PLAUR Human
Description
PLAUR produced in Sf9 Baculovirus cells is a single, glycosylated polypeptide chain containing 291 amino acids (23-305 a.a.) and having a molecular mass of 32.5kDa (Molecular size on SDS-PAGE will appear at approximately 40-57 kDa).
PLAUR is fused to a 8 amino acid His-tag at C-terminus & purified by proprietary chromatographic techniques.
Product Specs
PLAUR, Monocyte Activation Antigen Mo3, U-PAR, UPAR, U-Plasminogen Activator Receptor Form 2, CD87 Antigen , CD87, URKR, MO3.
Q&A
What is the primary biological role of PLAUR (uPAR) in human physiology and pathology?
PLAUR encodes the urokinase receptor (uPAR), a cell surface protein critical for regulating cell migration, invasion, and survival. In pathophysiological contexts, uPAR promotes epithelial-to-mesenchymal transition (EMT), enhances cancer cell resistance to targeted therapies, and contributes to atherosclerotic lesion progression . Its role is context-dependent: in glioblastoma, high PLAUR expression correlates with poor patient survival, particularly in mesenchymal subtypes , while in atherosclerosis, PLAUR expression predicts lesion severity and macrophage-mediated inflammation .
Methodological Note: To study PLAUR’s role, researchers often use:
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Neurosphere cultures to assess glioblastoma stem cell-like properties .
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Single-cell RNA sequencing (scRNA-seq) to identify macrophage-specific PLAUR expression in atherosclerosis .
How is PLAUR expression analyzed in experimental settings?
PLAUR expression is quantified via:
Key Consideration: Antibody selection (e.g., clone A20095I for capture in ELISA ) affects assay specificity. Validate with recombinant PLAUR protein standards .
What experimental models are used to study PLAUR’s function?
How does PLAUR regulate gene expression signatures in cancer?
PLAUR induces a mesenchymal gene expression profile in glioblastoma by interacting with oncogenic pathways (e.g., EGFRvIII). While EGFRvIII promotes neurosphere growth, uPAR uniquely upregulates mesenchymal biomarkers (e.g., CHI3L1, SPOCK1) and enhances survival . This suggests uPAR may act as a transcriptional co-regulator or signal through integrin/EGFR cross-talk.
Contradiction Analysis: Some studies show uPAR-independent EMT in other cancers. Researchers must validate mesenchymal signature induction using RNA-seq and network analysis (e.g., WGCNA) to distinguish context-specific mechanisms .
What epigenetic or post-transcriptional mechanisms regulate PLAUR expression?
Recent studies identify novel small RNAs encoded within Plaur, such as Plaur-miR1-5p, which may stabilize HIF1A mRNA via ceRNA networks (e.g., HCG17-hsa-miR-424-5p-HIF1A) . These miRNAs are processed via Drosha/DGCR8 complexes and show conservation across vertebrates, suggesting functional relevance .
Methodological Note: To study PLAUR’s non-coding RNA interactions:
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Perform miRNA-seq on Plaur-expressing glioblastoma cells.
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Use luciferase assays to validate miRNA targets (e.g., HIF1A).
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Analyze scRNA-seq data to map miRNA expression to specific cell clusters (e.g., hypoxic macrophages in atherosclerosis) .
What therapeutic strategies target PLAUR in disease?
Key Challenge: PLAUR is expressed in a subpopulation of cancer cells , necessitating combination approaches to target both uPAR+ and uPAR- cells.
How do researchers address contradictions in PLAUR’s role across diseases?
Conflicting findings (e.g., pro-tumor vs. pro-atherogenic roles) arise from context-specific signaling. To resolve discrepancies:
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Perform meta-analyses of PLAUR expression in TCGA cohorts vs. single-center studies.
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Use multi-omics integration (e.g., WGCNA + scRNA-seq) to identify disease-specific regulatory networks .
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Validate findings in orthogonal models (e.g., glioblastoma neurospheres vs. atherosclerotic mouse models) .
How is PLAUR’s diagnostic utility validated across species?
PLAUR’s diagnostic potential in atherosclerosis was validated using:
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Human transcriptomic datasets (e.g., GSE28829).
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Mouse models (e.g., ApoE-/- mice on high-fat diets).
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Cross-species scRNA-seq alignment to confirm macrophage-specific expression .
Critical Parameter: Ensure antibody cross-reactivity (e.g., mouse anti-human PLAUR clones like A20095I ) when translating findings to preclinical models.
What computational tools optimize PLAUR-related hypothesis generation?
Product Science Overview
PLAUR is a highly glycosylated protein with a molecular weight of approximately 55-60 kDa. It is anchored to the plasma membrane via a glycosylphosphatidylinositol (GPI) anchor . The primary function of PLAUR is to bind to urokinase plasminogen activator (uPA), facilitating the conversion of plasminogen to plasmin, a serine protease involved in the degradation of the extracellular matrix and fibrinolysis .
PLAUR is significantly implicated in cancer biology. Overexpression of PLAUR and uPA is strongly correlated with poor prognosis in various malignant tumors . The uPA/PLAUR system drives tumor progression by mediating directed extracellular proteolysis on the surface of migrating or invading cells . Targeting PLAUR has been proposed as a novel approach for inhibiting tumor progression, making it a potential therapeutic target in cancer treatment .
Recombinant PLAUR (Human) is produced using DNA sequences encoding the human UPAR isoform 1 (Q03405-1) expressed in HEK293 cells . The recombinant protein is typically tagged with a polyhistidine tag for purification purposes and is used in various research applications, including functional assays and structural studies .
Recombinant PLAUR is widely used in research to study its role in cancer and other diseases. Functional assays, such as ELISA, are employed to measure its binding ability and interactions with other proteins . Additionally, PLAUR’s involvement in the tumor microenvironment and its interaction with tumor-associated macrophages (TAMs) and glioma cells have been subjects of recent studies .
