| + |
CLOCK/BMAL1 | up-regulates quantity by expression 
transcriptional regulation
|
SERPINE1 |
0.506 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253712 |
|
|
Homo sapiens |
Colorectal Cancer Cell |
| pmid |
sentence |
| 22198637 |
Both CLOCK:ARNTL and CLOCK:ARNTL2 heterodimers powerfully activate the promoter of the PAI-1 gene, officially called SERPINE1 and located on the seventh chromosome (7q21.3-q22), underlying the circadian variation in circulating PAI-1 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Circadian clock |
| + |
SERPINE1 | down-regulates 
|
Fibrinolysis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267984 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19387897 |
Plasma PAI-1 levels robustly fluctuate in a circadian manner and consequently contribute to hypofibrinolysis during the early morning. The circadian expression of PAI-1 gene is thought to be directly regulated by the circadian clock proteins such as CLOCK and BMAL1/BMAL2 which drive the endogenous biological clock. Plasma PAI-1 levels are increased in the beginning of the active phase in both diurnal humans and in nocturnal rodents, suggesting that the rhythmic PAI-1 expression is commonly indispensable for organisms. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-68481 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10368279 |
Pai-1 is the physiological inhibitor of the fibrinolytic pathway |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Circadian clock |
| + |
TGFBR1 | up-regulates quantity by expression 
transcriptional regulation
|
SERPINE1 |
0.444 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260590 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 28520219 |
The transforming growth factor-β pathway is the major driver of fibrotic response. Plasminogen activator inhibitor-1 (PAI-1) is a crucial downstream target of this pathway. Transforming growth factor-β positively regulates PAI-1 gene expression via two main pathways including Smad-mediated canonical and non-canonical pathways. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
SERPINE1 | down-regulates activity 
binding
|
F12 |
0.311 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263516 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26707513 |
C1INH is a serine protease inhibitor (serpin) that acts on both the complement pathway and the contact system and is the main inhibitor of the contact system by targeting both FXIIa and PK 9. Additionally, FXIIa can be inhibited by α1‐antitrypsin and plasminogen activator inhibitor‐1 (PAI‐1). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Blood Plasma |
| + |
SMAD3/SMAD4 | up-regulates quantity by expression
transcriptional regulation
|
SERPINE1 |
0.575 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-57776 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9606191 |
Here we report the identification of smad3/smad4 binding sequences, termed caga boxes, within the promoter of the human pai-1 gene. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
SRF | down-regulates quantity by repression
transcriptional regulation
|
SERPINE1 |
0.268 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255228 |
|
|
Homo sapiens |
Lung Fibroblast Cell Line |
| pmid |
sentence |
| 15514113 |
We previously demonstrated that serum response factor (SRF), a critical smooth muscle transcription factor, is highly expressed in LAM cells. Here we show that a high SRF level alters the plasminogen (Plg) system. Specifically, overexpression of SRF in human lung fibroblasts upregulated urokinase-type plasminogen activator (uPA) and its substrate Plg, whereas it downregulated plasminogen activator inhibitor (PAI)-1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SERPINE1 | up-regulates
|
Fibrosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260588 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29474926 |
Plasminogen activator inhibitor-1 (PAI-1) formed in the injured alveolar epithelium also contributes to pulmonary fibrosis in a manner that involves vitronectin binding. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
CLOCK/BMAL2 | up-regulates quantity by expression
transcriptional regulation
|
SERPINE1 |
0.498 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253713 |
|
|
Homo sapiens |
Colorectal Cancer Cell |
| pmid |
sentence |
| 22198637 |
Both CLOCK:ARNTL and CLOCK:ARNTL2 heterodimers powerfully activate the promoter of the PAI-1 gene, officially called SERPINE1 and located on the seventh chromosome (7q21.3-q22), underlying the circadian variation in circulating PAI-1 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Circadian clock |
| + |
SNAI1 | up-regulates quantity by expression
transcriptional regulation
|
SERPINE1 |
0.428 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252262 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19055748 |
We demonstrated by both cDNA microarrays and real-time quantitative RT-PCR that the functional blockade of SNAI1 induces a significant decrease of PAI-1 and uPA transcripts. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SERPINE1 | up-regulates
|
Cell_adhesion |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-68478 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10368279 |
Pai-1 is now being identified as a key player in the link between coagulation and the cell adhesion pathways involved in tissue remodeling and metastasis. Active pai-1 (but not its latent or cleaved forms) binds tightly to the adhesive glycoprotein vitronectin in the extracellular matrix. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
N | up-regulates quantity by expression
transcriptional regulation
|
SERPINE1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260589 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18055455 |
In this study, we demonstrate that SARS-associated coronavirus (SARS-CoV) nucleocapsid (N) protein potentiates transforming growth factor-beta (TGF-beta)-induced expression of plasminogen activator inhibitor-1 but attenuates Smad3/Smad4-mediated apoptosis of human peripheral lung epithelial HPL1 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV FIBROSIS |
3.0
SERPINE1
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