| + |
CDK1 | down-regulates 
phosphorylation
|
HMGA2 |
0.374 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-74094 |
Ser44 |
QEPTGEPsPKRPRGR |
Homo sapiens |
|
| pmid |
sentence |
| 10636877 |
Architecture of high mobility group protein i-c dna complex and its perturbation upon phosphorylation by cdc2 kinase. Phosphorylation by cdc2 reduces binding strength of the mammalian and insect hmgi proteins to dna. After phosphorylation of the protein at ser-43 and ser-58 by cdc2 kinase multiple contacts of dbds, especially with the bases, are impaired and the protein binds to dna in a different way, extending the contacts to the sugar-phosphate backbone. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-74098 |
Ser59 |
PKGSKNKsPSKAAQK |
Homo sapiens |
|
| pmid |
sentence |
| 10636877 |
Architecture of high mobility group protein i-c dna complex and its perturbation upon phosphorylation by cdc2 kinase. Phosphorylation by cdc2 reduces binding strength of the mammalian and insect hmgi proteins to dna. After phosphorylation of the protein at ser-43 and ser-58 by cdc2 kinase multiple contacts of dbds, especially with the bases, are impaired and the protein binds to dna in a different way, extending the contacts to the sugar-phosphate backbone. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
SMAD2/SMAD4 | up-regulates activity 
binding
|
HMGA2 |
0.511 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281162 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 18832382 |
In the present study we investigated the molecular mechanisms by which HMGA2 induces EMT. We found that HMGA2 regulates expression of many important repressors of E-cadherin. Among these, we analyzed in detail the zinc-finger transcription factor SNAIL1, which plays key roles in tumor progression and EMT. We demonstrate that HMGA2 directly binds to the SNAIL1 promoter and acts as a transcriptional regulator of SNAIL1 expression. Furthermore, we observed that HMGA2 cooperates with the TGF-beta/Smad pathway in regulating SNAIL1 gene expression. The mechanism behind this cooperation involves physical interaction between these factors, leading to an increased binding of Smads to the SNAIL1 promoter |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SMAD3/SMAD4 | up-regulates activity
binding
|
HMGA2 |
0.555 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281163 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 18832382 |
In the present study we investigated the molecular mechanisms by which HMGA2 induces EMT. We found that HMGA2 regulates expression of many important repressors of E-cadherin. Among these, we analyzed in detail the zinc-finger transcription factor SNAIL1, which plays key roles in tumor progression and EMT. We demonstrate that HMGA2 directly binds to the SNAIL1 promoter and acts as a transcriptional regulator of SNAIL1 expression. Furthermore, we observed that HMGA2 cooperates with the TGF-beta/Smad pathway in regulating SNAIL1 gene expression. The mechanism behind this cooperation involves physical interaction between these factors, leading to an increased binding of Smads to the SNAIL1 promoter |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HMGA2 | up-regulates quantity by expression
transcriptional regulation
|
SNAI1 |
0.382 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281164 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 18832382 |
In the present study we investigated the molecular mechanisms by which HMGA2 induces EMT. We found that HMGA2 regulates expression of many important repressors of E-cadherin. Among these, we analyzed in detail the zinc-finger transcription factor SNAIL1, which plays key roles in tumor progression and EMT. We demonstrate that HMGA2 directly binds to the SNAIL1 promoter and acts as a transcriptional regulator of SNAIL1 expression. Furthermore, we observed that HMGA2 cooperates with the TGF-beta/Smad pathway in regulating SNAIL1 gene expression. The mechanism behind this cooperation involves physical interaction between these factors, leading to an increased binding of Smads to the SNAIL1 promoter |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281165 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 18832382 |
In the present study we investigated the molecular mechanisms by which HMGA2 induces EMT. We found that HMGA2 regulates expression of many important repressors of E-cadherin. Among these, we analyzed in detail the zinc-finger transcription factor SNAIL1, which plays key roles in tumor progression and EMT. We demonstrate that HMGA2 directly binds to the SNAIL1 promoter and acts as a transcriptional regulator of SNAIL1 expression. Furthermore, we observed that HMGA2 cooperates with the TGF-beta/Smad pathway in regulating SNAIL1 gene expression. The mechanism behind this cooperation involves physical interaction between these factors, leading to an increased binding of Smads to the SNAIL1 promoter |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
HMGA2 | up-regulates quantity by expression
transcriptional regulation
|
TWIST1 |
0.409 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-281171 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 18832382 |
We then analyzed the effect of Snail1 depletion on expression of the other four E-cadherin repressors, whose levels become increased by HMGA2 overexpression, Snail2, ZEB1, ZEB2, and Twist in the same panel of cells (Fig. 7, A–C). Depletion of the induced Snail1 levels by the shRNA led to a concomitant and significant decrease in Snail2, ZEB1, and ZEB2 mRNA levels. In the case of ZEB1 and ZEB2, their expression was decreased almost down to the levels of the parental epithelial cells (NMuMG-m). In contrast, Twist levels remained unaltered by the knock-down of endogenous Snail1 (Fig. 7C). These results demonstrate that Snail1 regulates specifically the expression of Snail2, ZEB1, and ZEB2 but not that of Twist. The data suggest that HMGA2 causes EMT by inducing at least two primary transcriptional mediators of this process, Snail1 and Twist. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HMGA2 | up-regulates 
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-205465 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25300915 |
This study unraveled a novel function ofhmga2in induction of apoptosis in human primary cell lines |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HMGA2 | down-regulates quantity by repression 
transcriptional regulation
|
SCNN1A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251946 |
|
|
Rattus norvegicus |
Parotid Acinar Cell |
| pmid |
sentence |
| 11390395 |
Expression of endogenous alpha-ENaC gene in salivary Pa-4 cells is suppressed by an ectopic HMGI-C overexpression. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
HMGA2 | down-regulates
binding
|
E4F1 |
0.371 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-119537 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14645522 |
Here we show that hmga2 associates with the e1a-regulated transcriptional repressor p120(e4f), interfering with p120(e4f) binding to the cyclin a promoter |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HMGA2 | up-regulates quantity by expression
transcriptional regulation
|
CCNA2 |
0.314 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-119496 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14645522 |
Transcriptional activation of the cyclin a gene by the architectural transcription factor hmga2 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
4.0
HMGA2
- 
- 