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ELISA Beta-type platelet-derived growth factor receptor,Canis familiaris,Canis lupus familiaris,CD140 antigen-like family member B,Dog,PDGFRB,PDGF-R-beta

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[#E2061c] ELISA Beta-type platelet-derived growth factor receptor,Canis familiaris,Canis lupus familiaris,CD140 antigen-like family member B,Dog,PDGFRB,PDGF-R-beta

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E2061c | ELISA Beta-type platelet-derived growth factor receptor,Canis familiaris,Canis lupus familiaris,CD140 antigen-like family member B,Dog,PDGFRB,PDGF-R-beta, 96T
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(1) [Platelet-derived growth factor-BB inhibited p21(WAF1) expression partially through transforming growth factor-beta signalling system in vascular smooth muscle cell].[TOP]

Pubmed ID :20398565
Publication Date : //
To assess if the modulating effect of platelet-derived growth factor (PDGF)-BB on p21(WAF1) was mediated by upregulating transforming growth factor (TGF)-beta(1) expression in vascular smooth muscle cells (VSMC).

Authors : Pan Da-Bin, Ke Yong-Sheng, Liu Wen-Jie, Wei You-Quan, Tang Jun, Cao Heng,



(2) TGF-beta type I receptor kinase inhibitor down-regulates rheumatoid synoviocytes and prevents the arthritis induced by type II collagen antibody.[TOP]

Pubmed ID :17135447
Publication Date : //
Rheumatoid arthritis (RA) is characterized by hypertrophic synovial tissues comprising excessively proliferating synovial fibroblasts and infiltrating inflammatory cells. Transforming growth factor-beta (TGF-beta) is a multifunctional cytokine that regulates cell growth, inflammation and angiogenesis by acting on various cell types. In RA synovial tissues, TGF-beta is expressed at high levels. However, the precise role of TGF-beta in RA remains unclear. We herein demonstrated a causal link between the TGF-beta-induced RA synovial cell proliferation and induction of platelet-derived growth factor (PDGF)-AA. In addition, TGF-beta induced IL-6 and vascular endothelial growth factor (VEGF) production by RA synovial fibroblasts associated with nuclear factor-kappa B activation. These effects of TGF-beta on RA synovial fibroblasts were suppressed by TGF-beta type I receptor kinase inhibitor HTS466284. Furthermore, HTS466284 significantly prevented anti-collagen type II antibody-induced arthritis in mice according to the clinical manifestations, histology, tumor necrosis factor-alpha, PDGF and VEGF expression and 5-bromo-2'-deoxyuridine incorporation. These in vitro and in vivo results suggest that TGF-beta plays a role in the development of synovial hyperplasia consisting of synovial cell proliferation, inflammation and angiogenesis. The blockade of TGF-beta signaling may thus become an additional strategy for the treatment of RA.

Authors : Sakuma Michitomo, Hatsushika Kyosuke, Koyama Kensuke, Katoh Ryohei, Ando Takashi, Watanabe Yoshiyuki, Wako Masanori, Kanzaki Mirei, Takano Shinichi, Sugiyama Hajime, Hamada Yoshiki, Ogawa Hideoki, Okumura Ko, Nakao Atsuhito,



(3) Analysis of growth factor-dependent signalling in human epithelioid sarcoma cell lines. clues To the role of autocrine, juxtacrine and paracrine interactions in epithelioid sarcoma.[TOP]

Pubmed ID :10854951
Publication Date : //
Human epithelioid sarcoma (ES) is an extremely aggressive soft tissue tumour of unknown histogenesis. Although growth factor-dependent signalling cascades significantly affect the biological behaviour of malignant tumours, little is known so far about their role in human ES. The present investigation, therefore, analyses the coexpression and function of different growth factors and their receptors in the human ES cell line GRU-1 and its clonal subpopulations (GRU-1A, GRU-1B and GRU-1C). As shown by Northern blot, flow cytometry, immunocytochemistry and MTT assay, all ES cell lines expressed transforming growth factor (TGF)-alpha and the epidermal growth factor receptor (EGF-R). Although no response to exogenous TGF-alpha was observed, antagonistic anti-EGF-R antibodies (at 20 microg/ml) induced significant (P<0.05) growth inhibition in all cell lines. All cell lines showed coexpression of platelet-derived growth factor (PDGF)-A and the corresponding receptors. Neutralisation of ES-derived PDGF by anti-hPDGF antibodies resulted in significant (P<0.05) growth inhibition of all clonal subpopulations. Although all cell lines expressed TGF-beta(1) as well as TGF-beta type I and type II receptors (TGF-BI-R and TGF-BII-R), growth inhibition (P<0.05) by exogenous TGF-beta(1) was achieved in the clonal subpopulations only and not in the parental cell line. No ES cell line expressed acidic fibroblast growth factor (FGF) but stimulation of FGF type 3 and type 4 receptors (FGF-3R and FGF-4R) by exogenous acidic FGF (aFGF) resulted in a marked (P<0.05) acceleration of proliferation in all cell lines. In conclusion, our investigation suggests an intricate network of autocrine, juxtacrine and paracrine signalling between ES tumour cells and adjacent non-neoplastic stromal cells.

Authors : Gerharz C D, Ramp U, Reinecke P, Schardt C, Friebe U, Déjosez M, Nitsch T, Gabbert H E,



(4) An antibody present in normal human serum inhibits the binding of cytokines to their receptors in an in vitro system.[TOP]

Pubmed ID :10493920
Publication Date : //
The presence of active transforming growth factor-beta (TGF-beta) in serum has not been widely accepted. In particular, although at least five studies have concluded that active TGF-beta is present in normal human plasma and serum, assays that use the extracellular domain of the TGF-beta type II receptor as a capture agent have given contradictory results. We show that there is an antagonist present in normal human serum which inhibits the binding of active TGF-beta to the extracellular domain of the TGF-beta type II receptor when it is coated on the well of an ELISA plate. This antagonist activity is due to a pool of immunoglobulins of the G2, D and M classes. Moreover, we show that this same pool of immunoglobulins also recognizes the extracellular domain of the platelet-derived growth factor alpha-receptor, insulin-like growth factor-1 receptor and interleukin-3 receptor, by serial transfer of serum over the different receptors. In addition, the same immunoglobulin pool inhibits the binding of platelet-derived growth factor-AA to its receptor, in an analogous way to the inhibition of binding of TGF-beta to its type II receptor. Circumstantial evidence suggests that the pool of immunoglobulins is recognizing a carbohydrate residue that is attached to the protein when it is synthesized by the mouse myeloma cell line, NSO, in which it is made. If the cytokine receptors are similarly glycosylated in vivo, then the presence of these antibodies in normal human serum may modulate physiological cytokine signalling.

Authors : Mosedale D E, Grainger D J,



(5) Functional intactness of stimulatory and inhibitory autocrine loops in human renal carcinoma cell lines of the clear cell type.[TOP]

Pubmed ID :9146668
Publication Date : //
The aim of the present study was to analyze the contribution of different stimulatory and inhibitory growth factors to the deregulated proliferation of human RCCs.

Authors : Ramp U, Jaquet K, Reinecke P, Schardt C, Friebe U, Nitsch T, Marx N, Gabbert H E, Gerharz C D,



(6) Transforming growth factor-beta receptor and fibronectin expressions in aortic smooth muscle cells in diabetic rats.[TOP]

Pubmed ID :9112014
Publication Date : //
Smooth muscle cells in arteries of diabetic rats and rabbits have unique properties including the overexpression of platelet-derived growth factor (PDGF) beta-receptor compared with controls. Fibronectin, one of the increased components of extra-cellular matrices in diabetic arteries, plays an important role in the phenotypic change of smooth muscle cells from the contractile to the synthetic type with the expression of the PDGF beta-receptor. Moreover, fibronectin synthesis is regulated by transforming growth factor-beta (TGF-beta). In this study, we report on the expression of TGF-beta receptors in diabetic smooth muscle cells, by immunohistochemistry, cross-linking of 125I-TGF-beta 1 to cells and quantitative reverse transcription-polymerase chain reaction. We also report on the effects of TGF-beta 1 on fibronectin synthesis of diabetic smooth muscle cells by use of ELISA and immunoprecipitation, in order to clarify the role of TGF-beta-fibronectin pathway in forming characteristic changes of diabetic smooth muscle cells. Cultured aortic smooth muscle cells of diabetic rats expressed TGF-beta type II receptor about 8.7 times that of controls at the protein level and 5.7 times at the mRNA level, whereas the expression of the type I receptor did not differ between the two types of smooth muscle cells. These changes were accompanied by increased fibronectin synthesis in diabetic smooth muscle cells in response to TGF-beta 1. Furthermore, protein expression of fibronectin, and mRNA and protein of TGF-beta type II receptor were increased in the diabetic aorta compared with the control aorta in vivo, implying the importance of the TGF-beta-fibronectin pathway for the unique biology of smooth muscle cells in the diabetic artery.

Authors : Kanzaki T, Shiina R, Saito Y, Zardi L, Morisaki N,



(7) Active and acid-activatable TGF-beta in human sera, platelets and plasma.[TOP]

Pubmed ID :7634487
Publication Date : //
Assays which measure active and latent forms of transforming growth factor beta (TGF-beta) separately in human serum and plasma are required to investigate the biological role of TGF-beta in a variety of human diseases. We have developed an enzyme-linked immunosorbent assay (ELISA) using two polyclonal antibodies against TGF-beta which rapidly determines the amount of active plus acid-activatable, latent TGF-beta forms ((a+l)TGF-beta) present in human serum and plasma in the range 4 pmol/l to 2000 pmol/l. To measure active TGF-beta alone, we have developed a second ELISA using the extracellular domain of the TGF-beta type II receptor as the capture reagent which detects active TGF-beta in serum and plasma samples in the range 20 pmol/l to 4000 pmol/l. Both assays detect TGF-beta 1 and TGF-beta 3 with similar sensitivity, are > 10-fold less sensitive to TGF-beta 2 and are not affected by a range of other peptide growth factors. The mean (a+l)TGF-beta present in human serum was 330 pmol/l but the range was very large (< 4 pmol/l to 1400 pmol/l). The mean active TGF-beta present was 230 pmol/l (range < 20 pmol/l to 1400 pmol/l) and the proportion of the (a+l)TGF-beta present which was active [a/(a+l)] varied from < 10% to 100%. The concentration of (a+l)TGF-beta and the proportion of TGF-beta which was active were very similar in the serum and platelet-poor plasma prepared from the same whole blood sample. The clot formed during serum preparation retained all of the TGF-beta which was detected by the (a+l)TGF-beta ELISA in the corresponding platelet releasate, although the PDGF in platelets was released into the serum. In contrast, platelet-poor plasma contained no detectable PDGF demonstrating that the (a+l)TGF-beta assayed in the plasma was not due to platelet degranulation after bleeding. Serum active TGF-beta and (a+l)TGF-beta concentrations therefore provide a reliable estimate of these forms of TGF-beta present in plasma.

Authors : Grainger D J, Mosedale D E, Metcalfe J C, Weissberg P L, Kemp P R,



(8) Characterization of platelet-derived growth factor and platelet-derived growth factor receptor expression in asbestos-induced rat mesothelioma.[TOP]

Pubmed ID :1309438
Publication Date : //
Although altered expression of platelet-derived growth factor (PDGF) is a hallmark of human mesothelioma, expression of PDGF receptors has not been characterized in this cell type. In addition, the expression of this growth factor and its cognate receptor in rodent mesothelioma has not been investigated. In this study, examination of transformed mesothelial cells derived from asbestos-induced rat mesotheliomas revealed that these cells expressed high affinity PDGF receptors (Kd = 0.5 nM) and receptor number was 1.6 x 10(5)/cell. Western analysis using antibodies specific for either the alpha-type or beta-type PDGF receptor and Northern analysis using probes specific for alpha- and beta-type receptor RNA transcripts indicated that these cells expressed beta-type PDGF receptors but that alpha-type receptors could not be detected. However, when the mesothelioma-derived cells were examined for the expression of PDGF, no expression of this growth factor could be detected. The transformed cells expressed no detectable A- or B-chain PDGF RNA transcripts; and using a competitive enzyme immunoassay specific for isoforms containing the B chain of PDGF and a sandwich enzyme-linked immunosorbent assay specific for A-chain-containing isoforms, neither AA, nor AB, nor BB isoforms of this growth factor could be detected in medium conditioned by these cells. The absence of alterations in PDGF expression in rat mesothelioma, in contrast to the data for the human disease, suggests that the production of this growth factor by transformed mesothelial cells may be species specific.

Authors : Walker C, Bermudez E, Stewart W, Bonner J, Molloy C J, Everitt J,