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anti-Mouse (Murine) PLAUR Antibodies:
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Mouse (Murine) Polyclonal PLAUR Primary Antibody for BR, CyTOF - ABIN5013025
Zhang, Cai, López-Guisa, Collins, Eddy: Mitogenic signaling of urokinase receptor-deficient kidney fibroblasts: actions of an alternative urokinase receptor and LDL receptor-related protein. in Journal of the American Society of Nephrology : JASN 2004
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Human Polyclonal PLAUR Primary Antibody for IHC (p), WB - ABIN966859
Wang, Yang, Jamaluddin, Boyd: The Kruppel-like KLF4 transcription factor, a novel regulator of urokinase receptor expression, drives synthesis of this binding site in colonic crypt luminal surface epithelial cells. in The Journal of biological chemistry 2004
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Mouse (Murine) Polyclonal PLAUR Primary Antibody for FACS, WB - ABIN4900558
van Zoelen, Florquin, de Beer, Pater, Verstege, Meijers, van der Poll: Urokinase plasminogen activator receptor-deficient mice demonstrate reduced hyperoxia-induced lung injury. in The American journal of pathology 2009
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Human Monoclonal PLAUR Primary Antibody for FACS - ABIN2472722
Gadd, Majdic, Kasinrerk, Stockinger, Maurer, Eher, Knapp: M5, a phosphoinositol-linked human myelomonocytic activation-associated antigen. in Clinical and experimental immunology 1990
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Human Monoclonal PLAUR Primary Antibody for IHC (fro), FACS - ABIN2472714
Sillaber, Baghestanian, Hofbauer, Virgolini, Bankl, Füreder, Agis, Willheim, Leimer, Scheiner, Binder, Kiener, Bevec, Fritsch, Majdic, Kress, Gadner, Lechner, Valent: Molecular and functional characterization of the urokinase receptor on human mast cells. in The Journal of biological chemistry 1997
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Human Monoclonal PLAUR Primary Antibody for FACS - ABIN2472717
Mondino, Blasi: uPA and uPAR in fibrinolysis, immunity and pathology. in Trends in immunology 2004
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Human Polyclonal PLAUR Primary Antibody for IP, Neut - ABIN223158
Viswanathan, Richardson, Togonu-Bickersteth, Dai, Liu, Vatsya, Sun, Yu, Munuswamy-Ramanujam, Baker, Lucas: Myxoma viral serpin, Serp-1, inhibits human monocyte adhesion through regulation of actin-binding protein filamin B. in Journal of leukocyte biology 2009
The results establish GDE3 as a negative regulator of the uPAR signaling network and, furthermore, highlight GPI-anchor hydrolysis as a cell-intrinsic mechanism to alter cell behavior.
The ratio of full-length versus cleaved uPAR as analysed by Western blotting and its regulation was assessed by addition of different protease inhibitors and transforming growth factor - beta1 (TGF-beta1). The role of uPAR cleavage in cell proliferation and migration was analysed using real-time cell analysis and invasion was assessed using the myoma invasion model
Plg-RKT is required for plasminogen binding and macrophage migration in vivo
The synergy of circulating factor suPAR and APOL1 G1 or G2 on alphavbeta3 integrin activation is a mechanism for CKD.
Results identify soluble uPAR as a functional connection between the bone marrow and the kidney, and they implicate bone marrow immature myeloid cells as a key source of soluble uPAR that leads to glomerular dysfunction.
Plaur deficiency does not increase susceptibility to epileptogenesis after traumatic brain injury in an animal model.
Significance of the urokinase-type plasminogen activator and its receptor in the progression of focal segmental glomerulosclerosis in clinical and mouse models.
Findings indicate a significant correlation of uPAR cleavage with breast cancer progression, but the precise biological consequence(s) of the cleavage or the cleavage products still remains to be elucidated.
interaction of full-length suPAR with alphavbeta3 integrin expressed on podocytes results in down-modulation of nephrin that may affect kidney functionality in different human pathologies characterized by increased concentration of suPAR.
In an in vivo murine angiogenesis model uPAR-deficient PTEN heterozygous animals increased the impaired angiogenic phenotype of uPAR knockout mice and were able to reverse the high invasive potential of PTEN heterozygotes.
uPAR contributes to macrophage driven atherosclerotic lesion formation.
we have firstly shown a fundamental mechanism of urokinase system(uPa and uPAR)-dependent regulation of the trajectory of growth and branching of blood vessels in early embryogenesis and in adults during the repair/regeneration of tissues.
our data show that uPAR is required for efficient skin tumor formation
Tumours with high levels of uPAR, as well as cells invading leiomyoma tissue with up-regulated uPAR expression, all displayed enhanced activity of gelatinolytic enzymes.
deficiency of uPAR and PSMD6 delays DNA repair and leads to decreased cell survival.
beta-elemene downregulates expression of uPA, uPAR, MMP-2, and MMP-9 in a murine intraocular melanoma model
Primary podocyte injury stimulates upregulation of endothelial PAI-1, with the uPA/uPAR complex on the podocyte surface, resulting in podocyte detachment secondary to beta1-integrin endocytosis.
uPA promotes remodeling of the fracture cartilage by osteoclasts that are associated with angiogenesis and suggest that uPA promotes angiogenesis and remodeling of the fracture cartilage at this time of bone fracture repair.
Binding of urokinase to uPAR promotes the reorganization of the actin cytoskeleton and re-emergence of dendritic filopodia after excitotoxic injury.
Inactivation of urokinase-type plasminogen activator receptor gene induces dermal and pulmonary fibrosis and peripheral microvasculopathy in mice.
Transient knockdown of urokinase/plasminogen activator urokinase receptor (uPAR) in basal-like breast cancer cells grown on vitronectin reduces FRA-1 phosphorylation and stabilization; and uPAR and FRA-1 are required for vitronectin-induced cell invasion
The pre-ovulatory follicular fluid level of suPAR was significantly lower in women developing severe ovarian hyperstimulation syndrome (OHSS), indicating that the plasminogen activator system could be involved in the pathophysiology of OHSS. However, suPAR did not provide a satisfying predictive value for the prediction of OHSS.
propose that a positive feedback mechanism between uPAR, plasmin and transforming growth factor beta1 (TGFbeta1) selects cells in the monolayer for matrix invasion
In acutely admitted patients with COPD, elevated PLAUR levels were associated with increased risk of mortality.
This study shows that the D2A sequence of the UPAR induces cell growth through alphaVbeta3 integrin and EGFR.
High expression of U-PAR is associated with breast cancer.
suPAR is associated with the Coronary Artery Calcification score and is a risk factor for new-onset CVD in patients undergoing hemodialysis.
Elevated baseline soluble urokinase receptor concentrations independently associate with new-onset microalbuminuria in subjects at increased risk of developing type 2 diabetes.
suPAR levels were significantly higher Behcet's disease patients.
To develop enzyme-resistant analogues, we applied here the Retro-Inverso (RI) approach, whereby the topology of the side chains is maintained by inverting the sequence of the peptide and the chirality of all residues. Molecular dynamics suggests that peptide RI-3 adopts the turn structure typical of uPAR-FPR1 antagonists
results demonstrated that PLAUR induces geftinib-resistance through EGFR/p-AKT/survivin signaling pathway in gefitinib-resistant human lung adenocarcinoma cells. PLAUR could be a novel therapeutic target for gefitinib-resistant NSCLC patients.
High Upar expression is associated with breast cancer.
Circulating soluble uPAR levels are higher in patients with peripheral arterial disease, particularly in those with extensive atherosclerosis and are predictive of long term cardiovascular and PAD-related outcomes.
Data confirmed PLAUR and CDH11, both targets of miR-335, to be overexpressed in gastric cancer tissues.
Serum and urine concentration of suPAR did not different between different clinical patterns of nephrotic syndrome in children, regardless the immunosuppressive treatment used.
the present study demonstrated that EGF induced aggressiveness of gastric cancer cells by activating epithelial to mesenchymal transition, which involved the activation of the ERK1/2 pathway and, subsequently, uPAR expression
uPAR and TF could potentially be attractive targets for molecular imaging and therapy in oral squamous cell carcinoma due to high positive expression rates and tumor-specific expression patterns. High uPAR expression was significantly associated with a reduced survival.
suPAR levels are significantly elevated in hemodialysis patients with ESRD and remain associated with adverse outcomes.
These findings may show that presenting a high level of suPAR in migraine patients with attack and aura results to predisposition to occurring on the symptoms and that high levels of suPAR, procalcitonin and fibrinogen in patients with migraine result in neurogenic inflammation during migraine headaches.
Data show that urokinase-type plasminogen activator (uPA) is only expressed in the cumulus cells of immature and in vitro matured cumulus-oocyte complexes (COCs), while uPA receptor (uPAR) and plasminogen activator inhibitor-1 (PAI-1) are expressed in both the cumulus cells and the immature and in vitro matured oocytes.
uPA/uPAR binding is involved in signaling pathways that activate transcription factors that regulate the synthesis of molecules concerned with the arrangement of a particular oviductal microenvironment.
Data indicate that superoxide dismutase (SOD) inhibited high glucose (HG)-induced expression of uPAR and VEGF in bovine retinal microvascular endothelial cell (REC).
These data indicated that E. coli LPS led to an increase in u-PA activity and RNA expression of u-PA and u-PAR in BME-UV1 cells, thus strengthening the role of the PA system during pathological processes.
the interaction between uPAR and Man-6-P/IGF2R is a low percentage binding event and that suPAR and full-length uPAR bind the Man-6-P/IGF2R by different mechanisms.
This gene encodes the receptor for urokinase plasminogen activator and, given its role in localizing and promoting plasmin formation, likely influences many normal and pathological processes related to cell-surface plasminogen activation and localized degradation of the extracellular matrix. It binds both the proprotein and mature forms of urokinase plasminogen activator and permits the activation of the receptor-bound pro-enzyme by plasmin. The protein lacks transmembrane or cytoplasmic domains and may be anchored to the plasma membrane by a glycosyl-phosphatidylinositol (GPI) moiety following cleavage of the nascent polypeptide near its carboxy-terminus. However, a soluble protein is also produced in some cell types. Alternative splicing results in multiple transcript variants encoding different isoforms. The proprotein experiences several post-translational cleavage reactions that have not yet been fully defined.
urokinase plasminogen activator surface receptor
, plasminogen activator, urokinase receptor
, urokinase plasminogen activator receptor
, urokinase-type plasminogen activator receptor
, monocyte activation antigen Mo3
, u-plasminogen activator receptor form 2
, urokinase-type plasminogen activator (uPA) receptor
, plasminogen activator urokinase receptor 3
, urinary plasminogen activator receptor 2
, urinary plasminogen activator receptor 3