Relevant bibliographies by topics / Cilia Flagella Kidney Kidney Diseases

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Academic literature on the topic 'Cilia Flagella Kidney Kidney Diseases'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Cilia Flagella Kidney Kidney Diseases"

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Pazour, Gregory J., Nathan Agrin, John Leszyk, and George B. Witman. "Proteomic analysis of a eukaryotic cilium." Journal of Cell Biology 170, no. 1 (July 4, 2005): 103–13. http://dx.doi.org/10.1083/jcb.200504008.

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Cilia and flagella are widespread cell organelles that have been highly conserved throughout evolution and play important roles in motility, sensory perception, and the life cycles of eukaryotes ranging from protists to humans. Despite the ubiquity and importance of these organelles, their composition is not well known. Here we use mass spectrometry to identify proteins in purified flagella from the green alga Chlamydomonas reinhardtii. 360 proteins were identified with high confidence, and 292 more with moderate confidence. 97 out of 101 previously known flagellar proteins were found, indicating that this is a very complete dataset. The flagellar proteome is rich in motor and signal transduction components, and contains numerous proteins with homologues associated with diseases such as cystic kidney disease, male sterility, and hydrocephalus in humans and model vertebrates. The flagellum also contains many proteins that are conserved in humans but have not been previously characterized in any organism. The results indicate that flagella are far more complex than previously estimated.
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Garcia-Gonzalo, Francesc R., and Jeremy F. Reiter. "Scoring a backstage pass: Mechanisms of ciliogenesis and ciliary access." Journal of Cell Biology 197, no. 6 (June 11, 2012): 697–709. http://dx.doi.org/10.1083/jcb.201111146.

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Cilia are conserved, microtubule-based cell surface projections that emanate from basal bodies, membrane-docked centrioles. The beating of motile cilia and flagella enables cells to swim and epithelia to displace fluids. In contrast, most primary cilia do not beat but instead detect environmental or intercellular stimuli. Inborn defects in both kinds of cilia cause human ciliopathies, diseases with diverse manifestations such as heterotaxia and kidney cysts. These diseases are caused by defects in ciliogenesis or ciliary function. The signaling functions of cilia require regulation of ciliary composition, which depends on the control of protein traffic into and out of cilia.
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Castaneda, Julio M., Rong Hua, Haruhiko Miyata, Asami Oji, Yueshuai Guo, Yiwei Cheng, Tao Zhou, et al. "TCTE1 is a conserved component of the dynein regulatory complex and is required for motility and metabolism in mouse spermatozoa." Proceedings of the National Academy of Sciences 114, no. 27 (June 19, 2017): E5370—E5378. http://dx.doi.org/10.1073/pnas.1621279114.

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Flagella and cilia are critical cellular organelles that provide a means for cells to sense and progress through their environment. The central component of flagella and cilia is the axoneme, which comprises the “9+2” microtubule arrangement, dynein arms, radial spokes, and the nexin-dynein regulatory complex (N-DRC). Failure to properly assemble components of the axoneme leads to defective flagella and in humans leads to a collection of diseases referred to as ciliopathies. Ciliopathies can manifest as severe syndromic diseases that affect lung and kidney function, central nervous system development, bone formation, visceral organ organization, and reproduction. T-Complex-Associated–Testis-Expressed 1 (TCTE1) is an evolutionarily conserved axonemal protein present from Chlamydomonas (DRC5) to mammals that localizes to the N-DRC. Here, we show that mouse TCTE1 is testis-enriched in its expression, with its mRNA appearing in early round spermatids and protein localized to the flagellum. TCTE1 is 498 aa in length with a leucine rich repeat domain at the C terminus and is present in eukaryotes containing a flagellum. Knockout of Tcte1 results in male sterility because Tcte1-null spermatozoa show aberrant motility. Although the axoneme is structurally normal in Tcte1 mutant spermatozoa, Tcte1-null sperm demonstrate a significant decrease of ATP, which is used by dynein motors to generate the bending force of the flagellum. These data provide a link to defining the molecular intricacies required for axoneme function, sperm motility, and male fertility.
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Verhey, Kristen J., John Dishinger, and Hooi Lynn Kee. "Kinesin motors and primary cilia." Biochemical Society Transactions 39, no. 5 (September 21, 2011): 1120–25. http://dx.doi.org/10.1042/bst0391120.

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Cilia and flagella play important roles in human health by contributing to cellular motility as well as sensing and responding to environmental cues. Defects in ciliary assembly and/or function can lead to a range of human diseases, collectively known as the ciliopathies, including polycystic kidney, liver and pancreatic diseases, sterility, obesity, situs inversus, hydrocephalus and retinal degeneration. A basic understanding of how cilia form and function is essential for deciphering ciliopathies and generating therapeutic treatments. The cilium is a unique compartment that contains a distinct complement of protein and lipid. However, the molecular mechanisms by which soluble and membrane protein components are targeted to and trafficked into the cilium are not well understood. Cilia are generated and maintained by IFT (intraflagellar transport) in which IFT cargoes are transported along axonemal microtubules by kinesin and dynein motors. A variety of genetic, biochemical and cell biological approaches has established the heterotrimeric kinesin-2 motor as the ‘core’ IFT motor, whereas other members of the kinesin-2, kinesin-3 and kinesin-4 families function as ‘accessory’ motors for the transport of specific cargoes in diverse cell types. Motors of the kinesin-9 and kinesin-13 families play a non-IFT role in regulating ciliary beating or axonemal length, respectively. Entry of kinesin motors and their cargoes into the ciliary compartment requires components of the nuclear import machinery, specifically importin-β2 (transportin-1) and Ran-GTP (Ran bound to GTP), suggesting that similar mechanisms may regulate entry into the nuclear and ciliary compartments.
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Pazour, Gregory J., Bethany L. Dickert, Yvonne Vucica, E. Scott Seeley, Joel L. Rosenbaum, George B. Witman, and Douglas G. Cole. "Chlamydomonas IFT88 and Its Mouse Homologue, Polycystic Kidney Disease Gene Tg737, Are Required for Assembly of Cilia and Flagella." Journal of Cell Biology 151, no. 3 (October 30, 2000): 709–18. http://dx.doi.org/10.1083/jcb.151.3.709.

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Intraflagellar transport (IFT) is a rapid movement of multi-subunit protein particles along flagellar microtubules and is required for assembly and maintenance of eukaryotic flagella. We cloned and sequenced a Chlamydomonas cDNA encoding the IFT88 subunit of the IFT particle and identified a Chlamydomonas insertional mutant that is missing this gene. The phenotype of this mutant is normal except for the complete absence of flagella. IFT88 is homologous to mouse and human genes called Tg737. Mice with defects in Tg737 die shortly after birth from polycystic kidney disease. We show that the primary cilia in the kidney of Tg737 mutant mice are shorter than normal. This indicates that IFT is important for primary cilia assembly in mammals. It is likely that primary cilia have an important function in the kidney and that defects in their assembly can lead to polycystic kidney disease.
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Pazour, Gregory J., Lynne Quarmby, Abigail O. Smith, Paurav B. Desai, and Miriam Schmidts. "Cilia in cystic kidney and other diseases." Cellular Signalling 69 (May 2020): 109519. http://dx.doi.org/10.1016/j.cellsig.2019.109519.

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7

Huang, Kaiyao, Dennis R. Diener, and Joel L. Rosenbaum. "The ubiquitin conjugation system is involved in the disassembly of cilia and flagella." Journal of Cell Biology 186, no. 4 (August 24, 2009): 601–13. http://dx.doi.org/10.1083/jcb.200903066.

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The disassembly of cilia and flagella is linked to the cell cycle and environmental cues. We have found that ubiquitination of flagellar proteins is an integral part of flagellar disassembly. Free ubiquitin and the ubiquitin-conjugating enzyme CrUbc13 are detected in flagella, and several proteins are ubiquitinated in isolated flagella when exogenous ubiquitin and adenosine triphosphatase are added, suggesting that the ubiquitin conjugation system operates in flagella. Levels of ubiquitinated flagellar proteins increase during flagellar resorption, especially in intraflagellar transport (IFT) mutants, suggesting that disassembly products are labeled with ubiquitin and transported to the cell body by IFT. Substrates of the ubiquitin conjugation system include α-tubulin (but not β-tubulin), a dynein subunit (IC2), two signaling proteins involved in the mating process, cyclic guanosine monophosphate–dependent kinase, and the cation channel polycystic kidney disease 2. Ubiquitination of flagellar proteins is enhanced early in mating, suggesting that ubiquitination also plays an active role in regulating signaling pathways in flagella.
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Adamiok-Ostrowska, Anna, and Agnieszka Piekiełko-Witkowska. "Ciliary Genes in Renal Cystic Diseases." Cells 9, no. 4 (April 8, 2020): 907. http://dx.doi.org/10.3390/cells9040907.

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Cilia are microtubule-based organelles, protruding from the apical cell surface and anchoring to the cytoskeleton. Primary (nonmotile) cilia of the kidney act as mechanosensors of nephron cells, responding to fluid movements by triggering signal transduction. The impaired functioning of primary cilia leads to formation of cysts which in turn contribute to development of diverse renal diseases, including kidney ciliopathies and renal cancer. Here, we review current knowledge on the role of ciliary genes in kidney ciliopathies and renal cell carcinoma (RCC). Special focus is given on the impact of mutations and altered expression of ciliary genes (e.g., encoding polycystins, nephrocystins, Bardet-Biedl syndrome (BBS) proteins, ALS1, Oral-facial-digital syndrome 1 (OFD1) and others) in polycystic kidney disease and nephronophthisis, as well as rare genetic disorders, including syndromes of Joubert, Meckel-Gruber, Bardet-Biedl, Senior-Loken, Alström, Orofaciodigital syndrome type I and cranioectodermal dysplasia. We also show that RCC and classic kidney ciliopathies share commonly disturbed genes affecting cilia function, including VHL (von Hippel-Lindau tumor suppressor), PKD1 (polycystin 1, transient receptor potential channel interacting) and PKD2 (polycystin 2, transient receptor potential cation channel). Finally, we discuss the significance of ciliary genes as diagnostic and prognostic markers, as well as therapeutic targets in ciliopathies and cancer.
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Wang, Shixuan, and Zheng Dong. "Primary cilia and kidney injury: current research status and future perspectives." American Journal of Physiology-Renal Physiology 305, no. 8 (October 15, 2013): F1085—F1098. http://dx.doi.org/10.1152/ajprenal.00399.2013.

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Cilia, membrane-enclosed organelles protruding from the apical side of cells, can be divided into two classes: motile and primary cilia. During the past decades, motile cilia have been intensively studied. However, it was not until the 1990s that people began to realize the importance of primary cilia as cellular-specific sensors, particularly in kidney tubular epithelial cells. Furthermore, accumulating evidence indicates that primary cilia may be involved in the regulation of cell proliferation, differentiation, apoptosis, and planar cell polarity. Many signaling pathways, such as Wnt, Notch, Hedgehog, and mammalian target of rapamycin, have been located to the primary cilia. Thus primary cilia have been regarded as a hub that integrates signals from the extracellular environment. More importantly, dysfunction of this organelle may contribute to the pathogenesis of a large spectrum of human genetic diseases, named ciliopathies. The significance of primary cilia in acquired human diseases such as hypertension and diabetes has gradually drawn attention. Interestingly, recent reports disclosed that cilia length varies during kidney injury, and shortening of cilia enhances the sensitivity of epithelial cells to injury cues. This review briefly summarizes the current status of cilia research and explores the potential mechanisms of cilia-length changes during kidney injury as well as provides some thoughts to allure more insightful ideas and promotes the further study of primary cilia in the context of kidney injury.
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Park, Kwon Moo. "Can Tissue Cilia Lengths and Urine Cilia Proteins Be Markers of Kidney Diseases?" Chonnam Medical Journal 54, no. 2 (2018): 83. http://dx.doi.org/10.4068/cmj.2018.54.2.83.

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Dissertations / Theses on the topic "Cilia Flagella Kidney Kidney Diseases"

1

Davenport, James Robert. "The role of the primary cilium in energy and glucose metabolism." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/davenport.pdf.

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Books on the topic "Cilia Flagella Kidney Kidney Diseases"

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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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Book chapters on the topic "Cilia Flagella Kidney Kidney Diseases"

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Hoshi, Masato, Jinzhi Wang, Sanjay Jain, and Moe R. Mahjoub. "Imaging centrosomes and cilia in the mouse kidney." In Methods in Cilia & Flagella, 1–17. Elsevier, 2015. http://dx.doi.org/10.1016/bs.mcb.2014.12.008.

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2

Rees, Lesley, Nicholas J. A. Webb, Detlef Bockenhauer, and Marilynn G. Punaro. "Renal cystic diseases and ciliopathies." In Paediatric Nephrology, 353–70. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198784272.003.0013.

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Inherited renal cystic diseases comprise a spectrum of disorders that are typically characterized by dysfunction of the so-called cilia. These hair-like cellular appendages are involved in numerous cellular signalling processes. During development, cilia are important for the development of the left–right axis and for the establishment of cell polarity. Consequently, depending on the specific nature of the underlying ciliary defect, renal cystic diseases can be associated with a large spectrum of other organ manifestations, including congenital heart disease, retinopathy, polydactyly, and hepatic abnormalities, such as ductal plate malformation. Based on clustering of such symptoms, specific clinical syndromes, such as nephronophthisis, Bardet–Biedl syndrome, Joubert syndrome, and the various forms of polycystic kidney diseases, have been assigned. Subsequent genetic investigations have shown that these clinical distinctions are not necessarily consistent with the underlying genetic alterations, so that, for example, genes initially associated with Joubert syndrome can phenocopy autosomal recessive polycystic kidney disease. Thus, identification of the genetic cause can inform the clinical management to assess for potentially involved organ manifestations.
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