medium 22100894
2012 Cutaneous papillomavirus E6 oncoproteins (BPV-1, HPV-1, HPV-8) bind an acidic LXXLL motif at the MAML1 C-terminus, repress MAML1 transactivation, and inhibit NOTCH-responsive promoters. BPV-1 E6 is found in a complex with MAML1 in stably transformed cells. Proteomic pulldown, co-immunoprecipitation, transcriptional reporter assays, LXXLL motif mapping Oncogene High 22249263
2012 MAML1 physically interacts with EGR1 and acts cooperatively to activate EGR1-regulated promoters (including EGR1 and p300 own promoters). MAML1 strongly induces p300-mediated acetylation of EGR1 and increases EGR1 protein expression in embryonic kidney cells. Co-immunoprecipitation, transcriptional reporter assays, acetylation assay, overexpression in HEK cells PloS one Medium 23029358
2013 MAML1 enhances the transcriptional activity of Runx2 in a Notch-independent manner (N-terminal Notch-binding domain deletion mutant retains activity; Notch inhibition does not affect Runx2 activation). MAML1 loss in mice impairs chondrocyte maturation and results in shorter bone lengths. Luciferase reporter assay, MAML1 deletion mutants, Maml1-KO mouse embryo analysis, alkaline phosphatase assay PLoS genetics High 23326237
2013 Snail suppresses NOTCH1 ICD-mediated transcription by physically interacting with NICD and competing with MAML1 for inclusion in the NICD/RBPJk transcription complex. Co-immunoprecipitation, transcriptional reporter assays, competition binding assay Biochemical and biophysical research communications Medium 23454378
2015 p53 associates with the Notch transcriptional complex via MAML1 (p53-NICD-MAML1 complex detected by co-IP and far-Western); formation of this complex is dependent on MAML1 (blocked by dominant-negative MAML1). In MCF-7 cells, this association results in inhibition of Notch-dependent transcription. Co-immunoprecipitation, far-Western blotting, chromatin immunoprecipitation (ChIP), dominant-negative MAML1 Journal of cellular physiology Medium 26033683
2017 MAML1 interacts with Gli family transcription factors (Gli1, Gli2) and functions as a potent transcriptional coactivator of Shh/Gli target genes. Maml1 silencing reduces Gli target gene expression and impairs cerebellar granule cell progenitor (GCP) proliferation; Maml1-null mice show compromised Shh pathway activity and impaired cerebellum development. Co-immunoprecipitation, transcriptional reporter assays, RNAi/siRNA knockdown, Maml1-KO mouse MEFs and GCPs Cell death & disease High 28726779
2020 MAML1 and MAML2 are required for YAP/TAZ nuclear localization and transcriptional activity. Ectopic MAML1 expression induces nuclear translocation of YAP/TAZ; MAML1 depletion causes cytoplasmic retention. Mutation of the MAML1 nuclear localization signal or its YAP/TAZ-interacting region abolishes this effect. MAML1 mRNA is regulated by miR-30c in a cell-density-dependent manner. Overexpression and siRNA knockdown with YAP/TAZ localization imaging, domain mutagenesis, co-immunoprecipitation, in vivo tumor models Proceedings of the National Academy of Sciences of the United States of America High 32482852
2020 MAML1 residues 151–350 are functionally essential for Notch-dependent transcriptional induction of both HES4 (promoter-driven) and DTX1 (enhancer-driven) target genes, as shown by add-back of MAML1 variants in MAML1-knockout cells. Fusion of the Notch-binding region of MAML1 to the p300 HAT domain rescues HES4 but not DTX1 expression, indicating that MAML1 has an additional recruitment activity beyond p300 HAT recruitment for enhancer-driven targets. MAML1 CRISPR knockout, add-back of deletion/truncation variants, HAT domain fusion constructs, H3K27ac ChIP Molecular and cellular biology High 32179552
2025 MAML1 interacts with the E3 ubiquitin ligase Itch via a PPQY motif and promotes K63-linked self-ubiquitylation of Itch, thereby deregulating Itch activity. Loss of MAML1 stabilizes Itch and suppresses Notch1 and Gli1 protein levels; MAML1 upregulation enhances Notch1 and Gli1 expression. Thus MAML1 acts as a post-translational regulator of Itch in addition to its transcriptional coactivator role. Co-immunoprecipitation, ubiquitylation assay (K63-linkage), Maml1-KO mouse model, domain mutagenesis (PPQY motif), in vivo tumor models Cell death and differentiation High 41272291
2025 MAML1 interacts with STAT3 and enhances STAT3 acetylation in a p300-dependent manner to promote hepatocellular carcinoma progression. YAP transcriptionally regulates MAML1 expression by directly binding its promoter, forming a YAP-MAML1-STAT3 signaling axis. Co-immunoprecipitation, acetylation assay, STAT3 inhibitor rescue experiments, ChIP for YAP binding to MAML1 promoter, knockdown/overexpression Experimental hematology & oncology Medium 41345959
2026 MAML1 activity in endocardial cells depends on liquid-liquid phase separation (LLPS) to form nuclear condensates required for efficient interaction with the NOTCH1 intracellular domain and downstream transcriptional activation. Patient-derived CHD-associated charge-altering variants (e.g., Q401K) within the intrinsically disordered region 2 of MAML1 abolish LLPS and downregulate Notch signaling. PKN2 kinase phosphorylates MAML1 at Ser314, destabilizing condensates and attenuating Notch transcriptional output. Knock-in mouse model (Q401K), endocardium-specific KO mouse, CRISPR-edited human heart organoids, biochemical LLPS assays, mass spectrometry (PTM identification), microscopy of condensates, echocardiography Circulation High 42246060

Source papers

Stage 0 corpus · 54 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 MAML1, a human homologue of Drosophila mastermind, is a transcriptional co-activator for NOTCH receptors. Nature genetics 467 11101851
2006 The Notch coactivator, MAML1, functions as a novel coactivator for MEF2C-mediated transcription and is required for normal myogenesis. Genes & development 134 16510869
1996 Prediction of the coding sequences of unidentified human genes. V. The coding sequences of 40 new genes (KIAA0161-KIAA0200) deduced by analysis of cDNA clones from human cell line KG-1. DNA research : an international journal for rapid publication of reports on genes and genomes 114 8724849
2012 Cutaneous papillomavirus E6 oncoproteins associate with MAML1 to repress transactivation and NOTCH signaling. Oncogene 113 22249263
2006 Inhibition of endothelial cell proliferation by Notch1 signaling is mediated by repressing MAPK and PI3K/Akt pathways and requires MAML1. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 96 16571776
2007 The notch regulator MAML1 interacts with p53 and functions as a coactivator. The Journal of biological chemistry 73 17317671
2011 Mastermind-like 1 (MamL1) and mastermind-like 3 (MamL3) are essential for Notch signaling in vivo. Development (Cambridge, England) 56 22069191
2009 The transcriptional coactivator MAML1 regulates p300 autoacetylation and HAT activity. Nucleic acids research 49 19304754
2011 Expression analysis elucidates the roles of MAML1 and Twist1 in esophageal squamous cell carcinoma aggressiveness and metastasis. Annals of surgical oncology 47 22006371
2020 MAML1/2 promote YAP/TAZ nuclear localization and tumorigenesis. Proceedings of the National Academy of Sciences of the United States of America 45 32482852
2017 Association of papillomavirus E6 proteins with either MAML1 or E6AP clusters E6 proteins by structure, function, and evolutionary relatedness. PLoS pathogens 44 29281732
2007 The transcriptional coactivator Maml1 is required for Notch2-mediated marginal zone B-cell development. Blood 44 17699740
2007 A proline repeat domain in the Notch co-activator MAML1 is important for the p300-mediated acetylation of MAML1. The Biochemical journal 40 17300219
2019 Methylation-mediated silencing of miR-133a-3p promotes breast cancer cell migration and stemness via miR-133a-3p/MAML1/DNMT3A positive feedback loop. Journal of experimental & clinical cancer research : CR 39 31660998
2019 Role of MAML1 in targeted therapy against the esophageal cancer stem cells. Journal of translational medicine 36 30992079
2018 MicroRNA-193b-3p regulates hepatocyte apoptosis in selenium-deficient broilers by targeting MAML1. Journal of inorganic biochemistry 36 29990747
2017 Maml1 acts cooperatively with Gli proteins to regulate sonic hedgehog signaling pathway. Cell death & disease 35 28726779
2010 The mastermind-like 1 (MAML1) co-activator regulates constitutive NF-kappaB signaling and cell survival. The Journal of biological chemistry 30 20231278
2009 GSK3beta is a negative regulator of the transcriptional coactivator MAML1. Nucleic acids research 30 19740771
2015 Role of Msi1 and MAML1 in Regulation of Notch Signaling Pathway in Patients with Esophageal Squamous Cell Carcinoma. Journal of gastrointestinal cancer 29 26294058
2010 Notch and MAML-1 complexation do not detectably alter the DNA binding specificity of the transcription factor CSL. PloS one 28 21124806
2019 NOTCH2/NOTCH3/DLL3/MAML1/ADAM17 signaling network is associated with ovarian cancer. Oncology letters 26 31186700
2015 p53 Modulates Notch Signaling in MCF-7 Breast Cancer Cells by Associating With the Notch Transcriptional Complex Via MAML1. Journal of cellular physiology 26 26033683
2011 Ubiquitination of Notch1 is regulated by MAML1-mediated p300 acetylation of Notch1. Biochemical and biophysical research communications 25 22100894
2009 Transcriptional mechanisms by the coregulator MAML1. Current protein & peptide science 24 19751190
2012 MAML1 acts cooperatively with EGR1 to activate EGR1-regulated promoters: implications for nephrogenesis and the development of renal cancer. PloS one 22 23029358
2013 MAML1 enhances the transcriptional activity of Runx2 and plays a role in bone development. PLoS genetics 21 23326237
2010 SUMO modification regulates the transcriptional activity of MAML1. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 18 20203086
2020 MAML1 promotes ESCC aggressiveness through upregulation of EMT marker TWIST1. Molecular biology reports 16 32180088
2019 MAML1 regulates EMT markers expression through NOTCH-independent pathway in breast cancer cell line MCF7. Biochemical and biophysical research communications 16 30732857
2012 A knockdown of Maml1 that results in melanoma cell senescence promotes an innate and adaptive immune response. Cancer immunology, immunotherapy : CII 16 22864395
2011 MAML1 regulates cell viability via the NF-κB pathway in cervical cancer cell lines. Experimental cell research 16 21640102
2021 Bone Marrow Mesenchymal Stem Cell-Derived Exosomal MicroRNA-133a Restrains Myocardial Fibrosis and Epithelial-Mesenchymal Transition in Viral Myocarditis Rats Through Suppressing MAML1. Nanoscale research letters 15 34215939
2018 MAML1 and TWIST1 co-overexpression promote invasion of head and neck squamous cell carcinoma. Asia-Pacific journal of clinical oncology 15 29333702
2018 Knockdown of MAML1 inhibits proliferation and induces apoptosis of T-cell acute lymphoblastic leukemia cells through SP1-dependent inactivation of TRIM59. Journal of cellular physiology 15 30370525
2017 Role of MAML1 and MEIS1 in Esophageal Squamous Cell Carcinoma Depth of Invasion. Pathology oncology research : POR 15 28462489
2004 Cloning and functional characterization of the murine mastermind-like 1 (Maml1) gene. Gene 13 15019995
2020 Soft tissue tumor with novel NR1D1-MAML1 fusion in a pediatric case. Virchows Archiv : an international journal of pathology 12 32474730
2023 NR1D1::MAML1 epithelioid and spindle cell sarcoma mimicking pseudomyogenic hemangioendothelioma in core biopsy: A case report and review of the literature. Genes, chromosomes & cancer 10 37326138
2021 Elucidated tumorigenic role of MAML1 and TWIST1 in gastric cancer is associated with Helicobacter pylori infection. Microbial pathogenesis 9 34818576
2020 MAML1-Dependent Notch-Responsive Genes Exhibit Differing Cofactor Requirements for Transcriptional Activation. Molecular and cellular biology 9 32179552
2017 Contribution of MAML1 in esophageal squamous cell carcinoma tumorigenesis. Annals of diagnostic pathology 8 28325367
2021 MAML1: a coregulator that alters endometrial epithelial cell adhesive capacity. Fertility research and practice 7 33773601
2023 MAML1-induced HPV E6 oncoprotein stability is required for cellular proliferation and migration of cervical tumor-derived cells. Journal of medical virology 6 36852660
2014 Arsenic-induced suppression of kidney cell proliferation and the transcriptional coregulator MAML1. Metallomics : integrated biometal science 5 24473123
2013 Snail inhibits Notch1 intracellular domain mediated transcriptional activation via competing with MAML1. Biochemical and biophysical research communications 4 23454378
2025 End Plate Chondrocyte-Derived Exosomal miR-133a-3p Alleviates Intervertebral Disc Degeneration by Targeting the NF-κB Signaling Pathway through the miR-133a-3p/MAML1 Axis. Molecular pharmaceutics 3 39898539
2020 First report of t(5;11) KMT2A-MAML1 fusion in de novo infant acute lymphoblastic leukemia. Cancer genetics 3 32992102
2022 Cottontail rabbit papillomavirus E6 proteins: Interaction with MAML1 and modulation of the Notch signaling pathway. Virology 2 36155393
2025 YAP-induced MAML1 cooperates with STAT3 to drive hepatocellular carcinoma progression. Experimental hematology & oncology 1 41345959
2026 CD4+ Tregs Drive Post-Ischemic Sprouting Angiogenesis via Endothelial YY1/MAML1 Reactivation. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 42159401
2026 Aberrant Phase Separation of Endothelial MAML1 Causes Congenital Heart Disease by Suppressing Notch Activity. Circulation 0 42246060
2025 [Danzhi Jiangtang Capsule improves renal vascular endothelial function in rats with diabetic nephropathy by downregulating the Notch1/NICD/MAML1 signaling pathway]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 0 41139455
2025 MAML1 drives Notch and Hedgehog oncogenic pathways by inhibiting Itch activity in triple-negative breast cancer. Cell death and differentiation 0 41272291

Missed literature

Know a paper Affinage missed for MAML1? Flag it for the maintainers and the community.

No submissions yet.