+ |
CSNK2A1 | down-regulates activity
phosphorylation
|
DNMT3A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-276650 |
Ser390 |
LFPVCHDsDESDTAK |
in vitro |
|
pmid |
sentence |
25066127 |
This modulation can be directly attributed to CK2-mediated phosphorylation of Dnmt3a. We also find that CK2-mediated phosphorylation is required for localization of Dnmt3a to heterochromatin. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-276649 |
Ser393 |
VCHDSDEsDTAKAVE |
in vitro |
|
pmid |
sentence |
25066127 |
This modulation can be directly attributed to CK2-mediated phosphorylation of Dnmt3a. We also find that CK2-mediated phosphorylation is required for localization of Dnmt3a to heterochromatin. |
|
Publications: |
2 |
Organism: |
In Vitro |
+ |
WT1 | up-regulates quantity by expression
transcriptional regulation
|
DNMT3A |
0.389 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255904 |
|
|
Homo sapiens |
|
pmid |
sentence |
23042785 |
Here, we show that Wilms' tumour 1 (WT1), a developmental master regulator that can also act as a tumour suppressor or oncoprotein, transcriptionally regulates the de novo DNA methyltransferase 3A (DNMT3A) and that cellular WT1 levels can influence DNA methylation of gene promoters genome-wide. we demonstrate that depletion of WT1 by short-interfering RNAs leads to reduced DNMT3A in Wilms' tumour cells and human embryonal kidney-derived cell lines. Chromatin immunoprecipitation assays demonstrate WT1 recruitment to the DNMT3A promoter region and reporter assays confirm that WT1 directly transactivates DNMT3A expression. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, Onco-fusion proteins in AML, miRNA in AML |
+ |
DNMT3A | down-regulates quantity by repression
transcriptional regulation
|
MEIS1 |
0.335 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256125 |
|
|
Homo sapiens |
|
pmid |
sentence |
28288143 |
Our results indicate that, in the absence of mixed lineage leukemia fusions, an alternative pathway for engaging an oncogenic MEIS1-dependent transcriptional program can be mediated by DNMT3A mutations.Under these circumstances, those AML patients carrying the alteration in the DNA methyltransferase would undergo a hypomethylation event at the MEIS1 promoter that would lead to the overexpression of this key oncogene in leukemia. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, AML_TRIPLETS, Triple mutant AML |
+ |
DNMT3A | form complex
binding
|
DNMT1/DNMT3A |
0.775 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-90842 |
|
|
Homo sapiens |
|
pmid |
sentence |
12145218 |
We show that the human de novo enzymes hdnmt3a and hdnmt3b form complexes with the major maintenance enzyme hdnmt1 /in vivo co-expression of hdnmt1 and hdnmt3a or hdnmt3b leads to methylation spreading in the genome, suggesting co-operation between de novo and maintenance enzymes during dna methylation |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
DNMT3A | down-regulates quantity by repression
transcriptional regulation
|
CDKN2C |
0.346 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261508 |
|
|
Homo sapiens |
|
pmid |
sentence |
26350239 |
Quantitative real-time PCR (qPCR) was used to investigate the effect of DNMT3A on p18INK4C expression, along with the other INK4 members, including p15INK4B, p16INK4A and p19INK4D. The results showed that the depletion of DNMT3A increased the transcriptional levels of the four members of the INK4 family |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
STAT5A | up-regulates quantity
transcriptional regulation
|
DNMT3A |
0.332 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255631 |
|
|
Homo sapiens |
|
pmid |
sentence |
26059451 |
… these data suggest that STAT5A positively regulates levels of DNMT3A, resulting in inactivation of tumor suppressor genes by epigenetic mechanisms in AML cells |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, miRNA in AML, AML_TRIPLETS, Triple mutant AML |
+ |
MECOM | up-regulates activity
binding
|
DNMT3A |
0.299 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-273432 |
|
|
|
|
pmid |
sentence |
21695170 |
The oncoprotein EVI1 and the DNA methyltransferase Dnmt3 co-operate in binding and de novo methylation of target DNA|Here we show that EVI1 physically interacts with DNA methyltransferases 3a and 3b (Dnmt3a/b), which are the only de novo DNA methyltransferases identified to date in mouse and man, and that it forms an enzymatically active protein complex that induces de novo DNA methylation in vitro. |
|
Publications: |
1 |
Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML |
+ |
DNMT3A | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255714 |
|
|
Homo sapiens |
|
pmid |
sentence |
27639498 |
The DNA methyltransferase 3 genes (DNMT3A and DNMT3B) encode methyltransferases that catalyze the addition of a methyl group to the cytosine residue of CpG dinucleotide; therefore they play an essential role in DNA methylation and gene silencing regulatory processes. DNMT3A function is involved in hematopoietic stem cells (HSCs) renewal and myeloid differentiation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, Onco-fusion proteins in AML, miRNA in AML, AML_TRIPLETS, Triple mutant AML |
+ |
DNMT3A | down-regulates quantity by repression
transcriptional regulation
|
CDKN2B |
0.355 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261509 |
|
|
Homo sapiens |
|
pmid |
sentence |
26350239 |
Quantitative real-time PCR (qPCR) was used to investigate the effect of DNMT3A on p18INK4C expression, along with the other INK4 members, including p15INK4B, p16INK4A and p19INK4D. The results showed that the depletion of DNMT3A increased the transcriptional levels of the four members of the INK4 family |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
DNMT3A | down-regulates quantity by repression
transcriptional regulation
|
CDKN2A |
0.388 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255809 |
|
|
Homo sapiens |
|
pmid |
sentence |
26350239 |
Quantitative real-time PCR (qPCR) was used to investigate the effect of DNMT3A on p18INK4C expression, along with the other INK4 members, including p15INK4B, p16INK4A and p19INK4D. The results showed that the depletion of DNMT3A increased the transcriptional levels of the four members of the INK4 family |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, Onco-fusion proteins in AML, Triple mutant AML |
+ |
miR-29b | down-regulates quantity by repression
post transcriptional regulation
|
DNMT3A |
0.4 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255927 |
|
|
Bos taurus |
|
pmid |
sentence |
28255176 |
Target prediction analysis revealed that ZNF423 was a potential target of bta-miR-23a. Dual-luciferase reporter assay revealed that bta-miR-23a directly targeted the 3′-UTR of ZNF423. |
|
Publications: |
1 |
Organism: |
Bos Taurus |
+ |
DNMT3A | down-regulates quantity by repression
transcriptional regulation
|
CDKN2D |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261510 |
|
|
Homo sapiens |
|
pmid |
sentence |
26350239 |
Quantitative real-time PCR (qPCR) was used to investigate the effect of DNMT3A on p18INK4C expression, along with the other INK4 members, including p15INK4B, p16INK4A and p19INK4D. The results showed that the depletion of DNMT3A increased the transcriptional levels of the four members of the INK4 family |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
DNMT3A | down-regulates quantity by repression
transcriptional regulation
|
HOXA9 |
0.346 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256128 |
|
|
Homo sapiens |
|
pmid |
sentence |
24280869 |
HOXA9 is significantly upregulated in both categories of DNMT3A modifications and this has been associated with poor prognosis in AML before (Figure 3d). In fact, almost the entire HOXA and HOXB cluster were significantly upregulated in AML samples with either epimutation or mutation in DNMT3A. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, Onco-fusion proteins in AML, AML_TRIPLETS, Triple mutant AML |
+ |
DNMT3A | down-regulates quantity by repression
transcriptional regulation
|
CCND1 |
0.485 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255808 |
|
|
Homo sapiens |
|
pmid |
sentence |
19786833 |
Based on one of these publications, we here showed that the interaction of Dnmt3a with c-myc promote the specific methylation of CG dinucleotides localized in c-myc boxes of promoter regions of CDKN2a, CCND1 and TIMP2 genes. Acellular experiments corroborated and complemented these results by revealing that the specificity of consensus sequence for DNA methylation of Dnmt3a is increased in presence of c-myc. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, AML_TRIPLETS, Triple mutant AML |
+ |
DNMT3A | down-regulates quantity by repression
transcriptional regulation
|
DPP6 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-268962 |
|
|
Mus musculus |
P-19 Cell |
pmid |
sentence |
23409053 |
In the absence of Dnmt3b, Dnmt3a was associated with Dpp6 gene promoter and regulated its expression and methylation in P19 cells. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
DNMT3A | down-regulates quantity by repression
transcriptional regulation
|
FGF21 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-262200 |
|
|
Homo sapiens |
|
pmid |
sentence |
29091029 |
Unbiased gene profiling studies revealed Fgf21 as a key negatively regulated Dnmt3a target gene in adipocytes with concordant changes in DNA methylation at the Fgf21 promoter region. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MYC | up-regulates activity
binding
|
DNMT3A |
0.701 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255806 |
|
|
Homo sapiens |
|
pmid |
sentence |
19786833 |
Based on one of these publications, we here showed that the interaction of Dnmt3a with c-myc promote the specific methylation of CG dinucleotides localized in c-myc boxes of promoter regions of CDKN2a, CCND1 and TIMP2 genes. Acellular experiments corroborated and complemented these results by revealing that the specificity of consensus sequence for DNA methylation of Dnmt3a is increased in presence of c-myc. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, miRNA in AML, AML_TRIPLETS, Triple mutant AML |
+ |
DNMT3A | down-regulates quantity by repression
transcriptional regulation
|
TIMP2 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255807 |
|
|
Homo sapiens |
|
pmid |
sentence |
19786833 |
Based on one of these publications, we here showed that the interaction of Dnmt3a with c-myc promote the specific methylation of CG dinucleotides localized in c-myc boxes of promoter regions of CDKN2a, CCND1 and TIMP2 genes. Acellular experiments corroborated and complemented these results by revealing that the specificity of consensus sequence for DNA methylation of Dnmt3a is increased in presence of c-myc. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |