| + |
HIPK2 |
phosphorylation
|
PDX1 |
0.361 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255539 |
Ser268 |
LPPGLSAsPQPSSVA |
Mus musculus |
Pancreatic Beta Cell, MIN-6 Cell |
| pmid |
sentence |
| 20637728 |
Our results suggest that HIPK2-mediated phosphorylation of PDX1 at Ser-269 might be a regulatory mechanism connecting signals generated by changes in extracellular glucose concentration to downstream effectors via changes in subnuclear localization of PDX1, thereby influencing islet cell differentiation and function |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
GSK3B | down-regulates quantity 
phosphorylation
|
PDX1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255566 |
Ser268 |
LPPGLSAsPQPSSVA |
Mus musculus |
MIN-6 Cell |
| pmid |
sentence |
| 19833727 |
We show that glucose levels modulate PDX1 protein phosphorylation at a novel C-terminal GSK3 consensus that maps to serines 268 and 272. A decrease in glucose levels triggers increased turnover of the PDX1 protein in a GSK3-dependent manner, such that PDX1 phosphomutants are refractory to the destabilizing effect of low glucose |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255567 |
Ser272 |
LSASPQPsSVAPRRP |
Mus musculus |
MIN-6 Cell |
| pmid |
sentence |
| 19833727 |
We show that glucose levels modulate PDX1 protein phosphorylation at a novel C-terminal GSK3 consensus that maps to serines 268 and 272. A decrease in glucose levels triggers increased turnover of the PDX1 protein in a GSK3-dependent manner, such that PDX1 phosphomutants are refractory to the destabilizing effect of low glucose |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255543 |
Ser61 |
LGALEQGsPPDISPY |
Mus musculus |
Pancreatic Beta Cell, MIN-6 Cell |
| pmid |
sentence |
| 16407209 |
Here we show that a minor portion of IPF1/PDX1 is phosphorylated on serine 61 and/or serine 66 in pancreatic beta-cells. This phosphorylated form of IPF1/PDX1 preferentially accumulates following proteasome inhibition, an effect that is prevented by inhibition of glycogen synthase kinase 3 (GSK3) activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255544 |
Ser66 |
QGSPPDIsPYEVPPL |
Mus musculus |
Pancreatic Beta Cell, MIN-6 Cell |
| pmid |
sentence |
| 16407209 |
Here we show that a minor portion of IPF1/PDX1 is phosphorylated on serine 61 and/or serine 66 in pancreatic beta-cells. This phosphorylated form of IPF1/PDX1 preferentially accumulates following proteasome inhibition, an effect that is prevented by inhibition of glycogen synthase kinase 3 (GSK3) activity. |
|
| Publications: |
4 |
Organism: |
Mus Musculus |
| Pathways: | Insulin Signaling |
| + |
PRKDC | down-regulates quantity by destabilization
phosphorylation
|
PDX1 |
0.311 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-225542 |
Thr11 |
EEQYYAAtQLYKDPC |
Mus musculus |
|
| pmid |
sentence |
| 16166097 |
The interaction of PDX-1 with Ku subunits and its phosphorylation on threonine 11 by the DNA-PK appear to be implicated in its degradation by the proteosome. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
SPOP | down-regulates quantity
ubiquitination
|
PDX1 |
0.331 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268859 |
|
|
Mus musculus |
Pancreatic Beta Cell |
| pmid |
sentence |
| 20811152 |
Pdx1 C terminus-interacting factor-1 (Pcif1, also known as SPOP) is a nuclear protein that inhibits Pdx1 transactivation. Here, we show that Pcif1 targets Pdx1 for ubiquitination and proteasomal degradation. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
PDX1 | up-regulates quantity by expression 
transcriptional regulation
|
NKX6-1 |
0.481 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255542 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 11309388 |
In conclusion, Pdx1 confers the expression of pancreatic β-cell-specific genes, such as genes encoding insulin, islet amyloid polypeptide, Glut2, and Nkx6.1. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
MAFA | up-regulates quantity by expression 
transcriptional regulation
|
PDX1 |
0.737 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254562 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17149590 |
the expression of important beta cell genes, e.g. those encoding solute carrier family 2 (facilitated glucose transporter), member 2 (formerly known as GLUT2), pancreatic and duodenal homeobox factor 1 (PDX1), NK6 transcription factor-related, locus 1 (NKX6-1), glucagon-like peptide 1 receptor (GLP1R), prohormone convertase 1/3 (PCSK1) and pyruvate carboxylase (PC), was regulated positively by MAFA and negatively by DN-MAFA. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
XRCC5 | down-regulates quantity by destabilization
binding
|
PDX1 |
0.311 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-225537 |
|
|
Mus musculus |
MIN-6 Cell |
| pmid |
sentence |
| 16166097 |
The interaction of PDX-1 with Ku subunits and its phosphorylation on threonine 11 by the DNA-PK appear to be implicated in its degradation by the proteosome. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
PDX1 | up-regulates quantity by expression
transcriptional regulation
|
Hexokinase |
0.59 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270264 |
|
|
Homo sapiens |
HIT-T15 Cell |
| pmid |
sentence |
| 8866550 |
The glycolytic enzyme glucokinase plays a primary role in the glucose-responsive secretion of insulin, and defects of this enzyme can cause NIDDM. As a step toward understanding the molecular basis of glucokinase (GK) gene regulation, we assessed the structure and regulation of the human GK gene beta-cell-type promoter. The results of reporter gene analyses using HIT-T15 cells revealed that the gene promoter was comprised of multiple cis-acting elements, including two primarily important cis-motifs: a palindrome structure, hPal-1, and the insulin gene cis-motif A element-like hUPE3. While both elements were bound specifically by nuclear proteins, it was the homeodomain-containing transcription factor insulin promoter factor 1 (IPF1)/STF-1/PDX-1 that bound to the hUPE3 site: IPF1, when expressed in CHO-K1 cells, became bound to the hUPE3 site and activated transcription. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267798 |
|
|
Homo sapiens |
HIT-T15 Cell |
| pmid |
sentence |
| 8866550 |
The glycolytic enzyme glucokinase plays a primary role in the glucose-responsive secretion of insulin, and defects of this enzyme can cause NIDDM. As a step toward understanding the molecular basis of glucokinase (GK) gene regulation, we assessed the structure and regulation of the human GK gene beta-cell-type promoter. The results of reporter gene analyses using HIT-T15 cells revealed that the gene promoter was comprised of multiple cis-acting elements, including two primarily important cis-motifs: a palindrome structure, hPal-1, and the insulin gene cis-motif A element-like hUPE3. While both elements were bound specifically by nuclear proteins, it was the homeodomain-containing transcription factor insulin promoter factor 1 (IPF1)/STF-1/PDX-1 that bound to the hUPE3 site: IPF1, when expressed in CHO-K1 cells, became bound to the hUPE3 site and activated transcription. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
PDX1 | up-regulates quantity by expression
transcriptional regulation
|
GCK |
0.59 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254911 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8866550 |
The glycolytic enzyme glucokinase plays a primary role in the glucose-responsive secretion of insulin, and defects of this enzyme can cause NIDDM. As a step toward understanding the molecular basis of glucokinase (GK) gene regulation, we assessed the structure and regulation of the human GK gene beta-cell-type promoter. The results of reporter gene analyses using HIT-T15 cells revealed that the gene promoter was comprised of multiple cis-acting elements, including two primarily important cis-motifs: a palindrome structure, hPal-1, and the insulin gene cis-motif A element-like hUPE3. While both elements were bound specifically by nuclear proteins, it was the homeodomain-containing transcription factor insulin promoter factor 1 (IPF1)/STF-1/PDX-1 that bound to the hUPE3 site: IPF1, when expressed in CHO-K1 cells, became bound to the hUPE3 site and activated transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PDX1 | up-regulates quantity by expression
transcriptional regulation
|
INS |
0.63 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255541 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 11309388 |
In conclusion, Pdx1 confers the expression of pancreatic β-cell-specific genes, such as genes encoding insulin, islet amyloid polypeptide, Glut2, and Nkx6.1. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Insulin Signaling |
| + |
PDX1 | up-regulates quantity by expression
transcriptional regulation
|
SLC2A2 |
0.538 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255540 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 11309388 |
In conclusion, Pdx1 confers the expression of pancreatic β-cell-specific genes, such as genes encoding insulin, islet amyloid polypeptide, Glut2, and Nkx6.1. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
3.0
PDX1
- 
- 