| + |
DOT1L |
methylation
|
H3C1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267141 |
Lys80 |
REIAQDFkTDLRFQS |
Homo sapiens |
|
| pmid |
sentence |
| 12123582 |
HDOT1L Is a Nucleosomal H3-K79-Specific HMTase. We identified a human DOT1-like (DOT1L) protein and demonstrated that this protein possesses intrinsic H3-K79-specific histone methyltransferase (HMTase) activity in vitro and in vivo. Furthermore, we found that K79 methylation level is regulated throughout the cell cycle. By using two different methods, we demonstrate that the K79 methylation level decreases during S phase, reaches its lowest level in G2, increases during M phase, and maintains at a high level during G1 phase. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DOT1L |
methylation
|
H3-3A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267143 |
Lys80 |
REIAQDFkTDLRFQS |
Homo sapiens |
|
| pmid |
sentence |
| 12123582 |
HDOT1L Is a Nucleosomal H3-K79-Specific HMTase. We identified a human DOT1-like (DOT1L) protein and demonstrated that this protein possesses intrinsic H3-K79-specific histone methyltransferase (HMTase) activity in vitro and in vivo. Furthermore, we found that K79 methylation level is regulated throughout the cell cycle. By using two different methods, we demonstrate that the K79 methylation level decreases during S phase, reaches its lowest level in G2, increases during M phase, and maintains at a high level during G1 phase. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DOT1L |
methylation
|
H3-4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267142 |
Lys80 |
REIAQDFkTDLRFQS |
Homo sapiens |
|
| pmid |
sentence |
| 12123582 |
HDOT1L Is a Nucleosomal H3-K79-Specific HMTase. We identified a human DOT1-like (DOT1L) protein and demonstrated that this protein possesses intrinsic H3-K79-specific histone methyltransferase (HMTase) activity in vitro and in vivo. Furthermore, we found that K79 methylation level is regulated throughout the cell cycle. By using two different methods, we demonstrate that the K79 methylation level decreases during S phase, reaches its lowest level in G2, increases during M phase, and maintains at a high level during G1 phase. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DOT1L | down-regulates quantity by repression 
transcriptional regulation
|
MYCBP2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267151 |
|
|
Homo sapiens |
LNCaP Cell |
| pmid |
sentence |
| 32814769 |
Overexpression of DOT1L decreased the expression of HECTD4 and MYCBP2 in LNCaP, C42B, and 22rv1 cells (Supplementary Fig. 5c), suggesting that DOT1L plays a role in repressing these targets either directly or indirectly. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DOT1L | up-regulates quantity by expression 
transcriptional regulation
|
MCL1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255881 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27856324 |
Previously, we found that MLL-AF4 binds to the BCL-2 gene and directly activates it through DOT1L recruitment and increased H3K79me2/3 levels. MLL-AF4 directly controls the active transcription of both BCL-2 and MCL-1 […]. Of all the BCL-2 family members, only BCL-2 and MCL-1 are directly activated by MLL-AF4. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
| + |
MLL-AF4 | up-regulates activity 
binding
|
DOT1L |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255882 |
|
|
Homo sapiens |
B-cell Leukemia Cell |
| pmid |
sentence |
| 27856324 |
Previously, we found that MLL-AF4 binds to the BCL-2 gene and directly activates it through DOT1L recruitment and increased H3K79me2/3 levels. MLL-AF4 directly controls the active transcription of both BCL-2 and MCL-1 […]. Of all the BCL-2 family members, only BCL-2 and MCL-1 are directly activated by MLL-AF4. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255871 |
|
|
Homo sapiens |
Pre-B-lymphocyte |
| pmid |
sentence |
| 18977325 |
Recent studies have identified association of multiple MLL-fusion partners including AF4, AF9, and AF10 with DOT1L, a histone H3K79 methyltransferase.This leads to a model where MLL-AF4 recruits DOT1L to MLL target genes, and promotes methylation of H3K79 at loci with existing H3K4 methylation (i.e., by wildtype MLL or other H3K4 methyltransferases) thus stimulating transcriptional elongation of genes that are normally primed but not fully transcribed. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
| + |
MLL Fusion | up-regulates activity
binding
|
DOT1L |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260095 |
|
|
Homo sapiens |
Pre-B-lymphocyte |
| pmid |
sentence |
| 18977325 |
Recent studies have identified association of multiple MLL-fusion partners including AF4, AF9, and AF10 with DOT1L, a histone H3K79 methyltransferase.This leads to a model where MLL-AF4 recruits DOT1L to MLL target genes, and promotes methylation of H3K79 at loci with existing H3K4 methylation (i.e., by wildtype MLL or other H3K4 methyltransferases) thus stimulating transcriptional elongation of genes that are normally primed but not fully transcribed. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, MLL fusion protein in AML |
| + |
DOT1L | up-regulates activity
binding
|
MYC |
0.342 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-239362 |
|
|
Homo sapiens |
MCF-10A Cell |
| pmid |
sentence |
| 26199140 |
Our data suggest that the c-Myc-dependent transcriptional switch is modulated by DOT1L, as in the presence of DOT1L c-Myc preferentially forms an active complex with p300 rather than a repressive complex containing HDAC1 and DNMT1 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
| + |
DOT1L | down-regulates quantity by repression
transcriptional regulation
|
HECTD4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267150 |
|
|
Homo sapiens |
LNCaP Cell |
| pmid |
sentence |
| 32814769 |
Overexpression of DOT1L decreased the expression of HECTD4 and MYCBP2 in LNCaP, C42B, and 22rv1 cells (Supplementary Fig. 5c), suggesting that DOT1L plays a role in repressing these targets either directly or indirectly. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DOT1L | up-regulates quantity by expression
transcriptional regulation
|
HOXA9 |
0.461 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256141 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20854876 |
Inhibition of EAP components pTEFb and Dot1l show that both contribute significantly to activation of Hoxa9 and Meis1 expression. EAP is dynamically associated with the Hoxa9 and Meis1 loci in hematopoietic cells and rapidly dissociates during induction of differentiation. In the presence of MLL fusion proteins, its dissociation is prevented. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, MLL fusion protein in AML |
| + |
DOT1L | up-regulates quantity by expression
transcriptional regulation
|
MEIS1 |
0.411 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256143 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20854876 |
Inhibition of EAP components pTEFb and Dot1l show that both contribute significantly to activation of Hoxa9 and Meis1 expression. EAP is dynamically associated with the Hoxa9 and Meis1 loci in hematopoietic cells and rapidly dissociates during induction of differentiation. In the presence of MLL fusion proteins, its dissociation is prevented. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
| + |
DOT1L | up-regulates quantity by expression
transcriptional regulation
|
BCL2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255880 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27856324 |
Previously, we found that MLL-AF4 binds to the BCL-2 gene and directly activates it through DOT1L recruitment and increased H3K79me2/3 levels. MLL-AF4 directly controls the active transcription of both BCL-2 and MCL-1 […]. Of all the BCL-2 family members, only BCL-2 and MCL-1 are directly activated by MLL-AF4. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
| + |
MLL-ENL | up-regulates activity
binding
|
DOT1L |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255870 |
|
|
Mus musculus |
Bone Marrow Stem Cell |
| pmid |
sentence |
| 23996074 |
In this work, we have identified and mapped the protein-protein interaction site between DOT1L and MLL fusion proteins, AF9 and ENL. The MLL fusion proteins, AF9 and ENL, activate target genes in part via recruitment of the histone methyltransferase DOT1L (disruptor of telomeric silencing 1-like). It is known that the recruitment of DOT1L results in hypermethylation of H3K79 on the prominent MLL fusion downstream target loci Hoxa9 and Meis1 |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
| + |
MLL-AF9 | up-regulates activity
binding
|
DOT1L |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255869 |
|
|
Mus musculus |
Bone Marrow Stem Cell |
| pmid |
sentence |
| 23996074 |
In this work, we have identified and mapped the protein-protein interaction site between DOT1L and MLL fusion proteins, AF9 and ENL.The MLL fusion proteins, AF9 and ENL, activate target genes in part via recruitment of the histone methyltransferase DOT1L (disruptor of telomeric silencing 1-like). It is known that the recruitment of DOT1L results in hypermethylation of H3K79 on the prominent MLL fusion downstream target loci Hoxa9 and Meis1 |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
3.0
DOT1L
- 
- 