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anti-Human PLG Antibodies:
anti-Rat (Rattus) PLG Antibodies:
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Human Polyclonal PLG Primary Antibody for WB - ABIN633957
Giraud, Dicristofaro, De Micco, Lejeune, Barbaria, Mallet: A plasminogen-like protein, present in the apical extracellular environment of thyroid epithelial cells, degrades thyroglobulin in vitro. in Biochemical and biophysical research communications 2005
Show all 2 references for ABIN633957
Human Polyclonal PLG Primary Antibody for EIA, IP - ABIN118044
Schott, Grosskinsky, Brenner, Kraiczy, Wallich: Molecular characterization of the interaction of Borrelia parkeri and Borrelia turicatae with human complement regulators. in Infection and immunity 2010
Human Polyclonal PLG Primary Antibody for EIA, IHC (fro) - ABIN336225
Fears: Binding of plasminogen activators to fibrin: characterization and pharmacological consequences. in The Biochemical journal 1989
Human Polyclonal PLG Primary Antibody for WB - ABIN2784539
Kinnby, Booth, Svensäter: Plasminogen binding by oral streptococci from dental plaque and inflammatory lesions. in Microbiology (Reading, England) 2008
Human Monoclonal PLG Primary Antibody for EIA, WB - ABIN112275
Hattey, Wojta, Binder: Monoclonal antibodies against plasminogen and alpha-2-antiplasmin: binding to native and modified antigens. in Thrombosis research 1987
Human Monoclonal PLG Primary Antibody for EIA, WB - ABIN112277
Wagner, Vetterlein, Binder: Purification of an active plasminogen activator inhibitor immunologically related to the endothelial type plasminogen activator inhibitor from the conditioned media of a human melanoma cell line. in The Journal of biological chemistry 1986
reduced proteolytic activity of plasmin on structures of growing thrombi, rather than on complement activation fragments, explains the association of plasminogen deficiency with aHUS.
Zinc modulates fibrinolysis by attenuating tPA (show PLAT Antibodies)-mediated plasminogen activation and plasmin-induced fibrin degradation.
Plasmin cleavage of iC3b provides a complement regulatory pathway that is as efficient as FI/CR1 (show CR1 Antibodies) but does not require a cellular cofactor.
PLG is the third replicated shared genetic risk factor of atherosclerosis and periodontitis.
Data show that preincubation with plasminogen, wild-type group A Streptococcus (GAS) NS88.2 degraded complement C3b.
whereas the presence of plasminogen did not affect the factor I cofactor activity of C4BP (show C4BPA Antibodies), the activation of plasminogen by urokinase-type plasminogen activator (show PLAU Antibodies) to active plasmin was significantly augmented in the presence of C4BP (show C4BPA Antibodies).
These studies demonstrate that GAS virulence can be explained by disparate hPg (show GNRH1 Antibodies) activation by SK2a and SK2b coupled with the coinherited M-proteins of these strains
PAM (show PAM Antibodies) activated Plasminogen Glycoform II.
High plasma fibrinogen and low plasminogen are associated with poor survival in CTEPH patients without modern therapy.
Data show that different subpopulations of platelets harbor plasminogen by diverse mechanisms
The plasminogen/plasminogen activator/plasmin system is activated during gamete interaction and regulates the sperm entry into the oocyte.
The current study suggests the existence of an active TNF-alpha (show TNF Antibodies)-plasminogen-plasmin autocrine/paracrine loop on the massively infiltrated polymorphonuclear neutrophils inside udders of drying-off cows.
examination of interaction with streptococcal plasminogen activator PauA
Plasminogen-deficient mice frequently develop colon lesions and rectal prolapses.
manganese transport protein (show SLC11A2 Antibodies) C (show PROC Antibodies) (MntC) is an extracellular matrix- and plasminogen-binding protein (show ENO1 Antibodies)
Plg from mouse plasma contains oxPtdPC adducts that are not affected by the action of Lp-PLA(2 (show Lp-PLA2 Antibodies)), suggesting that linkage to Plg protects oxPtdPCs from metabolism during their transport in the plasma.
plg-/- and tPA (show PLAT Antibodies)-/- mice exhibit brain parenchymal fibrin deposits that appear to result from reduced neurovascular integrity
plasminogen-dependent proteolysis has a beneficial effect during neurological recovery after stroke.
Pla-induced mononuclear cell recruitment in vivo was dependent on protease-activated receptor-1 activation of the MEK/ERK/NF-kappaB pathway, which led to the release of CCL2 and activation of CCR2.
Plg may play an important role in innate immunity by changing expression of genes that contribute to phagocytosis.
Plasminogen is a key molecular determinant of inflammatory joint disease capable of simultaneously driving or ameliorating arthritis pathogenesis in distinct anatomic locations in the same subject.
Plasmin suppresses brain metastasis in two ways: by converting membrane-bound astrocytic FasL (show FASL Antibodies) into a paracrine death signal for cancer cells, and by inactivating the axon pathfinding molecule L1CAM (show L1CAM Antibodies), which metastatic cells express for spreading along brain capillaries and for metastatic outgrowth.
Plasminogen stimulates autocrine cytokine production in human airway smooth muscle cells in a manner mediated by plasmin and annexin A2 (show ANXA2 Antibodies).
The protein encoded by this gene is a secreted blood zymogen that is activated by proteolysis and converted to plasmin and angiostatin. Plasmin dissolves fibrin in blood clots and is an important protease in many other cellular processes while angiostatin inhibits angiogenesis. Defects in this gene are likely a cause of thrombophilia and ligneous conjunctivitis. Two transcript variants encoding different isoforms have been found for this gene.
, lipoprotein, Lp(a)
, plasmin heavy chain A
, plasmin light chain B