| + |
PIM1 | up-regulates quantity by stabilization 
phosphorylation
|
EPAS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277310 |
Ser435 |
GKAILPPsQPWATEL |
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 34211090 |
PIM1 kinase directly phosphorylates HIF-1α at threonine 455, a previously uncharacterized site within its oxygen-dependent degradation domain. This phosphorylation event disrupts the ability of prolyl hydroxylases to bind and hydroxylate HIF-1α, interrupting its canonical degradation pathway and promoting constitutive transcription of HIF-1 target genes. Moreover, phosphorylation of the analogous site in HIF-2α (S435) stabilizes the protein through the same mechanism, indicating post-translational modification within the oxygen-dependent degradation domain as a mechanism of regulating the HIF-α subunits. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK1 | up-regulates quantity by stabilization
phosphorylation
|
EPAS1 |
0.252 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277585 |
Ser484 |
SSCSTPNsPEDYYTS |
Homo sapiens |
Glioma Stem Cell |
| pmid |
sentence |
| 35191554 |
The activation of ERK1/2 upon hypoxia promoted HIF-2alpha phosphorylation, enhancing its interaction with USP33.Here, we identified USP33 as essential deubiquitinase that stabilizes HIF-2alpha protein in an ERK1/2-dependent manner to promote hypoxia response in cancer cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK3 | up-regulates quantity by stabilization
phosphorylation
|
EPAS1 |
0.263 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277584 |
Ser484 |
SSCSTPNsPEDYYTS |
Homo sapiens |
Glioma Stem Cell |
| pmid |
sentence |
| 35191554 |
The activation of ERK1/2 upon hypoxia promoted HIF-2alpha phosphorylation, enhancing its interaction with USP33.Here, we identified USP33 as essential deubiquitinase that stabilizes HIF-2alpha protein in an ERK1/2-dependent manner to promote hypoxia response in cancer cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
KDM3A |
0.268 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271583 |
|
|
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 |
| + |
EPAS1 | up-regulates quantity by expression 
transcriptional regulation
|
CACNA1A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264332 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15833863 |
A second hypoxia-responsive factor, HIF-2, can activate many of the same genes as HIF-1. Ten genes were preferentially activated by HIF-2alpha, including two (CACNA1A and PTPRZ1) implicated in neurologic diseases. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
KDM7A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271587 |
|
|
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 |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
KDM4B |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271584 |
|
|
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 |
| + |
HIF3A | down-regulates quantity by repression 
transcriptional regulation
|
EPAS1 |
0.508 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261616 |
|
|
Homo sapiens |
HEP-3B Cell |
| pmid |
sentence |
| 21479871 |
None of the long HIF-3α variants was capable of efficient induction of an HRE reporter in overexpression experiments, but instead inhibited the transcriptional activation of the reporter by HIF-1 and HIF-2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
KDM5B |
0.288 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271578 |
|
|
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 |
| + |
EPAS1 | down-regulates quantity by repression
transcriptional regulation
|
KDM1A |
0.283 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271588 |
|
|
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 |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
PTPRZ1 |
0.266 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264333 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 15833863 |
A second hypoxia-responsive factor, HIF-2, can activate many of the same genes as HIF-1. Ten genes were preferentially activated by HIF-2alpha, including two (CACNA1A and PTPRZ1) implicated in neurologic diseases. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
KDM5A |
0.269 |
| 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 |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
KDM2B |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271582 |
|
|
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 |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
KDM5C |
0.282 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271579 |
|
|
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 |
| + |
EPAS1 | down-regulates activity
binding
|
AP1 |
0.351 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269042 |
|
|
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 24383088 |
Co-transfection experiments revealed that HIF-2α had greater potency on the GLIS1 promoter activation than HIF-1α. Subsequent studies using wild-type and mutant HIF-2α demonstrated that DNA binding activity was not necessary but TADs were critical for GLIS1 induction. Finally, co-transfection experiments indicated that HIF-2α cooperated with AP-1 family members in upregulating GLIS1 transcription. These results suggest that the hypoxic signaling pathway may play a pivotal role in regulating the reprogramming factor GLIS1, via non-canonical mechanisms involving partner transcription factor rather than by direct HIF transactivation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
KDM2A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271581 |
|
|
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 |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
KDM6B |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271586 |
|
|
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 |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
HBB |
0.289 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251791 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20534544 |
We used genomic and candidate gene approaches to search for evidence of such genetic selection. First, a genome-wide allelic differentiation scan (GWADS) comparing indigenous highlanders of the Tibetan Plateau (3,200-3,500 m) with closely related lowland Han revealed a genome-wide significant divergence across eight SNPs located near EPAS1. This gene encodes the transcription factor HIF2alpha, which stimulates production of red blood cells and thus increases the concentration of hemoglobin in blood. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
HBA1 |
0.25 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251792 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20534544 |
We used genomic and candidate gene approaches to search for evidence of such genetic selection. First, a genome-wide allelic differentiation scan (GWADS) comparing indigenous highlanders of the Tibetan Plateau (3,200-3,500 m) with closely related lowland Han revealed a genome-wide significant divergence across eight SNPs located near EPAS1. This gene encodes the transcription factor HIF2alpha, which stimulates production of red blood cells and thus increases the concentration of hemoglobin in blood. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
EPAS1 | up-regulates quantity by expression
transcriptional regulation
|
KDM4C |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271585 |
|
|
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 |
3.0
EPAS1
- 
- 