Relevant bibliographies by topics / KIF5

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'KIF5'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "KIF5"

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Aizawa, H., Y. Sekine, R. Takemura, Z. Zhang, M. Nangaku, and N. Hirokawa. "Kinesin family in murine central nervous system." Journal of Cell Biology 119, no. 5 (December 1, 1992): 1287–96. http://dx.doi.org/10.1083/jcb.119.5.1287.

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In neuronal axons, various kinds of membranous components are transported along microtubules bidirectionally. However, only two kinds of mechanochemical motor proteins, kinesin and brain dynein, had been identified as transporters of membranous organelles in mammalian neurons. Recently, a series of genes that encode proteins closely related to kinesin heavy chain were identified in several organisms including Schizosaccharomyces pombe, Aspergillus niddulans, Saccharomyces cerevisiae, Caenorhabditus elegans, and Drosophila. Most of these members of the kinesin family are implicated in mechanisms of mitosis or meiosis. To address the mechanism of intracellular organelle transport at a molecular level, we have cloned and characterized five different members (KIF1-5), that encode the microtubule-associated motor domain homologous to kinesin heavy chain, in murine brain tissue. Homology analysis of amino acid sequence indicated that KIF1 and KIF5 are murine counterparts of unc104 and kinesin heavy chain, respectively, while KIF2, KIF3, and KIF4 are as yet unidentified new species. Complete amino acid sequence of KIF3 revealed that KIF3 consists of NH2-terminal motor domain, central alpha-helical rod domain, and COOH-terminal globular domain. Complete amino acid sequence of KIF2 revealed that KIF2 consists of NH2-terminal globular domain, central motor domain, and COOH-terminal alpha-helical rod domain. This is the first identification of the kinesin-related protein which has its motor domain at the central part in its primary structure. Northern blot analysis revealed that KIF1, KIF3, and KIF5 are expressed almost exclusively in murine brain, whereas KIF2 and KIF4 are expressed in brain as well as in other tissues. All these members of the kinesin family are expressed in the same type of neurons, and thus each one of them may transport its specific organelle in the murine central nervous system.
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Matsuzaki, Fumiko, Michiko Shirane, Masaki Matsumoto, and Keiichi I. Nakayama. "Protrudin serves as an adaptor molecule that connects KIF5 and its cargoes in vesicular transport during process formation." Molecular Biology of the Cell 22, no. 23 (December 2011): 4602–20. http://dx.doi.org/10.1091/mbc.e11-01-0068.

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Neurons are highly polarized cells with long neurites. Vesicular transport is required for neurite extension. We recently identified protrudin as a key regulator of vesicular transport during neurite extension. Expression of protrudin in nonneuronal cells thus induces formation of neurite-like membrane protrusions. We adopted a proteomics approach to identify proteins that associate with protrudin. Among the protrudin-associated proteins, including many with a function related to intracellular trafficking, we focused on KIF5, a motor protein that mediates anterograde vesicular transport in neurons. A coimmunoprecipitation assay confirmed that endogenous protrudin and KIF5 interact in mouse brain. Overexpression of KIF5 induced the formation of membrane protrusions in HeLa cells, reminiscent of the effect of protrudin overexpression. Forced expression of both protrudin and KIF5 promoted protrusion extension in a synergistic manner, whereas depletion of either protein attenuated protrusion formation. Protrudin facilitated the interaction of KIF5 with Rab11, VAP-A and -B, Surf4, and RTN3, suggesting that protrudin serves as an adaptor protein and that the protrudin–KIF5 complex contributes to the transport of these proteins in neurons. Given that mutation of protrudin or KIF5 is a cause of human hereditary spastic paraplegia, the protrudin–KIF5 axis appears to be integral to neuronal function.
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Takemura, R., T. Nakata, Y. Okada, H. Yamazaki, Z. Zhang, and N. Hirokawa. "mRNA expression of KIF1A, KIF1B, KIF2, KIF3A, KIF3B, KIF4, KIF5, and cytoplasmic dynein during axonal regeneration." Journal of Neuroscience 16, no. 1 (January 1, 1996): 31–35. http://dx.doi.org/10.1523/jneurosci.16-01-00031.1996.

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Nakata, Takao, Shinsuke Niwa, Yasushi Okada, Franck Perez, and Nobutaka Hirokawa. "Preferential binding of a kinesin-1 motor to GTP-tubulin–rich microtubules underlies polarized vesicle transport." Journal of Cell Biology 194, no. 2 (July 18, 2011): 245–55. http://dx.doi.org/10.1083/jcb.201104034.

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Polarized transport in neurons is fundamental for the formation of neuronal circuitry. A motor domain–containing truncated KIF5 (a kinesin-1) recognizes axonal microtubules, which are enriched in EB1 binding sites, and selectively accumulates at the tips of axons. However, it remains unknown what cue KIF5 recognizes to result in this selective accumulation. We found that axonal microtubules were preferentially stained by the anti–GTP-tubulin antibody hMB11. Super-resolution microscopy combined with EM immunocytochemistry revealed that hMB11 was localized at KIF5 attachment sites. In addition, EB1, which binds preferentially to guanylyl-methylene-diphosphate (GMPCPP) microtubules in vitro, recognized hMB11 binding sites on axonal microtubules. Further, expression of hMB11 antibody in neurons disrupted the selective accumulation of truncated KIF5 in the axon tips. In vitro studies revealed approximately threefold stronger binding of KIF5 motor head to GMPCPP microtubules than to GDP microtubules. Collectively, these data suggest that the abundance of GTP-tubulin in axonal microtubules may underlie selective KIF5 localization and polarized axonal vesicular transport.
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Nakata, Takao, and Nobutaka Hirokawa. "Microtubules provide directional cues for polarized axonal transport through interaction with kinesin motor head." Journal of Cell Biology 162, no. 6 (September 15, 2003): 1045–55. http://dx.doi.org/10.1083/jcb.200302175.

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Post-Golgi carriers of various newly synthesized axonal membrane proteins, which possess kinesin (KIF5)-driven highly processive motility, were transported from the TGN directly to axons. We found that KIF5 has a preference to the microtubules in the initial segment of axon. Low dose paclitaxel treatment caused missorting of KIF5, as well as axonal membrane proteins to the tips of dendrites. Microtubules in the initial segment of axons showed a remarkably high affinity to EB1–YFP, which was known to bind the tips of growing microtubules. These findings revealed unique features of the microtubule cytoskeletons in the initial segment, and suggested that they provide directional information for polarized axonal transport.
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Chen, Ying-Chun, Hao-Ru Huang, Chia-Hao Hsu, and Chan-Yen Ou. "CRMP/UNC-33 organizes microtubule bundles for KIF5-mediated mitochondrial distribution to axon." PLOS Genetics 17, no. 2 (February 11, 2021): e1009360. http://dx.doi.org/10.1371/journal.pgen.1009360.

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Neurons are highly specialized cells with polarized cellular processes and subcellular domains. As vital organelles for neuronal functions, mitochondria are distributed by microtubule-based transport systems. Although the essential components of mitochondrial transport including motors and cargo adaptors are identified, it is less clear how mitochondrial distribution among somato-dendritic and axonal compartment is regulated. Here, we systematically study mitochondrial motors, including four kinesins, KIF5, KIF17, KIF1, KLP-6, and dynein, and transport regulators in C. elegans PVD neurons. Among all these motors, we found that mitochondrial export from soma to neurites is mainly mediated by KIF5/UNC-116. Interestingly, UNC-116 is especially important for axonal mitochondria, while dynein removes mitochondria from all plus-end dendrites and the axon. We surprisingly found one mitochondrial transport regulator for minus-end dendritic compartment, TRAK-1, and two mitochondrial transport regulators for axonal compartment, CRMP/UNC-33 and JIP3/UNC-16. While JIP3/UNC-16 suppresses axonal mitochondria, CRMP/UNC-33 is critical for axonal mitochondria; nearly no axonal mitochondria present in unc-33 mutants. We showed that UNC-33 is essential for organizing the population of UNC-116-associated microtubule bundles, which are tracks for mitochondrial trafficking. Disarrangement of these tracks impedes mitochondrial transport to the axon. In summary, we identified a compartment-specific transport regulation of mitochondria by UNC-33 through organizing microtubule tracks for different kinesin motors other than microtubule polarity.
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Raynaud, Fabrice, Vincent Homburger, Martial Seveno, Oana Vigy, Enora Moutin, Laurent Fagni, and Julie Perroy. "SNAP23–Kif5 complex controls mGlu1 receptor trafficking." Journal of Molecular Cell Biology 10, no. 5 (September 14, 2018): 423–36. http://dx.doi.org/10.1093/jmcb/mjy031.

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Iworima, Diepiriye G., Bryce A. Pasqualotto, and Gordon L. Rintoul. "Kif5 regulates mitochondrial movement, morphology, function and neuronal survival." Molecular and Cellular Neuroscience 72 (April 2016): 22–33. http://dx.doi.org/10.1016/j.mcn.2015.12.014.

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Gumy, Laura F., Eugene A. Katrukha, Ilya Grigoriev, Dick Jaarsma, Lukas C. Kapitein, Anna Akhmanova, and Casper C. Hoogenraad. "MAP2 Defines a Pre-axonal Filtering Zone to Regulate KIF1- versus KIF5-Dependent Cargo Transport in Sensory Neurons." Neuron 94, no. 2 (April 2017): 347–62. http://dx.doi.org/10.1016/j.neuron.2017.03.046.

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Chen, Yanmin, and Zu-Hang Sheng. "Kinesin-1–syntaphilin coupling mediates activity-dependent regulation of axonal mitochondrial transport." Journal of Cell Biology 202, no. 2 (July 15, 2013): 351–64. http://dx.doi.org/10.1083/jcb.201302040.

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Axonal mitochondria are recruited to synaptic terminals in response to neuronal activity, but the mechanisms underlying activity-dependent regulation of mitochondrial transport are largely unknown. In this paper, using genetic mouse model combined with live imaging, we demonstrate that syntaphilin (SNPH) mediates the activity-dependent immobilization of axonal mitochondria through binding to KIF5. In vitro analysis showed that the KIF5–SNPH coupling inhibited the motor adenosine triphosphatase. Neuronal activity further recruited SNPH to axonal mitochondria. This motor-docking interplay was induced by Ca2+ and synaptic activity and was necessary to establish an appropriate balance between motile and stationary axonal mitochondria. Deleting snph abolished the activity-dependent immobilization of axonal mitochondria. We propose an “Engine-Switch and Brake” model, in which SNPH acts both as an engine off switch by sensing mitochondrial Rho guanosine triphosphatase-Ca2+ and as a brake by anchoring mitochondria to the microtubule track. Altogether, our study provides new mechanistic insight into the molecular interplay between motor and docking proteins, which arrests axonal mitochondrial transport in response to changes in neuronal activity.
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Dissertations / Theses on the topic "KIF5"

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Röhlk, Christian. "Characterization of conventional kinesins Kif3 and Kif5 from Dictyostelium discoideum." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-73948.

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Barry, Joshua. "Function and Mechanism of Polarized Targeting of Neuronal Membrane Proteins." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1373971273.

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Lee, Han Kyu Verfasser], and Matthias [Akademischer Betreuer] [Kneussel. "Analysis of the adaptor proteins, gephyrin and GRIP1, in KIF5-driven neuronal transport in Mus musculus, (Linnaeus, 1758) / Han Kyu Lee. Betreuer: Matthias Kneussel." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2011. http://d-nb.info/1020458259/34.

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McHugh, Toni. "Single molecule mechanics of Kif15." Thesis, University of Warwick, 2015. http://wrap.warwick.ac.uk/77516/.

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Kinesin-12 is a motor protein that has a role in the processes of mitotic spindle formation and maintenance. The human Kinesin-12, Kif15, has been shown to have some functional redundancy with Eg5, a Kinesin-5 that plays key roles in the formation of the bipolar spindle and is a potential target for anti-cancer drugs. Eg5 is thought to contribute to spindle formation by cross-linking and sliding microtubules, however little is known about the mechanism of Kif15. We have used laser tweezers to investigate the mechanical properties of Kif15 compared to those of kinesin-1. We have found that Kif15 is plus end directed and takes multiple steps along the microtubule without detaching. Full-length Kif15 walks faster and supports more load than full-length Eg5. Kif15 is less processive under load than kinesin-1, although it has a similar stall force. A second, diffusive, microtubule binding site in Kif15 supports processivity at zero load, and slows flyback following a detachment in the optical trap. The microtubule-associated protein, Tpx2, is necessary for the localisation of Kif15 to spindle microtubules. We find that Tpx2 binding arrests the motion of Kif15 and creates a stable binding state that resists both assisting and hindering loads. We also find evidence of a tail-mediated auto-inhibitory mechanism that creates a stable MT binding state and causes pausing during processive runs. C-terminal truncation of the Kif15 tail relieves this inhibition leading to faster overall stepping and abrogates the effects of Tpx2. We examined the detachment behaviour of Kif15 from microtubules, under assisting and hindering loads. We find that assisting loads cause single Kif15 and Kinesin-1 motors to detach from the microtubule more easily than hindering loads. Kif15 shows a much more asymmetric response to load in low levels of ATP than Kinesin-1, and both show more asymmetry than Eg5: previous work has shown that the behaviour of Eg5 does not change dramatically with differing loading directions. This has interesting implications for the roles of Kif15 and Eg5 motors in both parallel and anti-parallel microtubule bundles. Overall our data supports an in vivo mechanism for Kif15 that it distinct from that of Eg5. We investigated the load-dependent detachment of Kinesin-1 and Kif15 in millimolar concentrations of ADP, AMPPNP and micromolar concentrations of ATP. Kinesin-1 in ADP detached at low loads, and in AMPPNP at two different loads, both higher than in ADP. These two AMPPNP states of Kinesin1 likely corresponding to single and double headed microtubule binding, as proposed by Ishiwata and colleagues. Kif15 behaved broadly similarly. At micromolar ATP concentrations and hindering loads, both Kinesin-1 and Kif15 again showed two different high load detachment states. This is inconsistent with the model proposed by Ishiwata and possible modifications are discussed.
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Lin, Raozhou, and 林饒洲. "Kif5b interaction with NMDA receptors regulates neuronal function." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/208429.

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Intracellular transportation is an essential cellular event controlling neuronal development, morphology, function and survival. Kinesin-1 is the molecular motor conveying cargo along microtubule by utilizing the chemical energy from ATP hydrolysis. This motor consists of two heavy chains and two light chains. Both heavy and light chains are responsible for cargo bindings. There are three kinesin-1 heavy chains in eukaryotic cells. Kif5a and Kif5c are neuronal specific, while Kif5b is ubiquitously expressed. Kif5b carries various cargos essential for neuronal functions, and the early embryonic death of Kif5b null mice suggests the importance of Kif5b in vivo. N-methyl-d-aspartate receptors (NMDARs) are glutamate elicited channel, which is permeable to calcium and crucial for synaptic plasticity in the central nervous system. NMDARs are heteromeric assemblies consisting of NR1, NR2 and NR3 subunits. These transmembrane subunits contain three parts. Other than the transmembrane domain, the extracellular domain serves as the ligand binding site while the intracellular domain interacts with various partners regulating downstream signaling and receptor trafficking. Synaptic NMDAR activation regulates synaptic plasticity, while extrasynaptic NMDAR activation leads to excitotoxicity. In this project, I find that kinesin-1 directly interacts with NMDAR subunit, NR1, NR2A and NR2B in vivo. NMDAR colocalizes with kinesin-1 in the cell body and neurites. By GST-pull-down assays with different Kif5b fragments, the cytoplasmic domains of NR1, NR2A and NR2B are found to directly bind with Kif5b via a Kif5b C-terminal region independent of kinesin light chains. To examine the role of Kif5b in NMDAR trafficking, dominant negative Kif5b fragments are expressed in cell lines together with NR1-1a and GFP-NR2B. Overexpression of dominant negative Kif5b significantly disrupts GFP-NR2B forward trafficking and prevents it from entering into Golgi apparatus. Furthermore, the surface NR1 and NR2B levels are significantly reduced whilst the NR2A levels are not affected in Kif5b+/- mice in which the Kif5b protein level is reduced by 50% compared with the wild-type littermates. Consistent with this observation, the NR1 and NR2B levels are decreased in fractions containing synaptosomal membrane but not the one containing only postsynaptic densities, suggesting that the extrasynaptic NMDAR levels are affected in Kif5b+/- mice. NMDARs are highly permeable to calcium while activated, thereby activating neuronal nitric oxide synthases (nNOS) to produce nitric oxide (NO). It is found that NMDA triggered calcium influx is perturbed in Kif5b+/- neurons, while the synaptic NMDA receptor mediated calcium influx is normal. In Kif5b+/- slices, the production of NO reduces significantly. Calcium ionophore, A23187, rescue this NO defect, indicating insufficient supply of calcium as the main contribution to this defect. Therefore, Kif5b-dependent extrasynaptic localization of NMDA receptors mediates calcium influx upon NMDA stimulation and controls NO production. In the summary, above results suggest kinesin-1 as a novel motor involving in NMDA receptor trafficking. This interaction may contribute to the extrasynaptic distribution of NMDARs. By regulating NO production through interaction with NMDARs, Kif5b may mediate neuronal survival in cerebral ischemia and certain aggressive behaviors. This provides a novel target for therapy development against stroke and schizophrenia.
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Hussain, Hamdi. "Structural organisation of the human kinesin-12 Kif15." Thesis, University of Warwick, 2018. http://wrap.warwick.ac.uk/111537/.

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Kinesin-12, Kif15 is a molecular motor involved in bipolar spindle assembly. Kif15 function is regulated through autoinhibition of its C-terminal tail and binding to the microtubule-associated protein Tpx2. Previous studies have reported Kif15 to function as a tetramer as well as a dimer. In this study, a cross-linking mass spectrometry (XL-MS) protocol and analysis workflow was developed to study the structural organisation of Kif15. Using XL-MS studies, it was found that Kif15 adopts a parallel tetramer conformation, which is autoinhibited by its C-terminal leucine zipper. Next, we show that this autoinhibited conformation is stabilised by the binding partner Tpx2. We also show that there is a shift in the binding interface between Kif15 and Tpx2 when microtubules are present and absent. In the presence of microtubules, Tpx2 mainly binds to the leucine-zipper of the Kif15 motor, whereas in the absence of the microtubules, this binding is exclusively localised to the fourth coiled-coil. We also reveal that Tpx2 adopts a dimeric conformation at physiological ionic strength. Finally, to understand the function of Kif15 in-vivo, we have developed putative Kif15 knock-out cell lines and developed a cross-linking protocol to cross-link Kif15 in cells.
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Hartel, Michaela. "Molecular Cloning and Functional Studies of Neurospora crassa KIF1, a New Member of the UNC-104/KIF1 Family of Kinesin-Like Proteins." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-22151.

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Wang, Jing, and 王景. "The study of KIF5B-mediated intracellular transport in neurons." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41633763.

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Wang, Jing. "The study of KIF5B-mediated intracellular transport in neurons." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41633763.

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唐裕婷 and Yu-ting Tracy Tong. "Study of kinesin family member 7 (KIF7) in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42904341.

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Books on the topic "KIF5"

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Ken Kiff. London: Thames & Hudson, 2001.

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Kiff, Ken. Ken Kiff. London: Fischer Fine Art, 1988.

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Kifo kisimani. Nairobi: Marimba Publications Ltd., 2001.

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Kifo cha uchungu. Dar es Salaam, Tanzania: FGD Tanzania Limited, 2009.

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Kifo cha mwalimu. Nairobi, Kenya: Jomo Kenyatta Foundation, 2011.

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Khalfani, Mwikoni Yusuf. Kifo cha huzuni. Peramiho, Tanzania: Benedictine Publications Ndanda, 1991.

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Kif: Roman. Paris: B. Grasset, 2014.

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Saitō, Sakae. Shin satsujin no kifu. Tōkyō: Chūō Kōronsha, 1996.

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Kifo ni haki yangu. [Dar es Salaam]: Global Publishers & General Enterprises Ltd., 2012.

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Kiff, Ken. Ken Kiff: New York. London: Fischer Fine Art, 1988.

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Book chapters on the topic "KIF5"

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Superko, H. Robert, Tom White, James Forrester, and Spencer King. "The Statin Response Gene: KIF6." In Pharmacogenomic Testing in Current Clinical Practice, 175–98. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-283-4_11.

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van Heesbeen, Roy G. H. P., and René H. Medema. "Kif15: A Useful Target for Anti-cancer Therapy?" In Kinesins and Cancer, 77–86. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-9732-0_5.

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Berčič, Boštjan, and Mirko Vintar. "Simple Life-Events Ontology in SU(M)O-KIF." In Knowledge Management in Electronic Government, 128–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-24683-1_14.

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Martin, Philippe. "Knowledge Representation in CGLF, CGIF, KIF, Frame-CG and Formalized-English." In Conceptual Structures: Integration and Interfaces, 77–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/3-540-45483-7_7.

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Hanayama, Nobutane, and Ryuichi Nogami. "A Method for Illustrating Shogi Postmortems Using Results of Statistical Analysis of Kifu Data." In Entertainment Computing – ICEC 2017, 277–83. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-66715-7_30.

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Anyango, Beatrice, Kate Wilson, and Ken Giller. "Competition in Kenyan soils between Rhizobium leguminosarum biovar phaseoli strain Kim5 and R. tropici strain CIAT899 using the gusA marker gene." In Molecular Microbial Ecology of the Soil, 69–78. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-017-2321-3_6.

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"DHU AL-KIFL." In The Qur'an, 210–12. Routledge, 2006. http://dx.doi.org/10.4324/9780203176443-32.

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"25. Ayyubid Kings (Lords) of Hisn Kifa." In The History of Tur Abdin, 123–26. Piscataway, NJ, USA: Gorgias Press, 2008. http://dx.doi.org/10.31826/9781463213336-027.

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Kezilahabi, Euphrase. "WASUBIRI KIFO (EN ESPERA DE LA MUERTE)." In África, translated by Leonard Lisanza Muaka and Germán Franco Toriz, 201–15. El Colegio de México, 2009. http://dx.doi.org/10.2307/j.ctv3dnr5z.12.

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Qugana, Hana, and Simon Layton. "Primitive Liberals and Pirate Tribes: Black-Flag Radicalism and the Kibbo Kift." In Liberal Ideals and the Politics of Decolonisation, 170–94. Routledge, 2020. http://dx.doi.org/10.4324/9781003053316-8.

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Conference papers on the topic "KIF5"

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Abdelnur, Humberto J., Radu State, and Olivier Festor. "KiF." In the 1st international conference. New York, New York, USA: ACM Press, 2007. http://dx.doi.org/10.1145/1326304.1326313.

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Hurst, Terril N. "Automated Model Generation Using the KIF Declarative Language." In ASME 1991 International Computers in Engineering Conference and Exposition. American Society of Mechanical Engineers, 1991. http://dx.doi.org/10.1115/cie1991-0018.

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Abstract Logic-based artificial intelligence researchers propound the declarative programming paradigm as a solution to problems arising from conventional procedural programming methods. A formal language possessing a declarative semantics, called Knowledge Interchange Format (or KIF), has been used for interchanging information between disparate programs, each containing specialized internal representations to support specific requirements. A simple system has been developed to evaluate the utility of KIF and declarative programming. The domain chosen for this evaluation was lumped-parameter dynamic systems analysis, due to its well-established vocabulary and concepts. In particular, bond graph theory formed the basis of the knowledge representation which was written in KIF. Models were generated to analyze the physical dynamics of a servomechanism used in a compact disc player. Fully automated model construction and solution was achieved, beginning with a set of library elements written in KIF and ending with solution of a set of first-order differential equations which characterize dynamic behavior. Work has begun to include assembly as well as bond graph information in order to evaluate the system’s utility for managing constraints in multiple domains. Based on demonstrated success in the dynamics and assembly domains, the next step will be to apply declarative programming to more-open domains, such as functional tolerancing, for which a comprehensive vocabulary and conceptual framework is still lacking. The hope is that the declarative paradigm will contribute to the formalization of several domains which can then be more easily integrated within a concurrent engineering environment, thus fostering conceptual product designs which are more robust with respect to manufacturability constraints.
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Shin, Jung-Young, Min-Young Kim, Kyoung-Hwa Son, Jeong-Oh Kim, and Jin-Hyoung Kang. "Abstract 2710: Tumorigenic activity of a novel KIF5B-RET fusion gene." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2710.

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Ho, Joanna, Oscar GW Wong, Michelle KY Siu, Hextan YS Ngan, and Annie N. Y. Cheung. "Abstract 3068: Tumor suppressor functions of Kinesin superfamily 7 (Kif7) in choriocarcinoma." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3068.

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Ningombam, Dhruba, Tejbanta Singh Chingtham, and Mrinal Kanti Ghose. "A Knowledge Interchange Format (KIF) for Robots in Cloud." In 2019 International Conference on Communication and Electronics Systems (ICCES). IEEE, 2019. http://dx.doi.org/10.1109/icces45898.2019.9002191.

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Wu, Te Hung, C. L. Lin, Ming Jui Chen, Zen Hsiang Tsai, Chen Yu Ao, H. C. Thuang, Jian Shin Liou, Chuen Huei Yang, and Ling Chieh Lin. "Improvement of OPC accuracy for 65nm node contact using KIF." In SPIE 31st International Symposium on Advanced Lithography, edited by Iraj Emami and Kenneth W. Tobin, Jr. SPIE, 2006. http://dx.doi.org/10.1117/12.657900.

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Schubert, Laura, Anh T. Le, Andrea E. Doak, and Robert C. Doebele. "Abstract 1842: Novel KIF5B-RET+ NSCLC cell lines demonstrate differential responses to RET inhibitors." 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.am2018-1842.

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Wates, Rebecca J., Anuradha Roy, Frank Schoenen, John Karanicolas, Scott Weir, and Andrew Godwin. "Abstract B03: Targeting the KIF11/KIF15/TPX2 axis to develop new therapies for ovarian cancer." In Abstracts: AACR Special Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; October 1-4, 2017; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-b03.

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Capelletti, Marzia, Doron Lipson, Geoff Otto, Roman Yelensky, Dalia Ercan, Jhingook Kim Kim, Hidefumi Sasaki, et al. "Abstract LB-88: Identification of recurrent oncogenic KIF5B-RET rearrangements in non-small cell lung cancer." 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-lb-88.

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Mazumdar, Manjari, Siddharth Dasari, and Jennifer Keen. "Abstract 934: Chromokinesin KIF4 facilitates chromatin organization critical for immunoglobulin class switch recombination and prevents lymphoma formation." 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.am2011-934.

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