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BCL6 inhibits transcription by competing for the Notch1 intracellular domain, preventing the coactivator Mastermind-like1 (MAM1) from binding.
XMam1 has the ability to induce the cell fate into the neurogenic lineage in a Notch-independent manner
The present study shows a new role for Maml1 as a component of Shh signaling, which plays a crucial role in both development and tumorigenesis.
Similar phenotypes were observed by conditionally misexpressing a dominant negative form of MAML1 in Mitral cells ( MCs)after their migration. Furthermore, the intracellular domain of Notch1 (NICD1) was localized to nuclei of MCs. These findings suggest that Notch signaling at embryonic stages is involved in the dendritic complexity of MCs
These observations suggest that chondrocyte maturation was impaired in MAML1(-/-) mice. MAML1 enhances the transcriptional activity of Runx2 and plays a role in bone development.
This study demonstrated that targeting Maml1-induced tumor cell senescence and differentiation may alter the tumor microenvironment and cytokine and chemokine profiles and may also promote innate and adaptive immune cell infiltration and function.
Maml-mediated Notch signaling plays a pivotal role in the initiation and maintenance of goblet cell differentiation for normal ocular surface morphogenesis.
Mastermind-like 1 (MamL1) and mastermind-like 3 (MamL3) are essential for Notch signaling in vivo.
Data demonstrate that Mesp2 potently represses Notch signaling by inducing the destabilization of mastermind-like 1, a core regulator of this pathway.
MAML1 is a novel modulator for NF-kappaB signaling and regulates cellular survival.
There seems to be close correlation of the spatial and temporal expression of Maml1, in the central nervous system (CNS) during early development, implicating a role for the Maml1 gene in neurogenesis.
a dominant negative mutant of MAML1 resulted in early inhibition of T-cell development and the appearance of intrathymic B cells, phenotypes consistent with Notch1 inhibition
MAML1 acts as a coactivator for MEF2C transcription and is essential for proper muscle development
Mam-1 is required to some extent for Notch-dependent stages in lymphopoiesis, thus supporting the notion that Mam is an essential component of the canonical Notch pathway in mammals.
Maml1 is specifically required for Notch2 signaling in marginal zone B cells.
These new findings suggest an oncogenic role for concomitant expression of MAML1 and TWIST1 genes in head and neck squamous cell carcinoma invasion and metastasis
Our results showed that MEIS1 may have a negative role in regulation of MAML1expression during the esophageal squamous cell carcinoma progression.
The divergence of E6 proteins from either MAML1 or E6AP binding preference is a major event in papillomavirus evolution.
Authors report that p300 and CBP acetylate Mastermind-like 1 (Maml1) on amino acid residues K188 and K189 to recruit NACK to the Notch1 ternary complex, which results in the recruitment of RNA polymerase II to initiate transcription.
Overexpression of Mastermind like1 was detected in 59% of tumor samples
MAML1 may play an important role in tumor progression of Hepatocellular Carcinoma.
Notch signaling was altered in almost half of the clear-cell renal cell carcinoma patients and copy number variances in MAML1 and KAT2B were predominant changes.
The transcriptional coregulator MAML1 affects DNA methylation and gene expression patterns in human embryonic kidney cells.
MMAL1 overexpression is associated with Esophageal Squamous Cell Carcinoma.
study identifies that MAML1 is ubiquitinated in the absence of Notch signaling to maintain low levels of MAML1 in the cell
In MCF-7 cells p53 associates with the Notch transcriptional complex (NTC) in a MAML1-dependent fashion, most likely through a p53-MAML1 interaction.
The impact of MAML1 genetic variants to heart rate was discovered.
Data indicate that EpCAM, CK19, and hMAM triple-marker-positive circulating tumor cells (CTCs) were detected in 86 of 98 (87.8 %) patients.
Snail decreased transcription of Notch1 intracellular domain (NICD) target genes via competing with MAML1, co-activator, in NICD complex.
Authors report that human papillomavirus type 8 E6 subverts NOTCH activation during keratinocyte differentiation by inhibiting RBPJ/MAML1 transcriptional activator complexes at NOTCH target DNA.
Bioinformatics assessment revealed a correlation between p300, EGR1 and MAML1 copy number and mRNA alterations in renal clear cell carcinoma and p300, EGR1 and MAML1 gene alterations were associated with increased overall survival.
MAML1 is best known as the co-activator and effector of NOTCH-induced transcription, and BPV-1 E6 represses synthetic NOTCH-responsive promoters, endogenous NOTCH-responsive promoters, and is found in a complex with MAML1 in stably transformed cells
Overexpression of MAML-1 and Twist1 were significantly associated with lymph node metastasis and the surgical staging of tumor
Association of CSL with NICD exerts remarkably little effect on the exchange kinetics of the ANK domain, whereas MAML1 binding greatly retards the exchange kinetics of ANK repeats 2-3.
This protein is the human homolog of mastermind, a Drosophila protein that plays a role in the Notch signaling pathway involved in cell-fate determination. There is in vitro evidence that the human homolog forms a complex with the intracellular portion of human Notch receptors and can increase expression of a Notch-induced gene. This evidence supports its proposed function as a transcriptional co-activator in the Notch signaling pathway.
, mastermind-like 1
, mastermind-like protein 1
, mastermind homolog