| + |
KDM5A | up-regulates activity 
demethylation
|
H3C1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264299 |
Lys5 |
kQTARKST |
Homo sapiens |
|
| pmid |
sentence |
| 30246379 |
KDM5 subfamily is capable of removing tri‐ and di‐ methyl marks from lysine 4 on histone H3 (H3K4). Depending on the methylation site, its effect on transcription can be either activating or repressing. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KDM5A | up-regulates activity
demethylation
|
H3-3A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264301 |
Lys5 |
kQTARKST |
Homo sapiens |
|
| pmid |
sentence |
| 30246379 |
KDM5 subfamily is capable of removing tri‐ and di‐ methyl marks from lysine 4 on histone H3 (H3K4). Depending on the methylation site, its effect on transcription can be either activating or repressing. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KDM5A | up-regulates activity
demethylation
|
H3-4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264300 |
Lys5 |
kQTARKST |
Homo sapiens |
|
| pmid |
sentence |
| 30246379 |
KDM5 subfamily is capable of removing tri‐ and di‐ methyl marks from lysine 4 on histone H3 (H3K4). Depending on the methylation site, its effect on transcription can be either activating or repressing. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AKT1 | up-regulates activity
phosphorylation
|
KDM5A |
0.31 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-274059 |
Ser1255 |
CLTERAMsWQDRARQ |
in vitro |
|
| pmid |
sentence |
| 27292631 |
We immunoprecipitated ectopically expressed wild-type KDM5A or KDM5Amut5A and performed an in vitro kinase assay using recombinant AKT1 in the presence or absence of AKT inhibition.Wild-type KDM5A is phosphorylated by AKT1 and this modification is sensitive to AKT inhibition, whereas KDM5Amut5A is not phosphorylated in the presence of AKT1 (Figure 3C).These results suggest that AKT-mediated KDM5A phosphorylation enhances KDM5A promoter recruitment. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-274060 |
Ser225 |
TRRVKTQsESGDVSR |
in vitro |
|
| pmid |
sentence |
| 27292631 |
We immunoprecipitated ectopically expressed wild-type KDM5A or KDM5Amut5A and performed an in vitro kinase assay using recombinant AKT1 in the presence or absence of AKT inhibition.Wild-type KDM5A is phosphorylated by AKT1 and this modification is sensitive to AKT inhibition, whereas KDM5Amut5A is not phosphorylated in the presence of AKT1 (Figure 3C).These results suggest that AKT-mediated KDM5A phosphorylation enhances KDM5A promoter recruitment. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-274062 |
Ser287 |
RQRKGTLsVNFVDLY |
in vitro |
|
| pmid |
sentence |
| 27292631 |
We immunoprecipitated ectopically expressed wild-type KDM5A or KDM5Amut5A and performed an in vitro kinase assay using recombinant AKT1 in the presence or absence of AKT inhibition.Wild-type KDM5A is phosphorylated by AKT1 and this modification is sensitive to AKT inhibition, whereas KDM5Amut5A is not phosphorylated in the presence of AKT1 (Figure 3C).These results suggest that AKT-mediated KDM5A phosphorylation enhances KDM5A promoter recruitment. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-274063 |
Thr1225 |
SRRPRLEtILSLLVS |
in vitro |
|
| pmid |
sentence |
| 27292631 |
We immunoprecipitated ectopically expressed wild-type KDM5A or KDM5Amut5A and performed an in vitro kinase assay using recombinant AKT1 in the presence or absence of AKT inhibition.Wild-type KDM5A is phosphorylated by AKT1 and this modification is sensitive to AKT inhibition, whereas KDM5Amut5A is not phosphorylated in the presence of AKT1 (Figure 3C).These results suggest that AKT-mediated KDM5A phosphorylation enhances KDM5A promoter recruitment. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-274061 |
Thr285 |
QMRQRKGtLSVNFVD |
in vitro |
|
| pmid |
sentence |
| 27292631 |
We immunoprecipitated ectopically expressed wild-type KDM5A or KDM5Amut5A and performed an in vitro kinase assay using recombinant AKT1 in the presence or absence of AKT inhibition.Wild-type KDM5A is phosphorylated by AKT1 and this modification is sensitive to AKT inhibition, whereas KDM5Amut5A is not phosphorylated in the presence of AKT1 (Figure 3C).These results suggest that AKT-mediated KDM5A phosphorylation enhances KDM5A promoter recruitment. |
|
| Publications: |
5 |
Organism: |
In Vitro |
| + |
KDM5A | down-regulates 
binding
|
RBPJ/NOTCH |
0.395 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-219250 |
|
|
Drosophila melanogaster |
T-lymphocyte |
| pmid |
sentence |
| 20231316 |
In this study, we show that the histone demethylase kdm5a associated with rbp-j protein and is essential for notch/rbp-j target gene silencing in vitro. |
|
| Publications: |
1 |
Organism: |
Drosophila Melanogaster |
| Pathways: | NOTCH Signaling |
| + |
KDM5A | down-regulates quantity by destabilization
transcriptional regulation
|
PTEN |
0.296 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260079 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 31374292 |
The retinoblastoma binding protein 2 (RBP2) belongs to the KDM5 family, and is also known as JARID1A or KDM5A. We found that histone H3 lysine 4 (H3K4) demethylase RBP2 expression is negatively correlated with BCR-ABL expression, which suggests a regulatory link between these two genes. We also discovered that RBP2 mediates the dephosphorylation of BCR-ABL by directly downregulating PTEN expression, depending on histone demethylase activity, while PTEN targets protein phosphatase activity of BCR-ABL, a phosphatase which directly dephosphorylates BCR-ABL. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, BCR-ABL in AML |
| + |
KDM5A | up-regulates activity
demethylation
|
Histone H3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-265334 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30246379 |
KDM5 subfamily is capable of removing tri‚Äê and di‚Äê methyl marks from lysine 4 on histone H3 (H3K4). Depending on the methylation site, its effect on transcription can be either activating or repressing. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
KDM5A |
0.27 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271580 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32938217 |
To this end, we confirm that KDM3A, KDM4B, KDM4C, KDM5B, KDM5C, and KDM62 are direct targets of HIF-1a while extent the list of known targets to KDM2A, KDM2B, KDM4D, KDM5A, and KDM6A. The results demonstrated that majority of the KDMs were similarly induced (KDM2A, KDM2B, KDM3A, KDM4B, KDM4C, KDM4D, KDM5A, KDM5B, KDM5C, KDM6B, and KDM7A) or repressed (KDM NO66 and KDM1A) by both HIF-1a and HIF-2a. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HIF1A | up-regulates quantity by expression
transcriptional regulation
|
KDM5A |
0.278 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271565 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32938217 |
To this end, we confirm that KDM3A, KDM4B, KDM4C, KDM5B, KDM5C, and KDM62 are direct targets of HIF-1a while extent the list of known targets to KDM2A, KDM2B, KDM4D, KDM5A, and KDM6A. The results demonstrated that majority of the KDMs were similarly induced (KDM2A, KDM2B, KDM3A, KDM4B, KDM4C, KDM4D, KDM5A, KDM5B, KDM5C, KDM6B, and KDM7A) or repressed (KDM NO66 and KDM1A) by both HIF-1a and HIF-2a. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | NOTCH Signaling |
| + |
2-oxoglutarate(2-) | up-regulates activity
chemical activation
|
KDM5A |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273467 |
|
|
|
|
| pmid |
sentence |
| 29981745 |
Histone lysine demethylases (KDMs) are 2-oxoglutarate-dependent dioxygenases (2-OGDDs) that regulate gene expression by altering chromatin structure. |2-OG is a central intermediate of the Krebs cycle, where it is produced by isocitrate dehydrogenase (IDH) isoenzymes 2 and 3. |
|
| Publications: |
1 |
| Pathways: | Acute Myeloid Leukemia |
3.0
KDM5A
- 
- 