Relevant bibliographies by topics / UPAR

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Academic literature on the topic 'UPAR'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "UPAR"

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Huang, M., Q. Huai, A. Zhou, A. Mazar, G. Parry, A. Kuo, D. Cines, Y. Li, B. Furie, and B. C. Furie. "ID: 86 Structural basis of uPAR-uPA and uPAR-vitronectin interactions." Journal of Thrombosis and Haemostasis 4, s1 (October 2006): 227. http://dx.doi.org/10.1111/j.1538-7836.2006.00086.x.

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Wei, Ying, Ralf-Peter Czekay, Liliane Robillard, Matthias C. Kugler, Feng Zhang, Kevin K. Kim, Jian-ping Xiong, Martin J. Humphries, and Harold A. Chapman. "Regulation of α5β1 integrin conformation and function by urokinase receptor binding." Journal of Cell Biology 168, no. 3 (January 31, 2005): 501–11. http://dx.doi.org/10.1083/jcb.200404112.

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Urokinase-type plasminogen activator receptors (uPARs), up-regulated during tumor progression, associate with β1 integrins, localizing urokinase to sites of cell attachment. Binding of uPAR to the β-propeller of α3β1 empowers vitronectin adhesion by this integrin. How uPAR modifies other β1 integrins remains unknown. Using recombinant proteins, we found uPAR directly binds α5β1 and rather than blocking, renders fibronectin (Fn) binding by α5β1 Arg-Gly-Asp (RGD) resistant. This resulted from RGD-independent binding of α5β1–uPAR to Fn type III repeats 12–15 in addition to type III repeats 9–11 bound by α5β1. Suppression of endogenous uPAR by small interfering RNA in tumor cells promoted weaker, RGD-sensitive Fn adhesion and altered overall α5β1 conformation. A β1 peptide (res 224NLDSPEGGF232) that models near the known α-chain uPAR-binding region, or a β1-chain Ser227Ala point mutation, abrogated effects of uPAR on α5β1. Direct binding and regulation of α5β1 by uPAR implies a modified “bent” integrin conformation can function in an alternative activation state with this and possibly other cis-acting membrane ligands.
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Li, Y., and P. J. Cozzi. "Targeting uPA/uPAR in prostate cancer." Cancer Treatment Reviews 33, no. 6 (October 2007): 521–27. http://dx.doi.org/10.1016/j.ctrv.2007.06.003.

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Sah, Dhiraj Kumar, Pham Ngoc Khoi, Shinan Li, Archana Arjunan, Jae-Uk Jeong, and Young Do Jung. "(-)-Epigallocatechin-3-Gallate Prevents IL-1β-Induced uPAR Expression and Invasiveness via the Suppression of NF-κB and AP-1 in Human Bladder Cancer Cells." International Journal of Molecular Sciences 23, no. 22 (November 13, 2022): 14008. http://dx.doi.org/10.3390/ijms232214008.

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(-)-Epigallocatechin-3-O-gallate (EGCG), a primary green tea polyphenol, has powerful iron scavengers, belongs to the family of flavonoids with antioxidant properties, and can be used to prevent cancer. Urokinase-type plasminogen activator receptors (uPARs) are glycosylphosphatidylinositol (GPI)-anchored cell membrane receptors that have crucial roles in cell invasion and metastasis of several cancers including bladder cancer. The mechanism of action of EGCG on uPAR expression has not been reported clearly yet. In this study, we investigated the effect of EGCG on interleukin (IL)-1β-induced cell invasion and uPAR activity in T24 human bladder cancer cells. Interestingly, nuclear factor (NF)-κB and activator protein (AP)-1 transcription factors were critically required for IL-1β-induced high uPAR expression, and EGCG suppressed the transcriptional activity of both the ERK1/2 and JNK signaling pathways with the AP-1 subunit c-Jun. EGCG blocked the IL-1β-stimulated reactive oxygen species (ROS) production, in turn suppressing NF-κB signaling and anti-invasion effects by inhibiting uPAR expression. These results suggest that EGCG may exert at least part of its anticancer effect by controlling uPAR expression through the suppression of ERK1/2, JNK, AP-1, and NF-κB.
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Uhrin, Pavel, and Johannes M. Breuss. "uPAR." Cell Adhesion & Migration 7, no. 1 (January 2013): 23–26. http://dx.doi.org/10.4161/cam.22124.

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Shang, Run-Ze. "Role of uPA/uPAR system in tumors." World Chinese Journal of Digestology 22, no. 9 (2014): 1235. http://dx.doi.org/10.11569/wcjd.v22.i9.1235.

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Lippert, Solvej, Kasper Drimer Berg, Peter Iversen, Gunilla Høyer-Hansen, Ib Jarle Christensen, Klaus Brasso, and M. Andreas Røder. "Urokinase plasminogen activator receptor (uPAR) as a novel biomarker in prostate cancer." Journal of Clinical Oncology 33, no. 7_suppl (March 1, 2015): 183. http://dx.doi.org/10.1200/jco.2015.33.7_suppl.183.

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183 Background: New biomarkers are warranted to distinguish between indolent and aggressive prostate cancer (PCa). The urokinase plasminogen activator receptor (uPAR) plays an important role in pericellular proteolysis by binding urokinase plasminogen activator (uPA). This is required for degradation of the extracellular matrix and for cancer invasion. In addition to binding uPAR, uPA cleaves uPAR liberating uPAR(I) and uPAR(II-III). Intact, uPAR(I-III), and uPAR(II-III) can be liberated from the cell surface resulting in three different uPAR forms in circulation. The different uPAR forms are strong prognostic markers in several cancers. We measured the uPAR forms in plasma from patients with different stages of PCa. Methods: Between February 1, 2012 and October 1, 2014, 400 patients with PCa (se table) had plasma samples obtained. The levels of intact uPAR [uPAR(I-III)], intact uPAR + cleaved uPAR domains II+III [uPAR(I-III) + uPAR(II-III)], and cleaved uPAR domain I [uPAR(I)] were determined in citrated plasma samples with two-site sandwich time-resolved fluorescence immunoassays (TR-FIAs). Results: Plasma uPAR(I-III) + uPAR(II-III) and uPAR(I) were significantly higher in hormone naïve patients and CRPC patients compared to patients with localized disease (see table). Quantification of intact uPAR(I-III) revealed no significant differences between the three groups. Conclusions: Our findings suggest that uPAR(I-III) + uPAR(II-III) and uPAR(I) are associated with higher tumor stage as well as advanced PCa disease. These associations suggest that uPAR domains in plasma harbour prognostic value for PCa patients. Further studies are warranted to validate the use of uPAR forms as biomarkers for PCa. [Table: see text]
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Gorrasi, Anna, Anna Maria Petrone, Anna Li Santi, Mariaevelina Alfieri, Nunzia Montuori, and Pia Ragno. "New Pieces in the Puzzle of uPAR Role in Cell Migration Mechanisms." Cells 9, no. 12 (November 24, 2020): 2531. http://dx.doi.org/10.3390/cells9122531.

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The urokinase (uPA) receptor (uPAR) plays a key role in cell migration. We previously showed that uPAR-negative HEK-293 cells efficiently migrate toward serum but, after uPAR ectopic expression, migrate only in a uPAR-dependent manner. In fact, migration of uPAR-transfected HEK-293 (uPAR-293) cells is impaired by anti-uPAR antibodies, without recovery of the uPAR-independent migration mechanisms formerly active. Prostate carcinoma PC3 cells, which express high endogenous uPAR levels, migrated only through a uPAR-dependent mechanism; in fact, the silencing of uPAR expression inhibited their migration. We hypothesize a crucial role of the uPAR glycosyl-phosphatidyl-inositol (GPI) tail, which promotes uPAR partitioning to lipid rafts, in uPAR-controlled cell migration. Here, we show that removal of the uPAR GPI-tail, or lipid rafts disruption by methyl-beta-cyclodextrin impairs migration of PC3 cells, incapable of uPAR-independent migration, whereas it restores uPAR-independent migration in uPAR-293 cells. We then show that, in PC3 cells, both uPAR signaling partners, β1 integrins and receptors for formylated peptides (FPRs), partly associate with lipid rafts. Inhibition of their interaction with uPAR impairs this association and impairs cell migration. Interestingly, blocking uPAR association with FPRs also impairs β1 integrin partitioning to lipid rafts, whereas blocking its association with β1 integrins has no effect on FPRs partitioning. On these bases, we propose that uPAR controls cell migration by connecting β1 integrins and FPRs and, through its GPI tail, by driving them into lipid rafts, thus promoting pro-migratory signals. uPAR-mediated partitioning of integrins to lipid rafts is strictly dependent on uPAR association with FPRs.
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Park, Young-Jun, Gang Liu, Yuko Tsuruta, Emmanuel Lorne, and Edward Abraham. "Participation of the urokinase receptor in neutrophil efferocytosis." Blood 114, no. 4 (July 23, 2009): 860–70. http://dx.doi.org/10.1182/blood-2008-12-193524.

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AbstractThe urokinase receptor (uPAR) plays an important role in regulation of fibronolysis, cell migration, and adhesion. In this study, we examined whether uPAR plays a role in modulating efferocytosis of neutrophils. Macrophages from uPAR−/− mice demonstrated enhanced ability to engulf viable wild-type (WT) neutrophils in vitro and in vivo in the lungs. The increased phagocytic activity of uPAR−/− macrophages was abrogated by incubation with soluble uPAR (suPAR), arginine-glycine-aspartic acid (RGD)–containing peptides, or anti-integrin antibodies. There was increased uptake of viable uPAR−/− neutrophils by WT macrophages. Incubation of uPAR−/− neutrophils with suPAR or anti-integrin antibodies diminished uptake by WT macrophages to baseline. Uptake of uPAR−/− neutrophils by uPAR−/− macrophages was not enhanced. However, incubation of uPAR−/− neutrophils or uPAR−/− macrophages, but not both, with suPAR enhanced the uptake of viable uPAR−/− neutrophils by uPAR−/− macrophages. The adhesion of WT neutrophils to uPAR−/− macrophages was higher than to WT macrophages. uPAR−/− neutrophils demonstrated increased adhesion to suPAR, which was abrogated by blocking of low-density lipoprotein related protein and integrins. Expression of uPAR on the surface of apoptotic neutrophils was reduced compared with levels on viable neutrophils. These results demonstrate a novel role for uPAR in modulating recognition and clearance of neutrophils.
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Kotzsch, Matthias, Axel Meye, Thomaz Langerholc, Susanne Füssel, Natalie Olbricht, Sybille Albrecht, Detlev Ockert, et al. "Identification of a novel urokinase receptor splice variant and its prognostic relevance in breast cancer." Thrombosis and Haemostasis 89, no. 04 (2003): 705–17. http://dx.doi.org/10.1055/s-0037-1613577.

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SummaryThe cellular receptor for urokinase-type plasminogen activator, uPAR, plays a central role in both cell surface-associated proteolysis and cellular adhesion. In the present study, we systematically searched for splice variants of uPAR mRNA in human cells and tumor tissues by qualitative RT-PCR using specific primers for uPAR exons 1 and 6. Beside the wild-type (wt) uPAR mRNA and the previously described splice variant lacking exon 5 (uPAR-del5), a novel splice variant lacking both exons 4 and 5 (uPAR-del4/5) was found predominantly in various cancer cell lines. To elucidate whether alternatively spliced uPAR mRNA may be translated and post-translationally processed, we generated stably transfected Chinese hamster ovary cells, which harbor expression plasmids of wt uPAR and various uPAR variants including uPAR-del5 and uPAR-del4/5. By ELISA, flow cytofluorometry, and Western blot analysis, we confirmed synthesis and secretion of wt uPAR and the uPAR variants by the use of domain-specific monoclonal antibodies against uPAR. For quantification of uPAR mRNA variants, we established two highly sensitive real-time RT-PCR assays based on LightCycler technology. Study of their expression in a representative set of breast cancer tissues indicated that the novel mRNA variant uPAR-del4/5 was expressed very frequently and independently of uPAR mRNA variants covering exon 4 (uPAR-wt and uPAR-del5). Higher uPAR-del4/5 expression was significantly associated with shorter disease-free survival (p = 0.0004) of breast cancer patients. These results suggest that uPAR-del4/5 mRNA may serve as a novel prognostic marker in breast cancer.Theme paper: Part of this paper was originally presented at the joint meetings of the 16th International Congress of the International Society of Fibrinolysis and Proteolysis (ISFP) and the 17th International Fibrinogen Workshop of the International Fibrinogen Research Society (IFRS) held in Munich, Germany, September, 2002.
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Dissertations / Theses on the topic "UPAR"

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Barson, Helen. "Studies on the cellular function of the uPA/uPAR system." Thesis, University of Aberdeen, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419648.

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The uPA receptor, uPAR, is GPI-linked and therefore contains no transmembrane domains.  Yet, uPA:uPAR binding can initiate cell signalling and may involve adaptor proteins, such as integrins.  Various responses to uPA binding have been described, but the exact mechanisms remain undefined. To identify potential downstream changes caused by uPA binding, MCF7 cells were treated ± uPA or ATF (the uPAR-binding part of uPA) for various times.  Gene expression was studied using custom cDNA microarrays, containing genes relating to a range of cellular processes.  Changes in expression were normalised to 0 min and buffer-only controls, and genes with a fold change less than 2.5-fold were discounted.  Gene expression changes that were observed in two or more treatments were shortlisted, from which thirteen were selected fro verification by real-time RT-PCR.  These experiments were done on cDNA from a further cell treatment with uPA.  The results did not reflect those of the microarrays; no changes in expression were observed.  The microarray data were then analysed in a different, more stringent, way, but not target genes were identified.  This study identified no clear candidate genes but gene expression after uPA:uPAR binding remains an important question. uPAR is present in lipid rafts and these may allow its association with signalling molecules.  This study investigated whether potential uPAR adaptor proteins, αv or β1 integrins, moved into rafts when cells bound uPA.  Mouse cells transfected with human uPAR were treated ±uPA, and lipid rafts were extracted from the cells.  uPAR was readily detectable in lipid rafts under al conditions, but the integrins were not found to associate with lipid rafts even after uPA treatment.
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Arendholz, Tanja [Verfasser]. "Bedeutung des uPA/uPAR-Systems für die Proliferation glatter Gefäßmuskelzellen / Tanja Arendholz." Gießen : Universitätsbibliothek, 2012. http://d-nb.info/1064024483/34.

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Petzinger, Jutta [Verfasser]. "Urokinase-Rezeptor (uPAR) und Zellkontakte : Mechanismen uPAR-abhängiger Zelladhäsion, Zellmigration und Signaltransduktion / Jutta Petzinger." Gießen : Universitätsbibliothek, 2011. http://d-nb.info/1063177480/34.

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Randle, Diandra Dominique. "Snail mediates cell invasion through uPa-uPar and mark signaling in human prostate cancer cells." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2014. http://digitalcommons.auctr.edu/dissertations/1648.

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Epithelial-mesenchymal transition (EMT) is a process by which cancer cells acquire mesenchymal properties, such as induction of vimentin, while epithelial-associated genes like E-cadherin are lost. This enables the cells to be more metastatic. Factors that can induce EMT include growth factors like transforming growth factor -P (TGF-P) and epidermal growth factor (EGF), and transcription factors like Snail. Snail-induced EMT promotes migration and invasion and we hypothesized that this may be mediated by urokinase (uPA) and its receptor (uPAR) activities. LNCaP, 22Rvl and ARCaP human prostate cancer (CaP) cells stably transfected with constitutively active Snail displayed increased cell invasion as compared to the empty vector control (Neo). Superarray analysis revealed an up-regulation in uPA and uPAR RNA expression in Snailtransfected ARCaP cells as compared to Neo control. Next, the protein expression levels of Snail, uPA, and uPAR were measured by western blot analysis in various prostate cancer cell lines which showed that overexpression of Snail increased uPA and uPAR protein levels. The activity of uPA in conditioned media was measured using an ELISA assay which revealed that uPA activity was elevated in LNCaP, 22Rvl and ARCaP cells overexpressing Snail. Additionally, transient silencing of uPAR in ARCaP cells overexpressing Snail using siRNA resulted in abrogation of Snail-mediated invasion. Snail overexpression was associated with increased ERK activity and antagonism of this activity with MAPK inhibitor, UO126, inhibited cell invasion and decreased uPA activity. Therefore, Snail-mediated cell invasion in human prostate cancer cells may occur via the regulation of uPA/ uPAR and the MAPK signaling pathways.
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Sandoval, Rubenstein Cynthia Priscilla, and Rubenstein Cynthia Priscilla Sandoval. "Laminin Binding α6β1 Integrin Regulation in Aggressive Cancer Cells and Tissue." Diss., The University of Arizona, 2017. http://hdl.handle.net/10150/625446.

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Despite recent advances in early detection, in 2017 prostate cancer is estimated to claim over 26,000 lives in the United States alone. Prostate cancer related morbidity and mortality is a result of secondary skeletal metastasis. Therefore, better understanding of the underlying molecular mechanisms of prostate tumor cell migration and subsequent metastasis is vital for improved clinical outcomes. Interestingly, integrin α6, a laminin receptor, is highly expressed in a number of aggressive tumor types including prostate and is associated with increased metastasis and reduced patient survival. Preliminary studies by our group found that α6 integrin undergoes a post-translational modification mediated by the serine protease, uPA and its receptor, uPAR, leading to the cleavage of α6 integrin and production of the tumor specific structural variant integrin α6p. Cleavage of this laminin receptor and production of α6p variant gives rise to an aggressive phenotype, markedly increasing tumor cell migration and invasion. Thus, the work conducted here sought to identify the function and efficacy of these prominent proteins in various aspects of tumor cell migration as well as the factors regulating α6 integrin cleavage. Interestingly, utilization of a co-culture system of prostate tumor cells and macrophages found that a direct and indirect interaction between the two cell populations influenced α6 integrin cleavage. Specifically, prostate tumor cell interactions with macrophages, a known immune cell population that is highly observed in a number of primary tumors, resulted in increased protein levels of uPAR on the surface of prostate tumor cells that led to a significant production of α6p and subsequently increased invasion. Additionally, key downstream effectors of integrin signaling, including FAK, ILK, and actin, were found to regulate production of the tumor specific variant integrin α6p. Depletion of FAK, ILK, or actin, resulted in a significant increase in uPAR protein expression and subsequent α6 integrin cleavage, a regulatory event previously not known of these integrin signaling effector molecules. In addition, silencing of another prominently expressed laminin receptor, integrin α3β1, led to a significant increase in the cohesive collective phenotype exhibited by aggressive prostate tumor cells that was found to be facilitated by α6 integrin cleavage. Depletion of integrin α3β1 resulted in increased surface uPAR expression and increased lateral association with α6 integrin, which resulted in a striking increase in α6p production, a novel finding showing the regulation of one laminin receptor is dependent on the expression of another. Furthermore, the expression of α6 integrin as well as uPAR, was found to be highly expressed in aggressive pancreatic tumor cells. This expression pattern was found to significantly increase in response to the development of drug resistance and increased invasive potential. This finding showed a never before seen efficacy of integrin and uPAR expression in dictating acquired drug resistance in pancreatic tumor cells and demonstrates their potential use as prognostic biomarkers for acquired chemotherapy resistance. Taken together, the work conducted here illustrates the utility in further understanding the role of integrins and their regulation in mediating tumor cell migration and subsequent metastasis in the progression of aggressive epithelial cancers.
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PIRAZZOLI, VALENTINA. "ROLE OF VITRONECTIN INTERACTION IN THE BIOLOGY OF THE UROKINASE RECEPTOR." Doctoral thesis, Università degli Studi di Milano, 2011. http://hdl.handle.net/2434/155510.

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Expression of uPAR has been extensively correlated with the malignant progression and metastasis of cancer; however, little evidence for a causal connection between increased uPAR expression and these processes has been documented to date. A complete functional alanine scan of human uPAR, pinpointed the extracellular matrix protein vitronectin (VN) as the critical uPAR-interactor required to induce cell adhesion, migration, and signaling in vitro, identifying this molecular interaction as a possible target for anti-cancer therapy (Madsen et al., 2007). The same study helped to determine the binding epitope in uPAR responsible for its interaction to VN in an integrin-independent fashion. The composite epitope is fully conserved in mouse and included three amino acids (W32, R58, I63) in domain 1 (D1) and 2 amino acids (R92, Y93) in the linker region between D1 and D2. We substituted these residues with alanine by site directed mutagenesis and analyzed the biological activity of resulting receptor variants in CHO Flp-In cells as compared to wild-type muPAR. All the mutant receptors displayed a deficiency for the binding to VN, preserving the receptor binding to its natural ligand uPA. They also failed to induce muPAR-induced cell morphology changes. These changes include the formation of actin-rich lamellipodia, loss of stress fibers, reduced cell-cell contact as well as a complete failure to form colonies when seeded at low density. The mouse uPARW32A (muPARW32A) was chosen for further experiments since it did not show folding problems. Moreover the W32 position is not a part of the receptor chemotactic epitope and is not involved in the receptor cleavage. Additional experiments using recombinant soluble muPAR confirmed the impaired VN-binding and a normal uPA-binding. To determine if uPAR and/or VN are involved in tumor formation and progression, and more specifically, if the direct uPAR/VN-interaction is important in this process, we exploited a xenograft mouse model. For this purpose muPAR or muPARW32A or a muPAR variant lacking of the D1, required for both VN and uPA binding (muPARΔD1), were expressed in HEK293 Flp-In GFP positive cells and injected in the fourth mammary fat pad of immunodeficient mice. In parallel the cells were tested for some in vitro assays. We demonstrated that HEK293 cells expressing muPAR are more proliferating and less apoptotic than the other cells. The interaction with VN is required to increased cell proliferation and to prevent from apoptosis. Moreover, muPAR-VN interaction induced cell spreading and migration. muPAR expressing cells formed palpable tumors earlier than cells expressing the mutant receptors and the tumor growth was significantly faster. Despite the expression of the muPARW32A didn’t affect the timing of the primary tumor formation, it drastically slowed down the growth of the primary tumor mass. Finally we conducted in vitro studies to determine the molecular mechanisms underlying the possible role of the uPAR/VN-interaction in vivo. From these tests emerged that VN may act as an adhesion “bridge” between different cells expressing uPAR and VN-integrins or cells expressing both uPAR, suggesting a possible role of the uPAR/VN-interaction not only in cell-ECM interactions but also in cell-cell adhesion events including the extravasation of metastatic cancer cells.
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MABILAT, PRAGNON CHRISTELLE. "Systeme upa/upar dans la migration cellulaire : localisation subcellulaire dans les cellules endotheliales et les eosinophiles." Paris 7, 1998. http://www.theses.fr/1998PA077253.

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Que ce soit dans des circonstances physiologiques ou pathologiques, la migration cellulaire est un phenomene ubiquitaire. Nous pouvons citer comme exemples, la migration des cellules endotheliales pendant la formation des vaisseaux sanguins (l'angiogenese) et la migration des globules blancs lors des reactions inflammatoires de l'organisme. Le systeme urokinase/recepteur de l'urokinase (upa/upar) joue un role majeur dans la migration cellulaire. L'objectif de ce travail etait 1) de caracteriser le systeme upa/upar dans deux types cellulaires differents ; 2) d'etudier l'effet du blocage de l'upar sur la migration cellulaire. Les resultats de cette these montrent que 1) la distribution subcellulaire du systeme upa/upar est tres differente entre les cellules endotheliales et les eosinophiles et qu'elle est tres finement controlee. Dans les cellules endotheliales, l'upar est associe a des structures membranaires particulieres, les caveoles, qui sont des invaginations specifiques de la membrane plasmique. Dans les eosinophiles, le systeme upa/upar, stocke dans des vesicules intracytoplasmiques, est retrouve au niveau de la membrane plasmique apres l'activation des cellules. Ainsi, la localisation du systeme upa/upar depend de l'etat d'activation et du potentiel migratoire de la cellule ; 2) la rupture de l'axe upa/upar, en bloquant l'upar avec une proteine chimerique, inhibe de maniere spectaculaire la migration des cellules endotheliales in vitro. Ainsi, le blocage de l'upar pourrait conduire a l'inhibition de l'angiogenese en inhibant la migration des cellules endotheliales. L'ensemble de ces resultats ouvre de larges perspectives de recherche sur le developpement d'agents bloquant l'upar, qui, en inhibant la migration des cellules endotheliales, peuvent etre utilises comme therapeutique anti-angiogenique pour le traitement du cancer.
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Moreau, Marie. "La ß-caténine et le NF-Kß coopèrent pour réguler le système uPA/uPAR dans des cellules tumorale." Paris 7, 2010. http://www.theses.fr/2010PA077113.

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La voie Wnt/ß-caténine est impliquée dans de nombreux événements comprenant l'adhésion, la migration, et la différenciation cellulaires. L'activateur du plasminogène de type urokinase (uPA) et son récepteur uPAR ont été décrits comme des gènes cibles de la voie Wnt/ß-caténine dans des cellules de cancer du colon. En utilisant deux lignées tumorales mammaires, MCF-7 et MDA-MB-231 et une lignée tumorale de colon, SW480, nous avons observé que l'inhibition de l'expression de la ß-caténine augmente l'expression d'uPA, d'uPAR et de l'inhibiteur de l'activateur du plasminogène PAI-1 ainsi que l'invasivité des cellules tumorales. La stabilisation de la ß-caténine par un traitement au chlorure de lithium (LiCl), inhibiteur de la glycogène synthase kinase-3beta (GSK-3ß) ou la co-transfection de vecteurs d'expression ß-caténine/Tcf-4 conduit à la diminution de l'expression des transcrits uPA, uPAR et PAI-1 dans les trois lignées. Le traitement des cellules transfectées par des siRNA ß-caténine avec un inhibiteur de la translocation nucléaire du nuclear factor-kappaB (NF-KB), le SN50, réduit significativement l'augmentation de l'expression des transcrits uPA, uPAR et PAI-1 et de l'invasivité cellulaire. De plus, nous avons observé une translocation nucléaire du NF-KB dans les cellules transfectées par un siRNA ß-caténine. Dans cette étude nous montrons un nouveau mécanisme de régulation du système uPA/uPAR par la ß-caténine, en coopération avec NF-KB, dans des cellules de cancer du sein et du colon. La ß-caténine peut exercer des effets inattendus dans les cellules tumorales et des stratégies thérapeutiques d'inhibition de son expression doivent être envisagées avec précaution
The Wnt/ß-catenin signaling influences many cellular processes including cell adhesion, growth and differentiation. Urokinase plasminogen activator (uPA) and urokinase plasminogen activator receptor (uPAR) have been reported as target genes of Wnt/ß-catenin signaling in colon cancer cells, since their expression is directly regulated through ß-catenin, binding to the T-cell factor binding element (TBE) motifs present in their promoters. Using three cancer cell models (MCF-7, MDA-MB-231 and SW480, breast and colon cancer cell lines, respectively) we demonstrated that silencing of ß-catenin increased uPA, uPAR and plasminogen activator inhibitor-1 (PAI-1) expression and the invasive potential of cancer cells. In addition, p-catenin stabilization and accumulation by lithium chloride (LiCl) treatment, an inhibitor of glycogen synthase kinase-3ß (GSK-3ß) or by ß-catenin/Tcf-4 expression vectors transfection led to a decrease in uPA, uPAR and PAI-1 mRNA expression in the studied cancer models. Moreover, the treatment of P-catenin siRNA transfected cells with a specific inhibitor of nuclear factor-kappaB (NF-KB) translocation, SN50, significantly reduced enhancement of uPA, uPAR and PAI-1 expression and cancer cell invasion. Furthermore, ß-catenin siRNA treated cells exhibited NF-KB nuclear translocation. In this study we present evidence of a novel cross-talk between ß-catenin and uPA/uPAR System through NF-KB cooperation in breast and colon cancer cells. Our results strengthen the emerging view that ß-catenin exerts different effects on tumor cells and that the therapeutic strategy of its inhibition could involve more complex mechanisms than originally anticipated
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Kean, Thomas. "Development of a synthetic uPAR targeted gene delivery system." Thesis, Cardiff University, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.635545.

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Planus, Emmanuelle. "Adherence et mecanotransduction via le complexe : recepteur de l'urokinase/urokinase/inhibiteur (upar/upa/pai-1) du systeme activateur du plasminogene." Paris 12, 1996. http://www.theses.fr/1996PA120085.

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Le systeme activateur du plasminogene (pas) via l'urokinase est un des principaux systemes proteolytiques des composants de la matrice extracellulaire. La voie de l'urokinase permet la formation d'un complexe compose d'un recepteur membranaire (upar), de l'urokinase (upa) et de l'inhibiteur de type 1 (pai-1). L'expression des composants de ce systeme est frequemment associee a la migration et a l'invasion cellulaire. Dans le but d'etudier l'implication du systeme pas dans ces phenomenes, nous avons voulu comprendre le role joue par le complexe tripartite upar/upa/pai-1 dans les mecanismes de l'adherence et de la mecanotransduction de signaux qui en decoule. Dans une premiere partie, nous avons montre que les cellules adheraient et s'etalent normalement sur une matrice uniquement constituee de pai 1. Dans une deuxieme partie, nous avons montre que ce processus etait dependant de la presence de l'upa a la surface cellulaire dans une derniere partie, nous avons montre qu'a travers le complexe upar/upa/pai-1 a la surface cellulaire, il etait possible de transmettre des forces mecaniques a l'interieur de la cellule. Nous en avons deduit que la formation du complexe tripartite upar/upa/pai-1 pouvait representer un des ponts moleculaires entre la cellule et le substrat, necessaires a l'adherence et a l'etalement des cellules. Enfin, nous avons discute des implications possibles du systeme pas comme 1) mediateur direct de l'adherence 2) mediateur eventuel de la deadherence par son activite proteolytique des composants de la matrice et 3) ainsi par ces deux actions son role dans la migration cellulaire.
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Books on the topic "UPAR"

1

Phull, Susheel Kumar. Parvaton ke upar. Delhi: Sharda Prakashan, 1990.

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Mitra, Vimal. Sabse upar kaun. Delhi: Sanmarg Prakashan, 1988.

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Osho. Shuli upar sej piyani. Surendanagar: Osho Bodhitaru Dhyan Kendra, 1991.

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Crónicas del Valle de Upar. [Valledupar, Colombia?: s.n.], 2000.

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Himachal Pradesh (India). Department of Information & Public Relations. 4 years of good governance: Sabse upar Himachal. Shimla: Information & Public Relations, 2011.

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Trespalacios, Pedro Castro. Culturas aborígenes cesarenses e independencia del Valle de Upar. 2nd ed. Santa Fé de Bogotá, D.C: Senado de la República, Congreso de Colombia, 2000.

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Vaughan, Marcia K. Upar and the great nut tree: A South American myth. Upper Saddle River, N.J: Pearson/Celebration Press, 2006.

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illustrator, Gaber Susan, ed. Upar and the great nut tree: A South American myth. Parsippany, N.J: Celebration Press, 2003.

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Araujonoguera, Consuelo. Lexicón del Valle de Upar: Voces, modismos, giros, interjecciones, locuciones, dichos, refranes y coplas del habla popular vallenata. Santafé de Bogotá: Instituto Caro y Cuervo, 1994.

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Araujonoguera, Consuelo. Lexicón del Valle de Upar: Voces, modismos, giros, interjecciones, locuciones, dichos, refranes y coplas del habla popular vallenata. Santafé de Bogotá: Instituto Caro y Cuervo, 1994.

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Book chapters on the topic "UPAR"

1

Blount, Mitsi A., Janet D. Klein, and Jeff M. Sands. "uPAR." In Encyclopedia of Signaling Molecules, 1945. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101430.

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Montuori, Nunzia, and Pia Ragno. "Role of uPA/uPAR in the Modulation of Angiogenesis." In Chemical Immunology and Allergy, 105–22. Basel: S. KARGER AG, 2013. http://dx.doi.org/10.1159/000353310.

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Büchler, P., H. A. Reber, O. J. Hines, M. W. Büchler, and H. Friess. "HIF-1 steuert Angioinvasion und Metastasierung durch Regulation der uPAR — Genexpression." In Zurück in die Zukunft, 610–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55611-1_419.

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Guthaus, Elke, Niko Schmiedeberg, Markus Bürgle, Viktor Magdolen, Horst Kessler, and Manfred Schmitt. "The Urokinase Receptor (uPAR, CD87) as a Target for Tumor Therapy: uPA-Silica Particles (SP-uPA) as a New Tool for Assessing Synthetic Peptides to interfere with uPA/uPA-Receptor Interaction." In Molecular Staging of Cancer, 3–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-59349-9_1.

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Leksa, Vladimir, Herbert B. Schiller, and Hannes Stockinger. "Biotin-Chasing Assay to Evaluate uPAR Stability and Cleavage on the Surface of Cells." In Methods in Molecular Biology, 39–47. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7595-2_4.

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Büchler, P., H. Friess, M. W. Müller, H. A. Reber, O. J. Hines, and M. W. Büchler. "HIF-1 steuert die Angioinvasion und Metastasierung durch Regulation der uPAR — Genexpression beim Pankreaskarzinom." In Deutsche Gesellschaft für Chirurgie, 29–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-19024-7_9.

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Kim, Cheorl-Ho. "GM3, Competing with GM1, Interaction with Urokinase Plasminogen Activator Receptor (uPAR) in Endothelial Caveolar-Lipid Rafts Inhibits Angiogenesis." In GM3 Signaling, 77–78. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5652-4_14.

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Blount, Mitsi A., Janet D. Klein, and Jeff M. Sands. "uPA Receptor." In Encyclopedia of Signaling Molecules, 1945. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101429.

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Umdale, Suraj Dhanyakumar, Pankaj Shivnarayan Mundada, and Mahendra Laxman Ahire. "Antiaris toxicaria (Upas Tree)." In Exploring Poisonous Plants, 129–37. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/b23017-11.

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Bottini, Cinzia. "The UPA Formula." In Redesigning Animation, 171–214. Boca Raton : Taylor & Francis, 2018.: Routledge, 2018. http://dx.doi.org/10.1201/9781351209595-5.

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Conference papers on the topic "UPAR"

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Ryu, Jinhyun, Jungil Choi, Dong Hoon Lee, Gu Seob Roh, Hyun Joon Kim, Gyeong Jae Cho, Wan Sung Choi, Jae-Yong Park, Jeong Woo Park, and Sang Soo Kang. "Abstract 3194: Tristetraprolin controls the stability of uPA/uPAR mRNA through binding to the 3’UTR of uPA/uPAR mRNA in U87MG glioma cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3194.

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Randle, Diandra D., and Valerie Odero-Marah. "Abstract 3430: Snail1 regulates invasion through uPA-uPAR signaling in prostate cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3430.

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Tucker, T. A., R. Logan, A. Jeffers, W. Qin, S. Owens, P. Chauhan, S. Komatsu, M. Ikebe, and S. Idell. "uPA and uPAR are Critical Mediators of Mesothelial Mesenchymal Transition and Pleural Fibrosis." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4419.

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Webster, Megan, Victoria Schroeder, Eva Peter, Ines Kollak, Jennifer Schuett, Bernd Guilliard, Ingrid Christ, et al. "Inhibition of uPA-uPAR signaling restores respiratory epithelial barrier function in asthma and COPD." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3856.

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Kwon, Yeo-Jung, and Young-Jin Chun. "Abstract 3469: CYP1B1 induces cancer progression through regulation of TRAIL pathway and uPA-uPAR system." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3469.

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Kwon, Yeo-Jung, and Young-Jin Chun. "Abstract 3469: CYP1B1 induces cancer progression through regulation of TRAIL pathway and uPA-uPAR system." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3469.

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Specker, Andreas, Mickael Cormier, and Jurgen Beyerer. "UPAR: Unified Pedestrian Attribute Recognition and Person Retrieval." In 2023 IEEE/CVF Winter Conference on Applications of Computer Vision (WACV). IEEE, 2023. http://dx.doi.org/10.1109/wacv56688.2023.00104.

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Kandela, Irawati, Andrey Ugolkov, Giulio Francia, Shafaat Rabbani, Robert S. Kerbel, and Andrew P. Mazar. "Abstract 863: Inhibition of breast cancer metastaticprogression by a novel uPAR targeted monoclonal antibody, ATN-658, correlateswith the uPAR expression." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-863.

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Randle, Diandra D., Shineka Clarke, and Valerie Odero-Marah. "Abstract 2407: Snail 1 regulates invasion through uPA-uPAR and MMP-9 signaling in prostate cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2407.

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Kwon, Yeo-Jung, Sangyun Shin, and Young-Jin Chun. "Abstract 2847: Human CYP1B1 induces cancer cell metastasis through Sp1-mediated activation of uPA-uPAR signaling pathway." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2847.

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Reports on the topic "UPAR"

1

López, Angel M. UPR/Mayaguez High Energy Physics. Office of Scientific and Technical Information (OSTI), October 2015. http://dx.doi.org/10.2172/1224213.

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Mendez, Hector. UPR/Mayaguez High Energy Physics. Office of Scientific and Technical Information (OSTI), October 2014. http://dx.doi.org/10.2172/1195544.

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Rao, Nitya, Sheetal Patil, Maitreyi Koduganti, Chandni Singh, Ashwin Mahalingam, Prathijna Poonacha, and Nishant Singh. Sowing Sustainable Cities: Lessons for Urban Agriculture Practices in India. Indian Institute for Human Settlements, 2023. http://dx.doi.org/10.24943/ssc12.2022.

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Despite growing interest and recognition of urban and peri-urban agriculture (UPA) as a nature- based solution, there is limited empirical evidence in countries like India on its role in reconfiguring goals on environmental functions (such as biodiversity, waste management, water recycling, micro-climate regulation, etc.) and social wellbeing (such as food and nutrition security, gender relations, work burdens, land tenure and community ties). A need to address this gap led to the ideation of the project ‘Urban and peri-urban agriculture as green infrastructures’ ( UPAGrI ). When UPAGrI started in 2019, the research on UPA in India was thin but growing. However, the practical experience of urban farming across Indian cities is thriving and diverse, built on decades of bottom-up experimentation. Within the landscape of our ever-changing cities, we found vibrant communities-of-practice sharing seeds and knowledge, engaged online influencers discussing composting and water reuse, and stories of farming becoming sites of multi-generational bonding and nutritional security. This compendium is a collection of 29 such innovative UPA practices from across the different cities in the country. These diverse case studies are loosely categorized into four themes: environment and sustainability; food, nutrition and livelihood; gender and subjective well-being; and urban policy and planning. Written mostly by practitioners themselves, the case studies collectively recognise and celebrate UPA innovations and practices, serving as a repository of lessons for peer-to-peer learning, and demonstrating how UPA can be one of the many solutions towards sustainable, liveable Indian cities.
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Rao, Nitya. Sowing Sustainable Cities: Lessons for Urban Agriculture Practices in India. Indian Institute for Human Settlements, 2023. http://dx.doi.org/10.24943/ssc12.2023.

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Despite growing interest and recognition of urban and peri-urban agriculture (UPA) as a nature- based solution, there is limited empirical evidence in countries like India on its role in reconfiguring goals on environmental functions (such as biodiversity, waste management, water recycling, micro-climate regulation, etc.) and social wellbeing (such as food and nutrition security, gender relations, work burdens, land tenure and community ties). A need to address this gap led to the ideation of the project ‘Urban and peri-urban agriculture as green infrastructures’ ( UPAGrI ). When UPAGrI started in 2019, the research on UPA in India was thin but growing. However, the practical experience of urban farming across Indian cities is thriving and diverse, built on decades of bottom-up experimentation. Within the landscape of our ever-changing cities, we found vibrant communities-of-practice sharing seeds and knowledge, engaged online influencers discussing composting and water reuse, and stories of farming becoming sites of multi-generational bonding and nutritional security. This compendium is a collection of 29 such innovative UPA practices from across the different cities in the country. These diverse case studies are loosely categorized into four themes: environment and sustainability; food, nutrition and livelihood; gender and subjective well-being; and urban policy and planning. Written mostly by practitioners themselves, the case studies collectively recognise and celebrate UPA innovations and practices, serving as a repository of lessons for peer-to-peer learning, and demonstrating how UPA can be one of the many solutions towards sustainable, liveable Indian cities.
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Lindberg, Michael J. Geochemical Charaterization of Sediments from UPR 200-E-81. Office of Scientific and Technical Information (OSTI), July 2008. http://dx.doi.org/10.2172/1024562.

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Clarke, Robert, Milton Brown, Ayesha N. Shajahan, and Jacqueline Smith. Targeting the UPR to Circumvent Endocrine Resistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613724.

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Gorman, Clare, Lucy Halton, and Kushum Sharma. Advocating for Change in Nepal’s Adult Entertainment Sector. Institute of Development Studies (IDS), July 2021. http://dx.doi.org/10.19088/clarissa.2021.010.

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The United Nations Human Rights Council has a powerful role to play in addressing the worst forms of child labour. Accountability mechanisms such as the Universal Periodic Review (UPR) – which work to support Member States to improve their human rights situation – are therefore widely seen as important opportunities to advocate for change. Ahead of Nepal’s third UPR cycle in 2021, the CLARISSA programme met with eight UN Permanent Missions to present recommendations addressing the exploitation of children within Nepal’s adult entertainment sector. This spotlight story shares the programme’s experience in advocacting within this process. It also highlights their approach of providing decision makers with recommendations to the Government of Nepal that were underpinned by the importance of integrating a participatory, adaptive and child-centred approach.
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Gallick, Gary E. Cellular Mechanisms Regulating uPA in Hormone Refractory Prostate Cancer: A Novel Therapeutic Target. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada398158.

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Czekay, Ralf-Pater, and Marilyn Farquhar. Relationship Between Scavenger Receptors and uPA:PAI-l and uPA Receptors in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 1997. http://dx.doi.org/10.21236/ada338927.

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Czekay, Ralf-Peter, and Marilyn Farquhar. Relationship Between Scavenger Receptors and uPA:PAI-1 and uPA Receptors in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/adb241037.

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