+ |
KLKB1 | up-regulates activity
cleavage
|
F12 |
0.588 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263520 |
Arg353 |
EQPPSLTrNGPLSCG |
Homo sapiens |
|
pmid |
sentence |
28966616 |
FXIIa converts PK to the active protease PKa, which reciprocally activates more FXII|In addition, PKa can initiate a further proteolysis of FXIIa into a ~30 kDa light chain fragment, termed β-FXIIa. The cleavage takes place at the peptide bond Arg353–Val354 and consequently, the active site released from the heavy chain and thus from surfaces. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Blood Plasma |
+ |
F12 | up-regulates activity
cleavage
|
KLKB1 |
0.588 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263518 |
Arg390 |
CTTKTSTrIVGGTNS |
Homo sapiens |
|
pmid |
sentence |
28966616 |
FXIIa activates two serine proteinases, factor XI (FXI) and plasma prekallikrein (PK) that drive the coagulation and kallikrein–kinin systems, respectively |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Blood Plasma |
+ |
MMP12 | down-regulates quantity by destabilization
cleavage
|
F12 |
0.335 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263611 |
Gly376 |
SMTRVVGgLVALRGA |
in vitro |
|
pmid |
sentence |
10930399 |
The data presented in this study show for the first time the degradation of Factor XII of the blood clotting system by matrix metalloproteinases. MMP-12, MMP-13, and MMP-14 cleave at Gly376Leu377|However, no activity of Factor XII can be observed after MMPinduced cleavage. |
|
Publications: |
1 |
Organism: |
In Vitro |
+ |
MMP13 | down-regulates quantity by destabilization
cleavage
|
F12 |
0.317 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263609 |
Gly376 |
SMTRVVGgLVALRGA |
in vitro |
|
pmid |
sentence |
10930399 |
The data presented in this study show for the first time the degradation of Factor XII of the blood clotting system by matrix metalloproteinases. MMP-12, MMP-13, and MMP-14 cleave at Gly376Leu377|However, no activity of Factor XII can be observed after MMPinduced cleavage. |
|
Publications: |
1 |
Organism: |
In Vitro |
+ |
MMP14 | down-regulates quantity by destabilization
cleavage
|
F12 |
0.336 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263610 |
Gly376 |
SMTRVVGgLVALRGA |
in vitro |
|
pmid |
sentence |
10930399 |
The data presented in this study show for the first time the degradation of Factor XII of the blood clotting system by matrix metalloproteinases. MMP-12, MMP-13, and MMP-14 cleave at Gly376Leu377|However, no activity of Factor XII can be observed after MMPinduced cleavage. |
|
Publications: |
1 |
Organism: |
In Vitro |
+ |
F12 | up-regulates activity
cleavage
|
F11 |
0.472 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263519 |
|
|
Homo sapiens |
|
pmid |
sentence |
8427954 |
Activation of factor XI in plasma is dependent on factor XII | Similar kinetics of factor XI cleavage are seen when 40 nmol/L factor XIIa (equal to 10% of factor XII activation) is added to factor XII-deficient plasma if an activating surface is provided. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Blood Plasma |
+ |
F12 | up-regulates activity
binding
|
GPIb-IX-V complex |
0.448 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261856 |
|
|
Homo sapiens |
Blood Platelet |
pmid |
sentence |
25297919 |
Besides VWF as a main ligand, GPIbα also binds multiple ligands such as thrombospondin, Factor XII, Factor XI, thrombin, High Molecular Weight kininogen, P-selectin and Mac-1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ESR1 | up-regulates quantity by expression
transcriptional regulation
|
F12 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254072 |
|
|
Homo sapiens |
Hep-G2 Cell |
pmid |
sentence |
9794469 |
Transcription of the FXII gene is stimulated by estrogens through specific interaction of the estrogen receptor alpha (ER alpha) with an estrogen response element present on FXII promoter. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
HNF4A | down-regulates quantity by repression
transcriptional regulation
|
F12 |
0.221 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254073 |
|
|
Homo sapiens |
Hep-G2 Cell |
pmid |
sentence |
9794469 |
Orphan receptor hepatocyte nuclear factor-4 antagonizes estrogen receptor alpha-mediated induction of human coagulation factor XII gene. In conclusion, our findings address a direct role for HNF-4 in modulating estrogen-dependent transcription of the FXII gene promoter. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
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 |
+ |
Blood vessel damage | up-regulates
|
F12 |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263514 |
|
|
|
|
pmid |
sentence |
NBK482253 |
It begins with the activation of Factor XII (a zymogen, inactivated serine protease) which becomes Factor XIIA (activated serine protease) after exposure to endothelial collagen. Endothelial collagen is only exposed when endothelial damage occurs. |
|
Publications: |
1 |
+ |
SERPING1 | down-regulates activity
binding
|
F12 |
0.631 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263517 |
|
|
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 |
+ |
SERPINA1 | down-regulates activity
binding
|
F12 |
0.337 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263515 |
|
|
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 |
+ |
SERPINC1 | down-regulates activity
cleavage
|
F12 |
0.587 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-264139 |
|
|
|
|
pmid |
sentence |
31030036 |
Antithrombin (AT), a member of the serine protease inhibitor (SERPIN) superfamily, is a major circulating inhibitor of blood coagulation proteases such as factor (F) IIa (known as thrombin), FXa and, to a lesser extent, FIXa, FXIa and FXIIa. SERPINC1, which encodes AT in humans, is located on chromosome 1q25.1 |
|
Publications: |
1 |