Map Key
Generic Enzyme
Generic kinase
Protein kinase
Lipid kinase
Generic phosphatase
Protein phosphatase
Lipid phosphatase
Generic phospholipase
Generic protease
Metalloprotease
G-alpha
RAS - superfamily
G beta/gamma
Regulators (GDI, GAP, GEF)
Generic channel
Ligand-gated channel
Voltage-gated channel
Transporter
Normal process
Pathological process
Positive effect
Negative effect
Unspecified effect
Technical link
Disrupts in disease
Emerges in disease
Enhances in disease
Weakens in disease
Organsim specific interaction

Generic binding protein
Receptor ligand
Cell membrane glycoprotein
Transcription factor
DNA
RNA
Compound
Inorganic ion
Predicted metabolite or user's structure
Reaction
Generic receptor
GPCR
Receptors with enzyme activity
Mitochondria
EPR
Golgi
Nucleus
Lysosome
Peroxisome
Cytoplasm
Extracellular

Normal process
Pathological process
Binding
Cleavage
Covalent modifications
Phosphorylation
Dephosphorylation
Transformation
Transport
Catalysis
Transcription regulation
MicroRNA binding
Competition
Influence on expression
Unspecified interactions
Pharmacological effect
Toxic effect
Group relation
Complex subunit
Similarity reaction
A complex or a group
Organism specific object

Cell adhesion Plasmin signaling


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Cell adhesion Plasmin signaling

Plasmin signaling

Plasmin is a major fibrinolytic protease with wide substratespecificity.

Plasminogen, a circulating plasma zymogen, can be converted toPlasmin by tissue-type Plasminogen activator ( PLAT ), Plasminogenactivator urokinase ( PLAU ), Coagulation factor XII, or Kallikrein Bplasma ( Plasma kallikrein ) [1].

Plasmin directly degrades Fibrinogen, Laminin,and Fibronectin. On the cell surface Plasmin activates a number ofMetalloproteinases ( MMPs ) [2] that degrade extracellular matrixproteins and components of basal membrane, such as Collagen, andFibrinogen, which leads to thrombolysis.

Plasmin can activate or release from extracellular matrix anumber of growth factors: Vascular endothelial growth factor ( VEGF ),Transforming growth beta ( TGF-beta ), or Fibroblast growth factor ( FGF2 )[3]. These growth factors bind to their receptors on the cell surface andactivate intracellular signaling pathways that regulate cellular behavior. VEGFdirectly activates Phosphatidylinositol-3-kinase ( PI3K ) and V-akt murine thymomaviral oncogene homolog 1 ( AKT(PKB) ) signaling pathways. TGF-betaactivates Mitogen activated protein kinase p38 signaling pathway via adaptorprotein X-linked inhibitor of apoptosis ( XIAP ), Mitogen-activated protein kinasekinase kinase 7 interacting protein 1 ( TAB1 ) and Mitogen-activated proteinkinase kinase kinase 7 ( TAK1 ) kinase.

Plasmin is also able to cleave TGF-beta receptor type IIIextracellular domain, suggesting possibility of yet another type of regulation of thereceptor [4].

Plasmin is inhibited by Serpin peptidase inhibitor clade I member 1 (Neuroserpin ), Serpin peptidase inhibitor clade G (C1 inhibitor) member 1 ( C1inhibitor ), T issue factor pathway inhibitor 2 ( TFPI-2 ), Pregnancy zoneprotein ( PZP ), and Serine protease inhibitor serine peptidase inhibitor Kazaltype 5 ( LEKTI ).