Relevant bibliographies by topics / Human renal epithelial cell

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Academic literature on the topic 'Human renal epithelial cell'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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Journal articles on the topic "Human renal epithelial cell"

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Demmers, M. W. H. J., S. S. Korevaar, M. Roemeling-van Rhijn, T. P. P. van den Bosch, M. J. Hoogduijn, M. G. H. Betjes, W. Weimar, C. C. Baan, and A. T. Rowshani. "Human renal tubular epithelial cells suppress alloreactive T cell proliferation." Clinical & Experimental Immunology 179, no. 3 (February 16, 2015): 509–19. http://dx.doi.org/10.1111/cei.12469.

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Elliott, Justine, Nadezhda N. Zheleznova, and Patricia D. Wilson. "c-Src inactivation reduces renal epithelial cell-matrix adhesion, proliferation, and cyst formation." American Journal of Physiology-Cell Physiology 301, no. 2 (August 2011): C522—C529. http://dx.doi.org/10.1152/ajpcell.00163.2010.

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c-Src is a non-receptor tyrosine kinase whose activity is induced by phosphorylation at Y418 and translocation from the cytoplasm to the cell membrane. Increased activity of c-Src has been associated with cell proliferation, matrix adhesion, motility, and apoptosis in tumors. Immunohistochemistry suggested that activated (pY418)-Src activity is increased in cyst-lining autosomal dominant polycystic kidney disease (ADPKD) epithelial cells in human and mouse ADPKD. Western blot analysis showed that SKI-606 (Wyeth) is a specific inhibitor of pY418-Src without demonstrable effects on epidermal growth factor receptor or ErbB2 activity in renal epithelia. In vitro studies on mouse inner medullary collecting duct (mIMCD) cells and human ADPKD cyst-lining epithelial cells showed that SKI-606 inhibited epithelial cell proliferation over a 24-h time frame. In addition, SKI-606 treatment caused a striking statistically significant decrease in adhesion of mIMCD and human ADPKD to extracellular collagen matrix. Retained viability of unattached cells was consistent with a primary effect on epithelial cell anchorage dependence mediated by the loss of extracellular matrix (ECM)-attachment due to α2β1-integrin function. SKI-606-mediated attenuation of the human ADPKD hyperproliferative and hyper-ECM-adhesive epithelial cell phenotype in vitro was paralleled by retardation of the renal cystic phenotype of Pkd1 orthologous ADPKD heterozygous mice in vivo. This suggests that SKI-606 has dual effects on cystic epithelial cell proliferation and ECM adhesion and may have therapeutic potential for ADPKD patients.
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Pathak, R. K., M. Yokode, R. E. Hammer, S. L. Hofmann, M. S. Brown, J. L. Goldstein, and R. G. Anderson. "Tissue-specific sorting of the human LDL receptor in polarized epithelia of transgenic mice." Journal of Cell Biology 111, no. 2 (August 1, 1990): 347–59. http://dx.doi.org/10.1083/jcb.111.2.347.

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The distribution of human low density lipoprotein (LDL) receptors was studied by immunofluorescence and immunoelectron microscopy in epithelial cells of transgenic mice that express high levels of receptors under control of the metallothionein-I promoter. In hepatocytes and intestinal epithelial cells, the receptors were confined to the basal and basolateral surfaces, respectively. Very few LDL receptors were present in coated pits or intracellular vesicles. In striking contrast, in the epithelium of the renal tubule the receptors were present on the apical (lumenal) surface where they appeared to be concentrated at the base of microvilli and were abundant in vesicles of the endocytic recycling pathway. Intravenously administered LDL colloidal gold conjugates bound to the receptors on hepatocyte microvilli and were slowly internalized, apparently through slow migration into coated pits. We conclude that (a) sorting of LDL receptors to the surface of different epithelial cells varies with each tissue; and (b) in addition to a signal for clustering in coated pits, the LDL receptor may contain a signal for retention in noncoated membrane that is manifest in hepatocytes and intestinal epithelial cells, but not in renal epithelial cells or cultured human fibroblasts.
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Balkovetz, Daniel F. "Claudins at the gate: determinants of renal epithelial tight junction paracellular permeability." American Journal of Physiology-Renal Physiology 290, no. 3 (March 2006): F572—F579. http://dx.doi.org/10.1152/ajprenal.00135.2005.

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The epithelial tight junction (TJ) is responsible for the control of paracellular transport between epithelial cells (gate function) and the maintenance of apical/basolateral polarity by preventing the diffusion of membrane lipids and/or proteins from one surface domain to another (fence function). Renal tubule epithelia in the mammalian nephron have TJs that determine paracellular transport characteristics. Paracellular transport across renal tubular epithelial TJs (gate function) varies in different segments of the nephron. A large family of recently identified TJ-associated transmembrane proteins named claudins appear to determine the paracellular permeability properties of the TJ. A combination of inherited human diseases, renal epithelial cell culture models, and nephron expression patterns of claudins is providing important clues about how claudin molecules determine the TJ gate function of renal epithelia in different segments of the nephron.
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Nadasdy, T., Z. Laszik, G. Lajoie, K. E. Blick, D. E. Wheeler, and F. G. Silva. "Proliferative activity of cyst epithelium in human renal cystic diseases." Journal of the American Society of Nephrology 5, no. 7 (January 1995): 1462–68. http://dx.doi.org/10.1681/asn.v571462.

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Increased proliferative activity of the renal tubular epithelium is thought to be a prerequisite for renal cyst formation by many investigators. However, in humans, the exact in vivo proliferation rate of epithelial cells lining these cysts is not known. In this study, which used immunohistochemical methods with an antibody to proliferating cell nuclear antigen (PCNA), the proliferation index (PI) (percentage of PCNA positive cell nuclei among epithelial cells lining the renal cysts) was determined in 10 cases of autosomal dominant polycystic kidney disease (ADPKD), 8 cases of autosomal recessive polycystic kidney disease (ARPKD), and 8 cases of acquired cystic kidney disease (ACKD). Cysts with proximal and distal nephron phenotype and cysts with markedly thickened basement membranes, as well as cysts lined by atrophic (flattened), "regular" (cuboidal or cylindrical), and hyperplastic epithelium, were evaluated separately. The overall PI of cyst epithelium (excluding hyperplastic cysts) was 2.58 in ADPKD, was 10.5 in ARPKD, and was 3.61 in ACKD. Overall, there were only minor differences in the PI between the various types of cysts. Cysts with hyperplastic epithelium in ACKD (unlike in ADPKD) showed a high PI (9.1). For comparison, the PI of two renal cell carcinomas occurring in two ACKD cases was also determined (13.70 and 8.67%). The PI of tubular epithelium in normal kidneys was only 0.22 to 0.33%, depending on the tubule segment. In contrast, in polycystic kidneys, those noncystic segments of the nephron from which the cysts are thought to originate (distal nephron (specifically collecting duct)) in ARPKD, primarily distal in ADPKD, proximal and distal in ACKD, had PI values similar to those of the cyst epithelium.(ABSTRACT TRUNCATED AT 400 WORDS)
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Nadasdy, T., Z. Laszik, K. E. Blick, L. D. Johnson, and F. G. Silva. "Proliferative activity of intrinsic cell populations in the normal human kidney." Journal of the American Society of Nephrology 4, no. 12 (June 1994): 2032–39. http://dx.doi.org/10.1681/asn.v4122032.

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The proliferative activity of various normal human renal cell populations is unknown. Recently, antibodies to cell proliferation-associated nuclear proteins, such as proliferating cell nuclear antigen (PCNA) and KI-67, which are applicable to archival paraffin sections, became available. With antibodies to PCNA and Ki-67 after microwave pretreatment of the paraffin sections, the proliferation indexes (ratio of positive nuclei with PCNA and Ki-67 antibodies/all nuclei counted x 100, i.e. percentage of positive cells) of 12 different intrinsic renal cell populations in 20 normal human kidneys have been determined. The following proliferation indexes (percentages of positive cells) were found with the PCNA and the Ki-67 antibodies, respectively: proximal tubular epithelium, 0.22, 0.24; thin limb of Henle, 0.29, 0.30; thick ascending limb of Henle, 0.32, 0.29; distal tubular epithelium (distal convoluted tubules and cortical collecting ducts, 0.33, 0.44; medullary collecting ducts, 0.32, 0.3; glomerular mesangial cells, 0.07, 0.12; glomerular visceral epithelial cells, 0.04, 0.08; glomerular parietal epithelial cells, 0.07, 0.1; glomerular capillary endothelium, 0.42, 0.47; peritubular capillary endothelial cells, 0.38, 0.43; endothelium of large intrarenal vessels (arteries and veins), 0.09, 0.12. Thus, normally capillary endothelium (glomerular and peritubular) appears to have the highest proliferation index in the human kidney by these techniques. These results indicate major variation in the proliferative activity of normal human renal cell populations, along with a significant correlation between PCNA and Ki-67 staining. Furthermore, this study provides normal values for the proliferative activity of different human renal cell populations.(ABSTRACT TRUNCATED AT 250 WORDS)
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Tasnim, Farah, and Daniele Zink. "Cross talk between primary human renal tubular cells and endothelial cells in cocultures." American Journal of Physiology-Renal Physiology 302, no. 8 (April 15, 2012): F1055—F1062. http://dx.doi.org/10.1152/ajprenal.00621.2011.

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Interactions between renal tubular epithelial cells and adjacent endothelial cells are essential for normal renal functions but also play important roles in renal disease and repair. Here, we investigated cocultures of human primary renal proximal tubular cells (HPTC) and human primary endothelial cells to address the cross talk between these cell types. HPTC showed improved proliferation, marker gene expression, and enzyme activity in cocultures. Also, the long-term maintenance of epithelia formed by HPTC was improved, which was due to the secretion of transforming growth factor-β1 and its antagonist α2-macroglobulin. HPTC induced endothelial cells to secrete increased amounts of these factors, which balanced each other functionally and only displayed in combination the observed positive effects. In addition, in the presence of HPTC endothelial cells expressed increased amounts of hepatocyte growth factor and vascular endothelial growth factor, which have well-characterized effects on renal tubular epithelial cells as well as on endothelial cells. Together, the results showed that HPTC stimulated endothelial cells to express a functionally balanced combination of various factors, which in turn improved the performance of HPTC. The results give new insights into the cross talk between renal epithelial and endothelial cells and suggest that cocultures could be also useful models for the analysis of cellular communication in renal disease and repair. Furthermore, the characterization of defined microenvironments, which positively affect HPTC, will be helpful for improving the performance of this cell type in in vitro applications including in vitro toxicology and kidney tissue engineering.
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Demmers, Martijn W. H. J., Carla C. Baan, Els van Beelen, Jan N. M. IJzermans, Willem Weimar, and Ajda T. Rowshani. "Differential Effects of Activated Human Renal Epithelial Cells on T-Cell Migration." PLoS ONE 8, no. 5 (May 22, 2013): e64916. http://dx.doi.org/10.1371/journal.pone.0064916.

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McAteer, James A., Stephen A. Kempson, and Andrew P. Evan. "Culture of human renal cortex epithelial cells." Journal of Tissue Culture Methods 13, no. 3 (September 1991): 143–47. http://dx.doi.org/10.1007/bf02388118.

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Kadomoto, Suguru, Kouji Izumi, Kaoru Hiratsuka, Taito Nakano, Renato Naito, Tomoyuki Makino, Hiroaki Iwamoto, et al. "Tumor-Associated Macrophages Induce Migration of Renal Cell Carcinoma Cells via Activation of the CCL20-CCR6 Axis." Cancers 12, no. 1 (December 30, 2019): 89. http://dx.doi.org/10.3390/cancers12010089.

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This study investigated tumor-associated macrophages activity in the microenvironment of renal cell carcinoma. Via a co-culture with macrophage-like cells differentiated from human monocyte cell line THP-1 and U937 cells, the migration ability of ACHN and Caki-1 cells, which are human renal cell carcinoma cell line cells, was significantly increased, as was the epithelial–mesenchymal transition change. A chemokine array identified the CCL20-CCR6 axis as a concentration-dependent signal in ACHN and Caki-1 cell migration. Akt in the ACHN and Caki-1 cells was activated by macrophage-like cells, and the CCL20 neutralizing antibody suppressed migration ability, epithelial–mesenchymal transition, and Akt phosphorylation in the ACHN and Caki-1 cells. Akt inhibitor AZD5363 also decreased the epithelial–mesenchymal transition change and migration ability in the ACHN and Caki-1 cells. In 42 renal cell carcinoma tissues, patients with CCR6 and macrophage infiltration indicated poor prognoses. In the tumor microenvironment of renal cell carcinoma, cancer cells are activated by CCL20 secreted by tumor-associated macrophages through Akt activation, followed by epithelial–mesenchymal transition and an acquired migration ability. Thus, inhibition of the CCL20-CCR6 axis may be a potential therapeutic strategy for renal cell carcinoma.
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Dissertations / Theses on the topic "Human renal epithelial cell"

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Tang, Chi-wai Sydney. "The many facets of the renal proximal tubular epithelial cell in human." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31992468.

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Colgin, Lorel Melanie. "Spontaneous mutations in aging human renal epithelia in vivo /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/6318.

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Orphanides, Chrystalla. "Hypoxia is a pro-fibrogenic stimulus for human renal tubular epithelial cells." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314192.

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Shah, Nileshkumar. "Expression and regulation of cadherin of human renal proximal tubule epithelial cells." Thesis, St George's, University of London, 2018. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.754076.

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Cadherins are a family of trans-membrane junctional proteins important in maintenance of cell-cell junction, phenotype regulation, tissue organisation and embryonic development. The proteins form calcium dependent homophilic cell junctional complexes and bind internally to the actin cytoskeleton and regulate intracellular signalling via the p- catenin pathway. Altered cadherin expression is essential for embryonic development, tissue repair or healing, fibrosis, cancer and metastasis. Much interest has developed in cadherin expression and its regulation along with signalling in renal proximal tubule epithelial cells (PTECs), an important cell type in the development of tubulointerstitial fibrosis and a potential source of myofibroblasts.
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Oates, Jeremy Edward. "Isolation and characterisation of an enriched side-population from human renal epithelial cells." Thesis, University of Manchester, 2010. https://www.research.manchester.ac.uk/portal/en/theses/isolation-and-characterisation-of-an-enriched-sidepopulation-from-human-renal-epithelial-cells(712fe1d5-12c4-4222-b6dc-687171450f86).html.

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Browne, James Alexander. "The expression and function of the atypical MAP kinase ERK5 in human renal epithelial cells." Thesis, St George's, University of London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511895.

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Winn, Simon. "An investigation of the actions of connective tissue growth factor on human renal epithelial cells." Thesis, St George's, University of London, 2018. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.754078.

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Introduction. Connective tissue growth factor (CTGF) is the only CCN member recognized as a mediator of chronic fibrotic disease. Accumulating evidence suggests that CTGF is important as a downstream effector of transforming growth factor (TGFβ) in modulating a sustained pro-fibrotic signal in in vivo models. Moreover, in cultured human proximal tubule epithelial cells (PTECs) CTGF mRNA is readily upregulated by TGFP and the nascent protein accumulates extracellularly. How pro-fibrotic signalling occurs is yet to be ascertained but it likely involves extracellular interactions with secreted CTGF. The tetra-modular structure of CTGF has been shown to possess multiple binding sites for ligands present in the extracellular milieu including matrix proteins, growth factors including the TGFβ superfamily and cell surface receptors. As such, CTGF can behave as a bridge between matrix and cell. Moreover, individual modules possess intrinsic biologic activity. Materials and Methods. Experiments were performed in cultured renal human renal epithelial cells. Recombinant human CTGF protein was generated in-house following plasmid transfection into context relevant PTECs. Immunoblotting and ELISA techniques were used to investigate protein expression in response to incubation with study protein in isolation or in combination with TGFP superfamily members. Protein-protein binding was investigated using surface plasmon resonance (SPR) in order to elucidate how CTGF might regulate TGFβ superfamily cell signalling. Additional experiments with an alternative CCN member, CCN3, were performed. Results. Both full-length and C-terminal CTGF bind to TGFβ and BMP7 and in human renal epithelial cells, this binding modulates the downstream Smad signalling pathways associated with fibrosis. In cultured human podocytes, CTGF drives TGFβ-dependent signalling in the absence of exogenous TGF(3 suggesting activation of latent TGFβ. Moreover, C-terminal CTGF increases the generation of pro-fibrotic markers aSMA and fibronectin, both of which are subsequently blocked by inhibiting the TGFp receptor. Unlike CTGF, an alternative CCN member CCN3 reduces TGFβ-induced signalling in PTECs. Conclusion. CTGF protein has multiple binding sites and modulates the cellular responses of TGFp superfamily members on human renal epithelial cells. Both full-length and C-terminal CTGF bind to TGFβ and BMP-7. CTGF also appears to bind to the receptors of the TGFβ superfamily. C-terminal CTGF has intrinsic profibrotic activity that differs from the full-length protein as demonstrated in cultured human podocytes. The pro-fibrotic activity is suppressed by CCN3 in the CTGF rich environment of the cultured PTEC. The interplay of different CCN proteins in modulating fibrotic pathways in renal epithelial cells warrants further investigation.
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Ho, Sau-kwan, and 何秀鈞. "Interactions of anti-dsDNA antibodies with human proximal renal tubular epithelial cells in the pathogenesis of lupus nephritis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/197161.

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Lupus nephritis is characterized by the production of anti-dsDNA antibodies, deposition of immune complexes within the kidney parenchyma, proliferation of resident renal cells and induction of inflammatory and fibrotic processes. Approximately 70% of patients with lupus nephritis show immune aggregates along the tubular basement membrane, which is accompanied by an influx of infiltrating cells and increased intra-renal expression of IL-6. Much attention has focused on the inflammatory processes in the kidney during pathogenesis of lupus nephritis whereas mechanisms of fibrogenesis are less well characterized. Tubulo-interstitial injury is a key indicator of poor prognosis of renal function. Given that the tubulo-interstitium occupies over 80% of the kidney volume, injury to this compartment will have a major impact on renal function. There is evidence to show that proximal tubular epithelial cells (PTEC) undergo epithelial-to-mesenchymal transition (EMT) during pathological disorders and adopt a fibroblastic morphology with increased fibrogenic potential. We have previously demonstrated that anti-dsDNA antibodies bound directly to the surface of PTEC through cross-reactive proteins, which were subsequently internalized and translocated to the nucleus where they induced functional changes. Using a proteomic approach, this study identified the cross-reactive antigens that mediated anti-dsDNA antibody binding and intracellular localization in PTEC and the functional consequences thereafter, focusing on EMT and fibrogenic events. Human polyclonal anti-dsDNA antibodies isolated from patients with lupus nephritis bound to Ku70 in plasma membrane extracts isolated from PTEC, and to Ku70, Ku80 and major vault protein in cytosolic and nuclear fractions. Anti-dsDNA antibodies increased synthesis of Ku70, Ku80 and major vault protein in PTEC in a time-dependent manner. Expression of these proteins was localized to proximal tubules especially those undergoing atrophy, and staining was more prominent in renal biopsies from patients with lupus nephritis compared to non-lupus renal disease or control specimens. Binding of anti-dsDNA antibodies to PTEC increased phosphorylation of MAPK and PKC signaling pathways that was accompanied by a concomitant increase in IL-6, IL-8 and TGF-1 secretion and synthesis of β-catenin, fibroblast specific protein-1, fibronectin and laminin. Inhibition of MAPK and PKC signaling pathways with specific inhibitors revealed differential regulation of inflammatory and fibrotic processes by these signaling pathways. In this respect, increased ERK, p38 MAPK, JNK and PKC phosphorylation in PTEC following anti-dsDNA antibody stimulation enhanced IL-6, IL-8 and fibronectin synthesis, whereas increased ERK and JNK phosphorylation upregulated TGF-β1 secretion. Increased β-catenin synthesis was mediated through JNK and PKC phosphorylation. Taken together, our data suggest that PTEC contribute to the pathogenesis of renal inflammation and fibrosis in lupus nephritis. We hypothesize that anti-dsDNA antibodies bind to Ku70 on the plasma membrane of PTEC to mediate inflammation, cell activation and increased fibrogenesis. Although synthesis of EMT markers was increased in PTEC after anti-dsDNA antibody stimulation, transition to a fibroblastic morphology was not observed under our experimental setting suggesting that induction of the EMT cascade is an early event before phenotypic alterations.
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Medicine
Master
Master of Philosophy
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Veerasamy, Mangalakumar. "The role of Id proteins 1 and 2 in regulating phenotypic changes by TGFB1 and BMP7 in human renal epithelial cells." Thesis, University of London, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589773.

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Tubulo-interstitial fibrosis (TIF) is a key feature of chronic kidney diseases (CKD). Epithelial mesenchymal transition of PTECs is considered to contribute to the interstitial fibroblast pool which secretes excessive matrix proteins seen in TIF. TGFpl plays a crucial role in TIF including mediating EMT. In animal models of CKD treatment with bone morphogenic protein 7 (BMP 7), a member of TGF superfamily improved the histology and renal function. However, the cellular signalling mechanisms involved in the anti- fibrotic effects of BMP 7, in particular whether BMP 7 inhibits TGFp 1 mediated EMT of human PTECs have not been studied. Experiments were performed in HKC 8 cells; a virally transformed human PTEC model. The expression of cell surface receptors for TGF superfamily and phosphorylation of TGFp 1 and BMP 7 Smads were studied by immunoblotting, and the nuclear translocation of Smad proteins was studied by immunofluorescence. The expressions of E-cadherin and (l-SMA were studied with TGFp 1 and BMP 7 treatment individually and in combination. siRNAs were used to knock-down Smadl and 5 proteins, to identify their role in BMP 7 regulation of markers of EMT. TGFp 1 and BMP 7 regulation of Id2 expression was studied at the protein level and the Smad signalling regulating this process was studied by '. silencing their expression with siRNA. siRNAs were used to study the role of Id2 on the expression of E-cadherin and (l-SMA with TGFp 1 and BMP 7 stimulation. Plasmid vector expressing Id2 was used to overexpress Id2 to study its role in TGFp 1 regulation of , markers ofEMT. Idl expression was studied at the protein level with BMP 7, and the Smad signalling involved in this process was studied by silencing their expression with siRNAs. The role of Id 1 in BMP 7 regulation of E-cadherin and (l-SMA was studied by silencing its expression by siRNA. The interaction of Idl and Id2 with E2A gene products was studied by nuclear co-immunoprecipitation. HKC 8 cells express TGF type 11, Alkl, Alk2, Alk3, Alk5 and Alk6 receptors. TGFpl and BMP 7 activated their respective receptor Smads concurrently during combined treatment. The nuclear translocation of their respective receptor Smads was not inhibited by the other during combined treatment. BMP 7 do~egulated E-cadherin, and it had an additive effect with TGFp 1 in this process and this was a Smad 1/5 dependent event. BMP 7 inhibited TGFp 1 induction of (l-SMA through Smad 1/5 signalling. TGFp 1 downregulated Id2 through Smad2/3 signalling and BMP 7 counter-regulated this through Smad1/5 signalling. IV Id2 gene silencing prevented BMP 7 inhibition of TGF~ I mediated a-SMA' expression. Id2 overexpression prevented TGF~ I mediated a-SMA expression. BMP 7 increased expression of Idl through non-Smadl/5 pathway and Id l gene silencing resulted in induction of a-SMA with BMP 7 stimulation. Both Idl and Id2 were co- immunoprecipitated with EI2 and E47 in the nuclear extract. In conclusion, these studies show that the anti-fibrotic effect of BMP 7 is mediated by inhibition of TGF~ 1 mediated induction of a-SMA and the myofibroblastic transition of PTECs in this in vitro model. The activation of Smadl/5 and Id2 signalling is involved in this counter-regulation. Although BMP 7 itself downregulated E-cadherin through Smadl/5 signalling, the concurrent induction of Idl through non-Smadl/5 pathway prevented de novo induction of a-SMA and myofibroblastic transition of PTECs. Id I and Id2 were shown to bind with E2A gene products, but their role in the expressions of markers of EMT in this model needs further confirmation.
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Sheremet, Andriy. "Bioinspired polyethersulfone-based hollow fiber membranes as the scaffolds in renal assist device for protein-bound toxins removal from blood." Master's thesis, Faculdade de Ciências e Tecnologia, 2014. http://hdl.handle.net/10362/13308.

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Dissertation for obtaining the Master degree in Membrane Engineering
Erasmus Mundus Master in Membrane Engineering
Using bioartificial kidney is the promising approach for removal of non-dializable, proteinbound uremic toxins, which are responsible for high mortality and morbidity in treating kidney failure related conditions. Additionaly, bioartificial kidney device could perform the physiological roles of the kidney such as metabolic replacement, endocrine function and immunomodulation. In the current work two commercial polyethersulfone-based membranes, Gambro HCO 1100 and Membrana MicroPES TF10 used in haemofiltration and plasma separation applications respectively were investigated. To provide adequate cytocompatibility of the membrane biomimetic, biomimetic double layer coating was developed. First, the membranes were coated with musselinspired synthetic polydopamine film, following with the coating of Collagen Type IV. Transport properties of the coated and native membranes were investigated. Increase in pure water permeability of the coated HCO 1100 membranes was observed. Membrane surface hydrophilization was assumed as the major factor responsible for the effect. Membrane permeabilities for bovine serum albumin and immunoglobulin G solutions were studied. Significant increase in protein rejection was observed for double coated HCO 1100 membranes with small or no effect of the double coated MicroPES TF10 membranes. Next, formation of confluent monolayers of the renal epithelial cells on the membrane scaffolds was studied. Cell seeding strategy was developed and two seeding conditions were tested. Specifically, the cells were allowed to adhere to the biomimetic membranes passively, and the negative pressure was applied to facilitate cell adhesion. After cultivation in semi-batch conditions the monolayer formation was examined. Confluent monolayers were observed for the conditions with passive cell adherence for the both membranes. Cell contacts formation and cell polarization were confirmed with the staining for ZO-1 protein. Applying the pressure to facilitate cell adhesion, on the contrary, resulted in the loss of cell ability to form functional monolayers.
EM3E Master is an Education Programme supported by the European Commission, the European Membrane Society (EMS), the European Membrane House (EMH), and a large international network of industrial companies, research centres and universities
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Books on the topic "Human renal epithelial cell"

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Abdul-Karim, Ahmad Bashur. A study of some of the aspects of epithelial and endothelial cels in relation to human renal transplantation. Birmingham: University of Birmingham, 1995.

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Tari, Shahryar Rafi. Characterization of AZT transport properties in a continuous renal epithelial cell line. Ottawa: National Library of Canada, 1995.

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Li, Qingxue. Epstein-Barr virus infection and replication in a human epithelial cell system. Birmingham: University of Birmingham, 1992.

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Beaulieu, Jean-François. Extracellular matrix components and integrins in relationship to human intestinal epithelial cell differentiation. Stuttgart: G. Fischer, 1997.

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Holcroft, Cynthia Jean. ATP threshold for loss of epithelial cell polarity and elaboration of fodrin cleavage products following in vivo ischemic renal injury. [New Haven, Conn: s.n.], 1996.

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Kühn, Wolfgang, and Gerd Walz. The molecular basis of ciliopathies and cyst formation. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0303.

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Abnormalities of the cilium, termed ‘ciliopathies’, are the prime suspect in the pathogenesis of renal cyst formation because the gene products of cystic disease-causing genes localize to them, or near them. However, we only partially understand how cilia maintain the geometry of kidney tubules, and how abnormal cilia lead to renal cysts, and the diverse range of diseases attributed to them. Some non-cystic diseases share pathology of the same structures. Although still incompletely understood, cilia appear to orient cells in response to extracellular cues to maintain the overall geometry of a tissue, thereby intersecting with the planar cell polarity (PCP) pathway and the actin cytoskeleton. The PCP pathway controls two morphogenetic programmes, oriented cell division (OCD) and convergent extension (CE) through cell intercalation that both seem to play a critical role in cyst formation. The two-hit theory of cystogenesis, by which loss of the second normal allele causes tubular epithelial cells to form kidney cysts, has been largely borne out. Additional hits and influences may better explain the rate of cyst formation and inter-individual differences in disease progression. Ciliary defects appear to converge on overlapping signalling modules, including mammalian target of rapamycin and cAMP pathways, which can be targeted to treat human cystic kidney disease irrespective of the underlying gene mutation.
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E, Milo George, Casto Bruce C, and Shuler Charles Fredric 1953-, eds. Transformation of human epithelial cells: Molecular and oncogenetic mechanisms. Boca Raton: CRC Press, 1992.

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Transformation of Human Epithelial Cells: Molecular and Oncogenetic Mechanisms. Taylor & Francis Group, 2017.

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Elger, Marlies, and Wilhelm Kriz. The renal glomerulus. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0043.

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The glomerulus performs its functions with three major cell types. Endothelial cells and visceral epithelial cells (podocytes) lie on the inside and outside of the glomerular basement membrane, and together these three structures form the glomerular filtration barrier. Mesangial cells sit in the axial region. Pathologies of all these regions and cell types can be identified. Parietal epithelial cells lining Bowman’s capsule participate in crescent formation, and at the tubular pole some of these cells seem to represent a stem cell population for tubular cells and podocytes. The extraglomerular mesangium and juxtaglomerular apparatus complete the description of the glomerular corpuscle. The structure of these elements, and how they relate to function, are illustrated in detail.
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Lechner, Mark Stewart. Mechanisms of epithelial cell transformation by human papillomavirus and simian virus 40. 1993.

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Book chapters on the topic "Human renal epithelial cell"

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Haugen, A., L. Maehle, D. Ryberg, and I. L. Hansteen. "A Human Renal Epithelial Multistep Model of in vitro Carcinogenesis." In Neoplastic Transformation in Human Cell Culture, 291–96. Totowa, NJ: Humana Press, 1991. http://dx.doi.org/10.1007/978-1-4612-0411-4_29.

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Wang, P. C., S. Kimura, Y. Gao, and M. Matsumura. "The Binding Effect of Immune Complex by Rat Renal Glomerular Epithelial Cell Expressed with Human CR1 Gene." In Animal Cell Technology: Basic & Applied Aspects, 279–83. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5161-0_48.

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Sharpe, Claire C., and Mark E. C. Dockrell. "Primary Culture of Human Renal Proximal Tubule Epithelial Cells and Interstitial Fibroblasts." In Methods in Molecular Biology, 175–85. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-367-7_12.

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Gildea, John J., Helen E. McGrath, Robert E. Van Sciver, Dora Bigler Wang, and Robin A. Felder. "Isolation, Growth, and Characterization of Human Renal Epithelial Cells Using Traditional and 3D Methods." In Methods in Molecular Biology, 329–45. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-125-7_20.

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Rhim, Johng S. "Human Prostate Epithelial Cell Cultures." In Basic Cell Culture Protocols, 383–93. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-128-8_24.

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Mullin, James M., and Arnost Kleinzeller. "Sugar Transport in the Renal Epithelial Cell Culture." In Tissue Culture of Epithelial Cells, 71–86. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4814-6_5.

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Boucher, Richard C., and Elaine H. C. Cheng. "Human Nasal Epithelial Cultures." In Pharmaceutical Applications of Cell and Tissue Culture to Drug Transport, 249–58. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4757-0286-6_20.

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Rhim, Johng S. "Novel Human Prostate Epithelial Cell Cultures." In Advances in Experimental Medicine and Biology, 91–99. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-22254-3_7.

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Meier, Kathryn E., and Paul A. Insel. "Hormone Receptors and Response in Cultured Renal Epithelial Cell Lines." In Tissue Culture of Epithelial Cells, 145–78. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4814-6_9.

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Vandekerckhove, Bart, Dominique Vanhecke, and Jean Plum. "T Cell Development in the Human Thymus." In Epithelial Tumors of the Thymus, 105–9. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0033-3_16.

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Conference papers on the topic "Human renal epithelial cell"

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Walters, Matthew S., Neil R. Hackett, Renat Shaykhiev, Rui Wang, Rachel K. Zwick, Jacqueline Salit, and Ronald G. Crystal. "The Human Airway Epithelial Basal Cell Transcriptome." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6019.

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Li, Ping, Jing Wang, Chengxiang Dai, Yingxuan Shi, Suke Li, and Tony Liu. "Cell therapeutic potential of human amniotic epithelial cells." In INTERNATIONAL SYMPOSIUM ON THE FRONTIERS OF BIOTECHNOLOGY AND BIOENGINEERING (FBB 2019). AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5110810.

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Marozkina, N., L. Smith, J. G. Zein, J. F. Chmiel, J. Kiselar, J. Kim, M. Denning, R. Cunningham, S. H. Randell, and B. M. Gaston. "Human Airway Epithelial Cell Hemoglobin and Airway Biology." 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.a4332.

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Wang, Lin, Paul Park, Huina Zhang, Frank La Marca, and Chia-Ying Lin. "Abstract 293: Characterization of renal tumor-initiating cells in human renal carcinoma cell lines." 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.am2011-293.

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Stemeier, K., J. Mertin, J. Pill, and F. Hartig. "EFFECTS OF THROMBOXANE RECEPTOR BLOCKER BM 13.505 ON THE DEVELOPMENT OF PROTEINURIA IN AUTOIMMUNE NZB/W MICE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643757.

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Female F1 hybrid of New Zealand black and white mice(NZB/W) spontaneouslydevelop an autoimmune disease characterize by afatal immune complex glomerulonephritis.Theyare considered to be a relevant model of human systemic lupus erythematosus. We observeda doubling of the concentration of TXB2 in urine at the same time when onset of proteinuria was noticed. This suggests that TXA2 synthetized by mesangial and epithelial cells of the glomeruli as well as by some inflammatory cells and platelets might be an important mediator in the pathogenesis of thi auto immune-mediated glomerular disease. Weused BM 13.505 as an long-acting TX receptor blocker for evaluating the importance of TXA2 on the development of proteinuria and compared its effects with that of the immunsuppressive agent cyclophosphamide.NZB/W mice were distributed to vehicle-treated (V-)group 20 mg/kg BM 13.505 (BM-) group and 20 mg/kgcyclophosphamide (C-) group( = 13 -14).Daily dosing by gavage was startedat the age of12 weeks. Every fourth week theurinary concentrations of proteins were measured by th biuret method and TXB2by a RIA. An increasein TXB2 was seen in the V- and BM-group, while in the C-group TXB2 was lowered. At 36 weeks of age 8of 14 animals of the V-group were proteinuria positive (>100 mg/100 ml). The study was finished at 44 weeks because more than 2/3 of the animals of the V-group haddeveloped a proteinuria. Previously four animals died and in most of other the disease was faradvanced. In the BM-group no animal had diedor showed signs of illness. However seven ofthe animals had slightly elevated protein concentrations in urine and two moderate elevated values. In the C-group no proteinuria was detected. Histological examinations of thekidneys showed a correlation in individualanimals of the V-group between the duration and extent of proteinuria and changes in the morphology of the glomeruli. In the BM-treated animals slight to moderate protein deposits were detectable, while in cyclophosphamide-treated animals glomeruli were of normal structure. This study presents someevidence that TXA2 may be an important mediator in the pathogenesis of this immune-mediated renal disease. Manifestation of this disease is delayed by the administration of thespecific TX receptor blocker BM 13.505.
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Millar, Fraser, Kate Gowers, Robert Hynds, Jessica Eley, Rachel Chambers, Sam Janes, and Adam Giangreco. "Cell intrinsic and environmental factors influencing human bronchial epithelial cell migration." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa6020.

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Zhilin-Roth, Alisa, and Jill A. Macoska. "Abstract 2021: The CXCL12/CXCR4 axis drives epithelial-mesenchymal transition in renal cell carcinoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2021.

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Lin, QS, T. Zhuang, and L. Gonzales. "Function of microRNAs in Human Lung Epithelial Cell Differentiation." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1909.

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Hansson, Jennifer, Kjell Hultenby, Catharina Cramnert, David Lindgren, Håkan Axelson, and Martin E. Johansson. "Abstract 5010: Characterization of a novel cell type in human renal proximal tubules with connection to renal cell carcinoma development." 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.am2013-5010.

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Bayramoglu, Neslihan, Juho Kannala, and Janne Heikkila. "Human Epithelial Type 2 cell classification with convolutional neural networks." In 2015 IEEE 15th International Conference on Bioinformatics and Bioengineering (BIBE). IEEE, 2015. http://dx.doi.org/10.1109/bibe.2015.7367705.

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Reports on the topic "Human renal epithelial cell"

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Band, Vimia. Human Mammary Epithelial Cell Transformation by Rho GTPase through a Novel Mechanism. Fort Belvoir, VA: Defense Technical Information Center, August 2008. http://dx.doi.org/10.21236/ada500910.

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Pauley, Robert J. Determinants of Human Breast Epithelial Cell Estrogen Expression and Differentiation: Organization and Environment. Fort Belvoir, VA: Defense Technical Information Center, June 1999. http://dx.doi.org/10.21236/ada374045.

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Williams, K., C. Chubb, E. Huberman, and C. S. Giometti. Analysis of differential protein expression in normal and neoplastic human breast epithelial cell lines. Office of Scientific and Technical Information (OSTI), July 1997. http://dx.doi.org/10.2172/501554.

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Stampfer, Martha R. Regulation of hTERT Expression and Function in Newly Immortalized p53(+) Human Mammary Epithelial Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, June 2008. http://dx.doi.org/10.21236/ada491221.

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Stampfer, Martha R. Regulation of hTERT Expression and Function in Newly Immortalized p53 (+) Human Mammary Epithelial Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada440296.

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Stampfer, Martha R. Regulation of hTERT Expression and Function in Newly Immortalized p53(+) Human Mammary Epithelial Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, June 2006. http://dx.doi.org/10.21236/ada457687.

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Richmond, Robert C. Cell and Molecular Biology of Ataxia Telangiectasia Heterozygous Human Mammary Epithelial Cells Irradiated in Culture. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412826.

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Stampfer, Martha R. Regulation of hTERT Expression and Function in Newly Immortalized p53(+) Human Mammary Epithelial Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, June 2007. http://dx.doi.org/10.21236/ada472883.

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Peehl, Donna M. Development of Methodology to Maintain Primary Cultures of Normal and Malignant Human Prostatic Epithelial Cell In Vivo. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada434013.

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Nicosia, Santo V., and Jin Q. Cheng. Cell Growth and Survival in Ovarian Epithelial Cancer Project 1: AKT2 Oncogene and Its Associated Protein APBP in Human Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada420904.

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