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Data suggest that protein aggregates interact with tissue-type plasminogen activator (show PLAT ELISA Kits) and plasminogen (show PLG ELISA Kits) to efficiently generate plasmin (show PLG ELISA Kits); this aggregate-bound plasmin (show PLG ELISA Kits) is shielded from inhibition by alpha-2-antiplasmin and degrades protein aggregates to release smaller, soluble but relatively hydrophobic peptide fragments; these fragments bind to and are cytotoxic to microglia (by not vascular endothelial cells).
Higher plasma concentrations of a-2-AP and PAI-1 (show SERPINE1 ELISA Kits) in patients with OSA indicated that these patients had increased prothrombotic activity. OSA increases the risk of cardiovascular complications as it enhances prothrombotic activity.
alpha2AP has a profibrotic effect probably not by the action as a plasmin (show PLG ELISA Kits) inhibitor, and the blocking of alpha2AP exerts an antifibrotic effect in humans and mice with systemic sclerosis
Possession of the alpha2AP 407Lys allele was negatively associated with AAA (show APP ELISA Kits), and thus changes in alpha2AP may affect aneurysm growth and development.
Two differentially expressed proteins, alpha-1-antitrypsin (SERPINA1 (show SERPINA1 ELISA Kits)) and alpha-2 antiplasmin (SERPINF2) are associated with purpura fulminans.
Data suggest serum A2AP (SERPINF2) level can serve as biomarker for diabetic retinopathy; levels of A2AP (but not fibrinogen, plasminogen (show PLG ELISA Kits), or plasminogen activator inhibitor 1 (show SERPINE1 ELISA Kits)) are up-regulated in hyperglycemic type 1 diabetes with retinopathy.
Study revealed that plasmin (show PLG ELISA Kits) was present in tumor tissue, and that it was responsible for processing progalanin to galanin (show GAL ELISA Kits)(1-20) in the extracellular environment.
Data suggest that decreased amounts of alpha2-plasmin (show PLG ELISA Kits) inhibitor in plasma vs serum ex vivo may reflect reduced factor XIII (show UGDH ELISA Kits) (FXIII) in vivo; thus, plasma vs serum alpha2-plasmin (show PLG ELISA Kits) inhibitor may be useful diagnostic marker for severe FXIII deficiency.
When the C terminus of alpha(2)-antiplasmin was removed, the binding affinity for active site-blocked plasmin (show PLG ELISA Kits) remained high, suggesting additional exosite interactions between the serpin core and plasmin (show PLG ELISA Kits).
Truncation of monocyte chemoattractant protein 1 (show CCL2 ELISA Kits) by plasmin (show PLG ELISA Kits) promotes blood-brain barrier disruption.
After cryotherapy of the sclera, pigment epithelium-derived factor (show SERPINF1 ELISA Kits) levels increased 44.8% compared to untreated controlsand stayed at that level until day 14. It returned to baseline by day 21. (untreated).
the inhibitory effect of PEDF appears to be mediated via the processing of VEGF-R2 by gamma-secretase
The renoprotective effects of PEDF (show SERPINF1 ELISA Kits) are mediated, at least partially, by inhibition of the Wnt (show WNT2 ELISA Kits) pathway in kidneys.
PEDF (show SERPINF1 ELISA Kits) deficiency has a significant impact on retinal endothelial cell adhesion and migration through altered production of extracellular matrix and junctional proteins in response to increased oxidative stress affecting their proangiogenic activity.
PEDF (show SERPINF1 ELISA Kits) is a hormone-regulated negative autocrine mediator of endometrial proliferation.
These results indicate that PEDF (show SERPINF1 ELISA Kits) counters Wnt (show WNT2 ELISA Kits) signaling to allow for osteoblast differentiation and provides a mechanistic insight into how the PEDF (show SERPINF1 ELISA Kits) null state results in OI type VI.
Furthermore, pigment epithelium-derived factor (PEDF (show SERPINF1 ELISA Kits)), a secreted glycoprotein known for its anti-tumor properties, blocked Wnt3a (show WNT3A ELISA Kits)-directed induction of autophagy proteins. Autophagy inhibition was complemented by reciprocal regulation of the oxidative stress enzymes, superoxide dismutase 2 (SOD2 (show SOD2 ELISA Kits)) and catalase (show CAT ELISA Kits).
Study demonstrated the inhibitory effect of PEDF (show SERPINF1 ELISA Kits) on insulin (show INS ELISA Kits)-dependent molecular mechanisms of glucose homeostasis, and suggests that PEDF (show SERPINF1 ELISA Kits) could be a specific target in the management of metabolic disorders.
Alpha-2-Antiplasmin mediated myofibroblast formation and the development of renal fibrosis in unilateral ureteral obstruction via induction of TGF-beta (show TGFB1 ELISA Kits).
PEDF (show SERPINF1 ELISA Kits) inhibits retinal microvascular dysfunction induced by 12/15-lipoxygenase-derived eicosanoids in diabetic retinopathy.
Data suggest that pigment epithelium-derived factor (PEDF (show SERPINF1 ELISA Kits)) and adipose triglyceride lipase (ATGL (show PNPLA2 ELISA Kits)) may serve as therapeutic targets for managing vascular hyperpermeability in sepsis.
This gene encodes a member of the serpin family of serine protease inhibitors. The protein is a major inhibitor of plasmin, which degrades fibrin and various other proteins. Consequently, the proper function of this gene has a major role in regulating the blood clotting pathway. Mutations in this gene result in alpha-2-plasmin inhibitor deficiency, which is characterized by severe hemorrhagic diathesis. Multiple transcript variants encoding different isoforms have been found for this gene.
, alpha-2-plasmin inhibitor
, serine (or cysteine) proteinase inhibitor, clade F (alpha-2 antiplasmin, pigment epithelium derived factor), member 2
, serpin F2
, serine (or cysteine) proteinase inhibitor, clade F, member 2
, alpha-2 antiplasmin
, pigment epithelium derived factor
, pigment epithelium-derived factor
, serpin peptidase inhibitor, clade F, member 1
, alpha-2-PI serine protease inhibitor
, alpha 2 antiplasmin
, plasmin inhibitor alpha 2
, serine (or cysteine) proteinase inhibitor, clade F (alpha-2 antiplasmin, pigment epithelium derived factor), member 1
, serine (or cysteine) proteinase inhibitor, clade F), member 1
, serine (or cysteine) proteinase inhibitor, clade F, member 1
, serpin F1
, stromal cell derived factor 3
, stromal cell-derived factor 3