The Experts below are selected from a list of 50271 Experts worldwide ranked by ideXlab platform
Carrie L Phillips - One of the best experts on this subject based on the ideXlab platform.
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analysis of multiple INVS transcripts in mouse and mdck cells
Genomics, 2004Co-Authors: Heather H Ward, Jinghong Wang, Carrie L PhillipsAbstract:Infantile nephronophthisis is associated with cystic kidneys, situs inversus, and INVS mutations. The function of the INVS product, inversin, is unknown but evidence suggests there are multiple inversin isoforms with differing molecular weights, cellular localization patterns, and binding partners. We used Northern blots, RT-PCR, and sequence analysis to identify alternative INVS transcripts. Northern blots probed with INVS cDNA detected four bands in normal mouse kidney. RT-PCR of mouse kidney RNA revealed INVS transcripts with skipping of exon 5, 11, or 13. We sequenced canine (MDCK-II cells) INVS and determined that the corresponding full-length protein shares identity with mouse (74%) and human (84%) inversin. Canine INVS produces a transcript that skips exon 12. Exon skips cause loss of inversin protein motifs, including ankyrin repeats, IQ domains, destruction boxes, and nuclear localization signals. Identification of INVS splice variants will help us determine which inversin protein motifs contribute to left-right asymmetry and kidney development.
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the INVS gene encodes a microtubule associated protein
Journal of The American Society of Nephrology, 2004Co-Authors: Jens Nurnberger, Anabelle Opazo Saez, Gerd Heusch, Thomas Philipp, Andreas Kribben, Carrie L PhillipsAbstract:ABSTRACT. Microtubule networks are important for many vital processes such as mitosis, cell polarity, and differentiation. Ciliary architecture and function closely depend on the microtubule cytoskeleton, and recent studies suggest a role of apical cilia of renal epithelia in the pathogenesis of polycystic kidney disease. This study evaluates the localization, potential interacting partners, and functional aspects of the INVS gene product inversin. Only recently, INVS has been identified as the gene that is mutated in nephronophthisis type 2, an autosomal recessive polycystic kidney disease. Using immunoprecipitation and co-pelleting assays, we show that the INVS gene product inversin forms a stable complex with tubulin in cultured renal epithelial cells. Inversin localizes to several components of the cytoskeleton including ciliary, random, and polarized microtubule pools. During cell divison, inversin is recruited to mitotic spindle fibers. After microtubule depolymerization using colcemid inversin and tubulin staining is no longer characterized by a network pattern but by homogeneous, diffuse distribution. Inversin does not coprecipitate with tubulin after addition of colcemid. After removal of colcemid, inversin immunofluorescence reappears together with tubulin in centrioles. Treatment with the microtubule stabilizing agent paclitaxel leads to severe alteration of the microtubule cytoskeleton with bundling and formation of long spindles of tubulin and inversin. In conclusion, inversin is closely associated with the microtubule cytoskeleton, and its spatial distribution is dependent on tubulin polymerization. Hence, altered inversin-tubulin interaction may impair ciliary function and thereby contribute to cyst development in nephronophthisis.
Sylvie Chetty - One of the best experts on this subject based on the ideXlab platform.
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disentangling the effects of post entry speed of internationalisation on export performance of INVS
International Small Business Journal, 2018Co-Authors: Arash Sadeghi, Elizabeth L Rose, Sylvie ChettyAbstract:This article aims to explore the under-researched topic of post-entry speed of internationalisation (PSI) in the context of international new ventures (INVS). We unbundle PSI and examine its relati...
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disentangeling the effects of post entry speed of internationalization on INVS export performance
2018Co-Authors: Sylvie Chetty, Arash Sadeghi, Elisabeth RoseAbstract:Disentangeling the effects of post-entry speed of internationalization on INVS' export performance
Daoguo Zhou - One of the best experts on this subject based on the ideXlab platform.
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INVS coordinates expression of prgh and fimz and is required for invasion of epithelial cells by salmonella enterica serovar typhimurium
Journal of Bacteriology, 2017Co-Authors: Lu Wang, Shuyan Wu, Rajdeep Bomjan, Ernesto S Nakayasu, Kristian Handler, Jay C D Hinton, Daoguo ZhouAbstract:: Deep sequencing has revolutionized our understanding of the bacterial RNA world and has facilitated the identification of 280 small RNAs (sRNAs) in Salmonella Despite the suspicions that sRNAs may play important roles in Salmonella pathogenesis, the functions of most sRNAs remain unknown. To advance our understanding of RNA biology in Salmonella virulence, we searched for sRNAs required for bacterial invasion into nonphagocytic cells. After screening 75 sRNAs, we discovered that the ablation of INVS caused a significant decrease of Salmonella invasion into epithelial cells. A proteomic analysis showed that INVS modulated the levels of several type III secreted Salmonella proteins. The level of PrgH, a type III secretion apparatus protein, was significantly lower in the absence of INVS, consistent with the known roles of PrgH in effector secretion and bacterial invasion. We discovered that INVS modulates fimZ expression and hence flagellar gene expression and motility. We propose that INVS coordinates the increase of PrgH and decrease in FimZ that promote efficient Salmonella invasion into nonphagocytic cells.IMPORTANCE Salmonellosis continues to be the most common foodborne infection reported by the CDC in the United States. Central to Salmonella pathogenesis is the ability to invade nonphagocytic cells and to replicate inside host cells. Invasion genes are known to be regulated by protein transcriptional networks, but little is known about the role played by small RNAs (sRNAs) in this process. We have identified a novel sRNA, INVS, that is involved in Salmonella invasion. Our result will likely provide an opportunity to better understand the fundamental question of how Salmonella regulates invasion gene expression and may inform strategies for therapeutic intervention.
Andreas Kribben - One of the best experts on this subject based on the ideXlab platform.
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differential tissue distribution of the INVS gene product inversin
Cell and Tissue Research, 2006Co-Authors: Jens Nurnberger, Rosmaria Kavapurackal, Shijun Zhang, Anabelle Opazo Saez, Gerd Heusch, Thomas Philipp, F Pietruck, Andreas KribbenAbstract:Nephronophthisis is a common genetic cause of end-stage renal disease in childhood. Recently, INVS was identified as the gene mutated in the infantile form of nephronophthisis. Humans with nephronophthisis develop a large number of extrarenal manifestations, including situs variations, anomalies of the hepatobiliary system, retinal degeneration and cerebellar ataxia. Mice homozygous for a mutation in the INVS gene (inv mouse) die during the first week after birth as a result of renal and liver failure. Although organ anomalies have been characterized in human nephronophthisis and the inv mouse, little is known about the tissue expression of the INVS gene product, inversin. We have used laser confocal microscopy of paraffin-embedded murine tissue sections to provide the first detailed characterization of the distribution of inversin in various organs. Our results show that inversin is localized to distal tubules in the kidney, hepatic bile ducts, acinar and ductal pancreatic cells, epithelial intestinal cells, splenic germinal centres, bronchiolar epithelial cells, dendrites of cerebellar Purkinje cells, retinal neural cells and spermatocytes and spermatids in the testis. The localization of inversin in distal tubules in the kidney and in extrarenal tissues suggests that the expression of this protein has an important function in a variety of organs. Further studies are required to understand the way in which mutations in the INVS gene lead to the multi-organ pathology of inv mouse and human nephronophthisis.
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the INVS gene encodes a microtubule associated protein
Journal of The American Society of Nephrology, 2004Co-Authors: Jens Nurnberger, Anabelle Opazo Saez, Gerd Heusch, Thomas Philipp, Andreas Kribben, Carrie L PhillipsAbstract:ABSTRACT. Microtubule networks are important for many vital processes such as mitosis, cell polarity, and differentiation. Ciliary architecture and function closely depend on the microtubule cytoskeleton, and recent studies suggest a role of apical cilia of renal epithelia in the pathogenesis of polycystic kidney disease. This study evaluates the localization, potential interacting partners, and functional aspects of the INVS gene product inversin. Only recently, INVS has been identified as the gene that is mutated in nephronophthisis type 2, an autosomal recessive polycystic kidney disease. Using immunoprecipitation and co-pelleting assays, we show that the INVS gene product inversin forms a stable complex with tubulin in cultured renal epithelial cells. Inversin localizes to several components of the cytoskeleton including ciliary, random, and polarized microtubule pools. During cell divison, inversin is recruited to mitotic spindle fibers. After microtubule depolymerization using colcemid inversin and tubulin staining is no longer characterized by a network pattern but by homogeneous, diffuse distribution. Inversin does not coprecipitate with tubulin after addition of colcemid. After removal of colcemid, inversin immunofluorescence reappears together with tubulin in centrioles. Treatment with the microtubule stabilizing agent paclitaxel leads to severe alteration of the microtubule cytoskeleton with bundling and formation of long spindles of tubulin and inversin. In conclusion, inversin is closely associated with the microtubule cytoskeleton, and its spatial distribution is dependent on tubulin polymerization. Hence, altered inversin-tubulin interaction may impair ciliary function and thereby contribute to cyst development in nephronophthisis.
Jens Nurnberger - One of the best experts on this subject based on the ideXlab platform.
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differential tissue distribution of the INVS gene product inversin
Cell and Tissue Research, 2006Co-Authors: Jens Nurnberger, Rosmaria Kavapurackal, Shijun Zhang, Anabelle Opazo Saez, Gerd Heusch, Thomas Philipp, F Pietruck, Andreas KribbenAbstract:Nephronophthisis is a common genetic cause of end-stage renal disease in childhood. Recently, INVS was identified as the gene mutated in the infantile form of nephronophthisis. Humans with nephronophthisis develop a large number of extrarenal manifestations, including situs variations, anomalies of the hepatobiliary system, retinal degeneration and cerebellar ataxia. Mice homozygous for a mutation in the INVS gene (inv mouse) die during the first week after birth as a result of renal and liver failure. Although organ anomalies have been characterized in human nephronophthisis and the inv mouse, little is known about the tissue expression of the INVS gene product, inversin. We have used laser confocal microscopy of paraffin-embedded murine tissue sections to provide the first detailed characterization of the distribution of inversin in various organs. Our results show that inversin is localized to distal tubules in the kidney, hepatic bile ducts, acinar and ductal pancreatic cells, epithelial intestinal cells, splenic germinal centres, bronchiolar epithelial cells, dendrites of cerebellar Purkinje cells, retinal neural cells and spermatocytes and spermatids in the testis. The localization of inversin in distal tubules in the kidney and in extrarenal tissues suggests that the expression of this protein has an important function in a variety of organs. Further studies are required to understand the way in which mutations in the INVS gene lead to the multi-organ pathology of inv mouse and human nephronophthisis.
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the INVS gene encodes a microtubule associated protein
Journal of The American Society of Nephrology, 2004Co-Authors: Jens Nurnberger, Anabelle Opazo Saez, Gerd Heusch, Thomas Philipp, Andreas Kribben, Carrie L PhillipsAbstract:ABSTRACT. Microtubule networks are important for many vital processes such as mitosis, cell polarity, and differentiation. Ciliary architecture and function closely depend on the microtubule cytoskeleton, and recent studies suggest a role of apical cilia of renal epithelia in the pathogenesis of polycystic kidney disease. This study evaluates the localization, potential interacting partners, and functional aspects of the INVS gene product inversin. Only recently, INVS has been identified as the gene that is mutated in nephronophthisis type 2, an autosomal recessive polycystic kidney disease. Using immunoprecipitation and co-pelleting assays, we show that the INVS gene product inversin forms a stable complex with tubulin in cultured renal epithelial cells. Inversin localizes to several components of the cytoskeleton including ciliary, random, and polarized microtubule pools. During cell divison, inversin is recruited to mitotic spindle fibers. After microtubule depolymerization using colcemid inversin and tubulin staining is no longer characterized by a network pattern but by homogeneous, diffuse distribution. Inversin does not coprecipitate with tubulin after addition of colcemid. After removal of colcemid, inversin immunofluorescence reappears together with tubulin in centrioles. Treatment with the microtubule stabilizing agent paclitaxel leads to severe alteration of the microtubule cytoskeleton with bundling and formation of long spindles of tubulin and inversin. In conclusion, inversin is closely associated with the microtubule cytoskeleton, and its spatial distribution is dependent on tubulin polymerization. Hence, altered inversin-tubulin interaction may impair ciliary function and thereby contribute to cyst development in nephronophthisis.
