+ |
PRKCA | up-regulates
phosphorylation
|
NKX3-1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-86723 |
Ser48 |
RQGGRTSsQRQRDPE |
Homo sapiens |
Prostate Gland Cancer Cell |
pmid |
sentence |
11980664 |
Phosphorylation of wild-type nkx3.1 decreased the apparent binding affinity of the protein for the consensus sequence by 3-fold relative to the nonphosphorylated protein (fig. 3) _ . |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ATM | down-regulates quantity by destabilization
phosphorylation
|
NKX3-1 |
0.371 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-276499 |
Thr134 |
SRAAFSHtQVIELER |
Homo sapiens |
HEK-293T Cell |
pmid |
sentence |
23890999 |
ATM phosphorylates NKX3.1 on T166 and then T134, resulting in NKX3.1 ubiquitination and degradation resulting from an apparent regulatory interaction. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-276500 |
Thr166 |
KNLKLTEtQVKIWFQ |
Homo sapiens |
HEK-293T Cell |
pmid |
sentence |
23890999 |
ATM phosphorylates NKX3.1 on T166 and then T134, resulting in NKX3.1 ubiquitination and degradation resulting from an apparent regulatory interaction. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
PTEN | up-regulates quantity by stabilization
dephosphorylation
|
NKX3-1 |
0.455 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-277026 |
Thr179 |
FQNRRYKtKRKQLSS |
Homo sapiens |
|
pmid |
sentence |
31213464 |
Loss of PTEN Accelerates NKX3.1 Degradation to Promote Prostate Cancer Progression.|PTEN was also able to dephosphorylate NKX3.1 at threonine 179, a target of protein kinase C, but not threonine residues 89 and 93, targeted by casein kinase 2 . |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Prostate Cancer |
+ |
CSNK2A2 | up-regulates
phosphorylation
|
NKX3-1 |
0.321 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-145501 |
Thr89 |
AAPEEAEtLAETEPE |
Homo sapiens |
Prostate Gland Cancer Cell |
pmid |
sentence |
16581776 |
In vitro kinase assays followed by mass spectrometric analyses demonstrated that ck2 phosphorylated recombinant nkx3.1 on thr89 and thr93. We have also determined that nkx3.1 is degraded primarily through a proteasomal pathway, suggesting that phosphorylation by ck2 protects nkx3.1 from degradation. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-145505 |
Thr93 |
EAETLAEtEPERHLG |
Homo sapiens |
Prostate Gland Cancer Cell |
pmid |
sentence |
16581776 |
In vitro kinase assays followed by mass spectrometric analyses demonstrated that ck2 phosphorylated recombinant nkx3.1 on thr89 and thr93. We have also determined that nkx3.1 is degraded primarily through a proteasomal pathway, suggesting that phosphorylation by ck2 protects nkx3.1 from degradation. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
NKX3-1 | down-regulates activity
binding
|
HDAC1 |
0.376 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251549 |
|
|
Homo sapiens |
|
pmid |
sentence |
16697957 |
NKX3.1 also binds HDAC1 and releases p53 from p53-MDM2-HDAC1 complex, promoting p53 acetylation and activity. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Prostate Cancer |
+ |
NKX3-1 | up-regulates quantity by stabilization
|
TP53 |
0.364 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251548 |
|
|
Homo sapiens |
|
pmid |
sentence |
16697957 |
NKX3.1 stabilizes p53.NKX3.1 can physically associate with HDAC1 and promotes p53 acetylation by recruiting HDAC1 from p53-MDM2-HDAC1 complex |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Prostate Cancer |
+ |
NKX3-1 | form complex
binding
|
NKX3-1/SRF |
0.405 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-82087 |
|
|
Homo sapiens |
|
pmid |
sentence |
10993896 |
A novel complex element containing a juxtaposed nkx-binding site (nke) and an srf-binding element (sre) in the proximal promoter region was found to be necessary for the nkx3-1/srf coactivation of smga transcription. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Muscle, Smooth Muscle |
+ |
AR | up-regulates quantity by expression
transcriptional regulation
|
NKX3-1 |
0.518 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251546 |
|
|
Homo sapiens |
|
pmid |
sentence |
16697957 |
Whereas androgen receptor (AR) positively regulates NKX3.1 expression, NKX3.1 negatively modulates AR transcription and consequently the AR-associated signaling events. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Prostate Cancer |
+ |
NKX3-1 | up-regulates quantity by expression
transcriptional regulation
|
ACTG2 |
0.291 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254619 |
|
|
Homo sapiens |
|
pmid |
sentence |
19797053 |
These results demonstrate the ability of MYOCD to discriminate among several juxtaposed CArG elements, presumably through its novel partnership with NKX3.1, to optimally transactivate the human ACTG2 promoter. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
NKX3-1 | down-regulates quantity by repression
transcriptional regulation
|
AR |
0.518 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251547 |
|
|
Homo sapiens |
|
pmid |
sentence |
16697957 |
Whereas androgen receptor (AR) positively regulates NKX3.1 expression, NKX3.1 negatively modulates AR transcription and consequently the AR-associated signaling events. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Prostate Cancer |
+ |
NKX3-1 | down-regulates activity
|
AKT |
0.503 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251552 |
|
|
Homo sapiens |
|
pmid |
sentence |
16697957 |
NKX3.1 negatively regulates AKT activity in an AR-dependent manner |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Prostate Cancer |
+ |
ERG | down-regulates quantity by repression
transcriptional regulation
|
NKX3-1 |
0.342 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251556 |
|
|
Homo sapiens |
|
pmid |
sentence |
25277175 |
Increased expression of ERG or other ETS factors under control of androgen responsive promoter (TMPRSS2) is an inevitable consequence of the fusion events, and it activates transcriptional program that contributes to oncogenesis by upregulating expression of, among others, MYC, EZH2 and SOX9 and repressing NKX3. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Prostate Cancer |