| + |
MAP2K1 | up-regulates quantity by stabilization 
phosphorylation
|
TET2 |
0.249 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277891 |
Ser1107 |
VLNNFIEsPSKLLDT |
Homo sapiens |
HCC-827 Cell |
| pmid |
sentence |
| 38461173 |
TET2 was stabilized by MEK1 phosphorylation at Ser 1107, while MEK1 inactivation promoted its proteasome degradation by enhancing the recruitment of CUL7FBXW11. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AMPK | up-regulates quantity by stabilization
phosphorylation
|
TET2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256135 |
Ser99 |
GGIKRTVsEPSLSGLL |
Homo sapiens |
Peripheral Blood Mononuclear Cell |
| pmid |
sentence |
| 30022161 |
We identify the tumour suppressor TET2 as a substrate of the AMP-activated kinase (AMPK), which phosphorylates TET2 at serine 99, thereby stabilizing the tumour suppressor. Increased glucose levels impede AMPK-mediated phosphorylation at serine 99, which results in the destabilization of TET2 followed by dysregulation of both 5-hydroxymethylcytosine (5hmC) and the tumour suppressive function of TET2 in vitro and in vivo |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, IDH-TET in AML, NPM1_new |
| + |
PRKAA1 | up-regulates quantity by stabilization
phosphorylation
|
TET2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256134 |
Ser99 |
GGIKRTVsEPSLSGLL |
Homo sapiens |
Peripheral Blood Mononuclear Cell |
| pmid |
sentence |
| 30022161 |
We identify the tumour suppressor TET2 as a substrate of the AMP-activated kinase (AMPK), which phosphorylates TET2 at serine 99, thereby stabilizing the tumour suppressor. Increased glucose levels impede AMPK-mediated phosphorylation at serine 99, which results in the destabilization of TET2 followed by dysregulation of both 5-hydroxymethylcytosine (5hmC) and the tumour suppressive function of TET2 in vitro and in vivo |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FGFR3 | down-regulates quantity by destabilization 
phosphorylation
|
TET2 |
0.253 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277535 |
Tyr1902 |
TRISLVFyQHKSMNE |
Homo sapiens |
HEp-2 Cell |
| pmid |
sentence |
| 33097695 |
FGFR3∆7-9, but not wild-type FGFR3, directly interacts with TET2 and phosphorylates TET2 at Y1902 site, leading to the ubiquitination and proteasome-mediated degradation of TET2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JAK2 | up-regulates activity
phosphorylation
|
TET2 |
0.428 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277290 |
Tyr1939 |
CEKYGPDyVPQKSHG |
in vitro |
|
| pmid |
sentence |
| 30944118 |
Specifically, cytokine receptor-associated JAK2 phosphorylates TET2 at tyrosines 1939 and 1964. Phosphorylated TET2 interacts with the erythroid transcription factor KLF1, and this interaction with TET2 is increased upon exposure to erythropoietin. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277289 |
Tyr1964 |
HETSEPTyLRFIKSL |
in vitro |
|
| pmid |
sentence |
| 30944118 |
Specifically, cytokine receptor-associated JAK2 phosphorylates TET2 at tyrosines 1939 and 1964. Phosphorylated TET2 interacts with the erythroid transcription factor KLF1, and this interaction with TET2 is increased upon exposure to erythropoietin. |
|
| Publications: |
2 |
Organism: |
In Vitro |
| Pathways: | Acute Myeloid Leukemia |
| + |
TET2 | up-regulates
binding
|
OGT |
0.455 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-200695 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23353889 |
Tet2 and tet3 associate with the o_glcnac transferase ogt / tet2 and tet3 promote ogt_mediated glcnacylation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
2-oxoglutarate(2-) | up-regulates activity
binding
|
TET2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255706 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25699704 |
A second group of AML patients (15%–33% of all cases) harbor mutations in either the isocitrate dehydrogenase (IDH) 1 or 2 gene (Shih et al., 2012). These enzymes produce α-ketoglutarate (α-KG), which is required for TET activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, AML-IDH/TET, IDH-TET in AML, NPM1_new |
| + |
miR-29b | down-regulates quantity by repression
post transcriptional regulation
|
TET2 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256310 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18568019 |
In leukaemic cell lines PLZF overexpression downmodulated miR-146a and upregulated CXCR4 protein, whereas PLZF knockdown induced the opposite effects. Our data indicate that megakaryopoiesis is controlled by a cascade pathway, in which PLZF suppresses miR-146a transcription and thereby activates CXCR4 translation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
miR-29c | down-regulates quantity by repression
post transcriptional regulation
|
TET2 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268854 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22983574 |
Transcriptional regulation of miR-10a/b by TWIST-1 in myelodysplastic syndromes |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
(R)-2-hydroxyglutarate(2-) | down-regulates activity
chemical inhibition
|
TET2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261829 |
|
|
Homo sapiens |
Acute Myeloid Leukemia Cell Line |
| pmid |
sentence |
| 29090344 |
Various studies have tried to investigate how the accumulation of R2-HG promotes leukemogenesis in cooperation with other frequently observed mutations in AML. An important role appears to be the ability of R2-HG to competitively inhibit multiple αKG-dependent dioxygenases. While TET2 normally catalyzes the conversion of 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC), inhibition of TET2 by R2-HG has been found to result in a hypermethylated gene signature in HSPCs, which overlaps with the signatures of both IDH and TET2-mutated leukemic cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AMPK | up-regulates activity
phosphorylation
|
TET2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260097 |
|
|
Homo sapiens |
U-937 Cell |
| pmid |
sentence |
| 31900833 |
Inactivation of AMPK suppressed the expression of ten-eleven translocation methylcytosine dioxygenase 2 (TET2) in tumor cells. Compound C-induced AMPK suppression causes downregulation TET2 and FOXP3 expression, leading to death of parental and HQ-selected U937 cells. These results confirm the connection of AMPK with the TET2–FOXP3 axis in modulating the survival of AML cells and suggest that suppression of the AMPK–TET2–FOXP3 axis suppresses the progression of AML and HQ-induced malignant transformation of AML cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, IDH-TET in AML, NPM1_new |
| + |
TET2 | up-regulates activity
binding
|
WT1 |
0.459 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255703 |
|
|
Homo sapiens |
KG-1 Cell, HL-60 Cell |
| pmid |
sentence |
| 25601757 |
In this study, we demonstrate that WT1 binds directly to TET2 and recruits TET2 to specific genomic sites to regulate the expression of WT1 target genes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | AML-IDH/TET, Acute Myeloid Leukemia, DNMT3A in AML, AML-IDH/TET, IDH-TET in AML, miRNA in AML, NPM1_new |
| + |
ASXL2 | up-regulates quantity by expression 
transcriptional regulation
|
TET2 |
0.343 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260074 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 28516957 |
Interestingly, this identified a number of genes known to promote leukemogenesis (either alone or in the context of AML1-ETO leukemia) as differentially expressed by ASXL2 loss. These include downregulation of TET2 as well as NOTCH2 with ASXL2 loss in human AML1-ETO-expressing cells, downregulation of which have been previously shown to functionally promote myeloid leukemogenesis when altered in expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, IDH-TET in AML |
| + |
miR-29a | down-regulates quantity by repression
post transcriptional regulation
|
TET2 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264703 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 17994015 |
Here, we show that MeCP2 levels are repressed by miR132, a brain-enriched microRNA (miRNA). We propose that the interaction of miR132 with its miRNA recognition element (MRE) in the MeCP2 3′ UTR prevents MeCP2 levels from becoming deleteriously high during neuronal maturation. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| Pathways: | Rett syndrome |
| + |
TET2 | down-regulates 
|
Proliferation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255704 |
|
|
Homo sapiens |
HL-60 Cell |
| pmid |
sentence |
| 25601757 |
Cell proliferation was stimulated by the knockdown of either TET2 or WT1 gene in KG-1 cells, but not additively by the co-depletion of both genes. Collectively, these results suggest that TET2 and WT1 function in the same pathway to inhibit leukemia cell proliferation and colony formation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | AML-IDH/TET, Acute Myeloid Leukemia, DNMT3A in AML, AML-IDH/TET, IDH-TET in AML, miRNA in AML, NPM1_new |
3.0
TET2
- 
- 