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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.published_or_final_version
Biochemistry
Doctoral
Doctor of Philosophy
6
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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Tong, Yu-ting Tracy. "Study of kinesin family member 7 (KIF7) in breast cancer." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B42904341.
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Zhu, Guixia, and 朱貴霞. "Study of the function of Kinesin-1 (KIF5B) in long bone development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B41757919.
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Gan, Huiyan, and 甘慧妍. "Understanding the role of KIF5B in long bone development and chondrocyte cytokinesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/211554.
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Kinesins are motor proteins responsible for the anterograde transport on microtubules. Kinesin-1 is the first characterized kinesin, and it consists of two heavy chains and two light chains. KIF5B is a form of Kinesin-1 heavy chains that is ubiquitously expressed in mammals. The head domain of KIF5B is responsible for ATP-dependent mechanical movement along microtubules, while the tail region is well-known for its interaction with cell specific cargos. Recent studies reveal a second microtubule binding site in the tail, suggesting special functions of KIF5B in microtubule sliding and bundling.
To understand the role of KIF5B in long bone development, a conditional knockout mouse model was generated, in which Kif5b is deleted in early limb mesenchyme using Prx1-cre/LoxP mediated recombination. Unlike Col2a1-cre directed Kif5b knockout in chondrocytes, the expression of Prx1-cre in limb mesenchyme results in Kif5b knockout in both chondrocyte and osteoblast lineages. The Prx1-cre mediated Kif5b conditional knockout mice develop malformed long bones characterized by their bowed shape, shortened length and multiple fractures, which reflects a combination of defects in bone matrix and growth plate. The mutant mice demonstrate impaired bone matrix formation, as indicated by both collagen density reduction and collagen matrix disorganization. Also, the growth plate does not retain its normal organization, and the hypertrophic zone is absent. The KIF5B deficient chondrocytes not only lose planar cell polarity, but also undergo early apoptosis and fail in terminal differentiation. Interestingly, the binucleation rate is significantly increased in these chondrocytes, suggesting a severe cytokinesis defect. Besides, the intracellular retention of extracellular matrix (ECM) molecules and the uneven distribution of ECM in the cartilage imply both blockage and inappropriate direction of secretion.
Cytokinetic defect in chondrocytes is closely associated with growth plate abnormality and growth retardation. In Kif5b knockout chondrocytes, cytokinetic defect is also one of the earliest and principal phenotypes. Therefore the underlying mechanism of cytokinetic defect was further investigated at cellular level. Since Kif5b knockout chondrocytes cannot survive in primary culture, RNA interference approach was adopted to generate a Kif5b-knockdown chondrogenic cell line. As expected, the Kif5b knockdown cells demonstrate cytokinetic defects characterized by increased binucleation rate and prolonged cytokinesis phase. In control cells, KIF5B becomes concentrated in the midbody during cytokinesis, and the midbody organization is disrupted in Kif5b knockdown cells. Furthermore, transient expression of full-length KIF5B significantly reduces the binucleation rate of these KIF5B deficient cells, whereas over-expression of a truncated KIF5B (without microtubule binding sites in tail region) cannot rescue the defect. Additionally, KIF5B is found to interact with midbody components PRC1 and Aurora B kinase by GST pull-down assay.
This study demonstrates the multiple functions of KIF5B in long bone development and emphasizes its significant role as a key modulator in chondrocyte cytokinesis. More importantly, the study also brings new insights into the mechanisms of cytokinesis: we propose that KIF5B may participate in cytokinesis by regulating the midbody organization and stability via microtubule bundling and transporting or anchoring important components to the midbody.published_or_final_version
Biochemistry
Doctoral
Doctor of Philosophy
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Zhu, Guixia. "Study of the function of Kinesin-1 (KIF5B) in long bone development." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B41757919.
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Cheng, Rachel K. "'Something radically wrong somewhere' : the Kindred of the Kibbo Kift, 1920-1932." Thesis, University of Glasgow, 2016. http://theses.gla.ac.uk/7693/.
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This thesis examines the Kindred of the Kibbo Kift, a co-educational outdoors organisation that claimed to be a youth organisation and a cultural movement active from August 1920 to January 1932. Originally part of the Boy Scouts and Girl Guides, the Kibbo Kift offers rich insight into the interwar period in Britain specifically because it carried forward late Victorian and Edwardian ideology in how it envisioned Britain. Members constructed their own historical narrative, which endeavoured to place the organisation at the heart of British life. The organisation’s internal life revolved around the unique mythology members developed, and the movement aspired to regenerate Britain after the First World War physically and spiritually. This thesis argues Kibbo Kift was a distinctive movement that drew upon its members’ intellectual preoccupations and ideals and inspired its members to create unique cultural artefacts. While the Kibbo Kift was ultimately too politically ambiguous to have lasting political impact on a national scale, examining the organisation offers important insight into intellectual thought and cultural production during the British interwar period. This thesis charts the changes the organisation underwent through its membership and the different trends of intellectual thought brought in by individual members, such as its leader, John Hargrave, brought to the group. It examines the cultural production of the organisation’s unique mythology, which created a distinctive historical narrative. It surveys gender issues within the organisation through the “roof tree”, an experimental family unit, and the group’s increasing anti-feminism. Finally, it considers how Clifford H. Douglas’ economic theory of social credit caused the Kibbo Kift to transform into the Green Shirts Movement for Social Credit and later into the Social Credit Party of Great Britain and Northern Ireland.
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Craven, Josef Francis Charles. "Redskins in Epping Forest : John Hargrave, the Kibbo Kift and the woodcraft experience." Thesis, University College London (University of London), 1999. http://discovery.ucl.ac.uk/1348858/.
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This thesis attempts to locate and explore the world of the Kibbo Kift, a camping and handicraft organisation established in 1920, by John Hargrave. The Kibbo Kift proved to be the most controversial, complex and colourful component of the English Woodcraft movement. The aim of this thesis is three-fold. First, to explain what is meant by the term Woodcraft and to examine the varied cultural influences that lay behind its growth in Edwardian England. Second, to give a more balanced and detailed historical account of the development of the Kibbo Kift, its secession from the Boy Scouts and its transformation into the Green Shirt Movement for Social Credit. Finally, it will orientate the movement within the English pro-rural tradition. In doing so, I hope to develop the idea of there being a collection of diverse and often contradictory strands within this culture, with the Kibbo Kift occupying a so-called pastoral Liberal-Transcendentalist stance, in contrast to the more agrarian Tory- Organic wing of the movement. It will be argued that the Kibbo Kift was 'progressive', forward looking and essentially 'modern', representing, in effect, a suburban interest in the inter-war countryside. However, the ultimate failure of the Kibbo Kift's Woodcraft strategy adds to the argument that the English rural revival of this period was not as hegemonic as once thought and that pro-ruralism was limited in its cultural scope and impact.
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Lin, Yangjun, and 林扬骏. "Kif5b may play a role in impairing mouse memory : a behaviour and cellular study." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193575.
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Alzheimer's Disease is one of the most fearsome diseases worldwide. The study of Alzheimer's Disease (AD) is broad and many have focused on investigating the various proteins involved in neurons. A popular hypothesis of the cellular mechanism of AD is the accumulation of beta-Amyloid. Kinesin is a large group of motor proteins, which plays an extensive role in mitosis and intracellular cargo transport, including that of the Amyloid Protein Precursor. In the present study we have performed fear conditioning behaviour tests on Kif5b conditional knockout (CKO) mouse. Kif5b CKO mouse shows an impair contextual memory compared to the wild type, but does not display an impaired auditory memory. Heterozygous Kif5b knock out mouse shows no significant difference to the wild type. The study has also generated Kif5b fragments and used them to pull-down proteins in mouse brain lysate. The study has identified Clathrin and alpha-Adaptin as binding partners of Kif5b in mouse neuronal cells. The binding domain of Kif5b for these proteins is between amino acid residue 891-935. Finally this study has made a number of recommendations for further study.published_or_final_version
Biochemistry
Master
Master of Medical Sciences
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de, Kiff Alan [Verfasser]. "Photooxygenierungen in Dominoprozessen und für die Organokatalyse und Luminolderivate als Ionenpaar-Fluoreszenzsonden / Alan de Kiff." München : Verlag Dr. Hut, 2013. http://d-nb.info/1045125733/34.
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Araujo, Tânia Kawasaki de 1985. "Utilização da técnica de Open Array para investigação de genes associados a fendas labiopalatais em amostra da população brasileira." [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313118.
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Orientador: Vera Lúcia Gil da Silva LopesTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A fenda de labiopalatal (FLP) isolada é o defeito craniofacial mais comum em humanos. O objetivo deste estudo foi avaliar associações entre 39 genes e a etiologia de FLP isolada em uma amostra da população brasileira. Este estudo de associação do tipo caso-controle foi desenhado com um poder estatístico de 81,29% por meio de regressão logística. O grupo de casos foi composto por 182 pacientes com FLP isolada registrados na Base Brasileira de Dados Clínicos e Familiais de Fendas Orofaciais Típicas. O grupo controle foi formado por 355 indivíduos saudáveis, sem história de fendas orais em três gerações. Toda a amostra foi genotipada por meio do sistema OpenArray®TaqManTM para 253 polimorfismos de nucleotídeo único (SNPs) em 39 genes, incluindo dois genes que, recentemente, haviam sido descritos por este grupo de pesquisa. A seleção de SNPs foi feita com o programa SNPbrowser 4.0 (Applied Biosystems) para verificar o número e a localização dos SNPs apropriados para explorar a associação de cada gene com FLP isolada. A análise de associação foi realizada por meio de regressão logística e regressão stepwise. Os resultados foram corrigidos para múltiplos testes (correção de Bonferroni). Vinte e quatro SNPs em 16 genes foram significativamente associados com a etiologia da FLP isolada, incluindo MSX1, SPRY1, MSX2, PRSS35, TFAP2A, SHH, VAX1, TBX10, WNT11, PAX9, BMP4, JAG2, AXIN2, DVL2, KIF7 e TCBE3. A análise de regressão stepwise revelou que 11 genes contribuiram em 15,5% do fenótipo de FLP isolada nessa amostra. Este é o primeiro estudo a associar os genes KIF7 e TCEB3 à FLP isolada
Abstract: Nonsyndromic cleft lip and palate (NSCLP) is the most common craniofacial birth defect. The aim of this study was to evaluate associations between 39 genes and the etiology of NSCLP in a Brazilian population. This case-control association study was designed with 81.29% statistical power according to logistic regression. The case group was composed of 182 patients with NSCLP enrolled in the Brazilian Database on Orofacial Clefts. The controls included 355 healthy individuals with no history of oral clefting in the past three generations. All samples were genotyped by TaqMan®OpenArrayTM system for 253 single nucleotide polymorphisms (SNPs) in 39 genes, including two that had recently been associated with this process. The SNPs selection was made by SNPbrowser 4.0 (Applied Biosystems) in order to establish the best SNPs to explor the association between each gene and NSCLP. The association analysis was performed using logistic regression and stepwise regression. The results were corrected for multiple testing (Bonferroni correction). Twenty-four SNPs in 16 genes were significantly associated with the etiology of NSCLP, including MSX1, SPRY1, MSX2, PRSS35, TFAP2A, SHH, VAX1, TBX10, WNT11, PAX9, BMP4, JAG2, AXIN2, DVL2, KIF7 and TCBE3. Stepwise regression analysis revealed that 11 genes contributed to 15.5% of the phenotype of NSCLP in the sample. This is the first study to associate KIF7 and TCEB3 with NSCLP
Doutorado
Ciencias Biomedicas
Doutora em Ciências Médicas
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Qugana, Hana Fe. "The cultural politics of Englishness : John Gordon Hargrave, the Kibbo Kift and Social Credit, 1920-1939." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1575562/.
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This thesis explores the idea of Englishness in the context of a social movement that lasted from 1920 to 1951, known as the Kindred of the Kibbo Kift and later, the Green Shirts and Social Credit Party. It is primarily a study of the movement’s founding leader John Gordon Hargrave (1894-1982), who sheds light on the reinvention of English identity, politics and culture in interwar Britain. It surveys how Hargrave and his Kindred constructed their Englishness against the backdrop of cultural change in the 1920s, before assessing their engagement with young, likeminded national movements on the European continent. It concludes with an appraisal of Hargrave’s attempts, after he adopted the ideology of Social Credit in 1925, to translate his movement’s cultural sensibilities into a mainstream political directive, positioning it against (and at times within) contemporaneous projects elsewhere, including European fascism. Assessing these thematic treatments collectively, I argue that the Kibbo Kift was an innovative expression of Englishness that embodied a libertarian impulse to ‘decolonise’ the metropole, before turning in on itself and finally fragmenting. This study seeks specifically to interrogate cosmopolitan Englishness—a patriotic sensibility associated with the breakdown of the imperial system and premised on notions of cultural relativism. Many of its proponents have posited it as a means of bridging class, gender and ethnic divisions at home and abroad. This concept elucidates, in the first instance, the logic of Hargrave and his followers in blending professed traditions of colonised and so-called primitive peoples with those of England’s pre-imperial past. They domesticated these elements in various ways, thereby conveying a compelling response to Britain’s perceived decline following the Great War of 1914-1918. Concurrently, the Kindred’s utopian proposals, which resonated most profoundly with the literary and artistic intelligentsia, former Suffragists and European youth movements, alluded to an alien, totalitarian quality that became more pronounced, distorted and inhibiting as the group ventured into British mass politics in the guise of the Social Credit Party. It was not merely political extremism and violence that limited the SCP’s success, however. This thesis attributes the decline of the movement to tensions inherent to its cultural politics—between intellectualism and activism, and cosmopolitanism and Englishness.
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Dafinger, Claudia [Verfasser], Peter [Akademischer Betreuer] Nürnberg, and Bernd [Akademischer Betreuer] Wollnik. "Molekulare Pathogenese des Joubert-Syndroms - Die Rolle des Proteins KIF7 / Claudia Dafinger. Gutachter: Peter Nürnberg ; Bernd Wollnik." Köln : Universitäts- und Stadtbibliothek Köln, 2013. http://d-nb.info/1056999667/34.
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Glaeser, Volker. "Toward a process-oriented knowledge transfer framework for a Knowledge Intensive Firm (KIF)." Thesis, University of Gloucestershire, 2017. http://eprints.glos.ac.uk/5833/.
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Managing and transferring knowledge within a corporation becomes the ultimate key for survival in the Knowledge Age. Internal knowledge is often unique and lays the foundation for a company’s competitiveness. Effective and fast knowledge transfer (KT) is particularly critical to KIFs such as IT consultancies, R&D based companies or firms in the software industry. Intrafirm KT is a complex undertaking though and a number of initiatives fail. Therefore, achieving optimal KT is a compelling need. The aim of this thesis is to explore what kind of process-oriented framework helps create optimal KT practices in a KIF by applying and adapting the Scrum management and control practices. Scrum was initially formalised for the development of software and can be used to manage complex projects. Enhancing Scrum to enable intra-firm KT represents a novel approach, involving diverse roles across a team of employees and making use of their respective capabilities. The work makes a contribution to knowledge by introducing clearly defined KT process steps and documentation tools - underpinned by motivational practices, transparency and accountability of individual employees to find ways for them to impart their knowledge. It proffers an extension to existing frameworks and models. The study could be highly relevant for practitioners concerned with intra-firm KT for two reasons. Employing the newly developed approach helps investigate appropriate organisational contexts and, more importantly, provides a practical set of tools to assist with the task of enabling KT. The form of a case study within a KIF, a consultancy firm focussed on digital business transformation, has been chosen as the foundation for the inquiry. The research strategy is rooted in a participatory paradigm. Qualitative data captured in the company were specifically developed through participatory action research (PAR). Documentary analysis, non-participant observation, and open-ended interviews ahead of iterative action-reflection cycles contributed to providing new learning for a team of highly qualified Knowledge Workers (KWs). Overall the team of consultants that was the focus of this case study believes that knowledge in the firm will be transferred faster and sustainably by employing practices of interaction and adaptation within a knowledge-friendly and motivational environment. The time required to phase new consultants into existing projects, where KT was indispensable, was reduced significantly by 50% from four to two weeks. The research suggests that the newly developed process-oriented framework can greatly improve KT practices in a KIF by applying practices of gathering data and information (Aggregating), prioritising them (Featuring), reviewing KT progress (Reviewing), and utilising newly acquired knowledge (Doing). The key findings of this work, the AFRD-process and the AFRD-framework, were subject to an audit by an expert panel from the Fresenius University of Applied Science in Munich, Germany, and practitioners in a machine engineering company in Augsburg, Germany.
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TAUBENBLATT, PATRICE. "Tri intracellulaire de la vamp et etude de la proteine moteur kif 1a." Paris 11, 2001. http://www.theses.fr/2001PA112142.
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La vamp 2 est une proteine de la vesicule synaptique essentielle au phenomene d'exocytose. La formation d'un complexe entre la vamp et 2 proteines de la membrane presynaptique (syntaxine et snap 25) va permettre la fusion entre ces 2 structures membranaires et la liberation du neurotransmetteur. Dans un premier temps, nous nous sommes interesses a la localisation subcellulaire de la vamp a la terminaison nerveuse. Grace a une technique de marquages apres cryofracture, nous montrons que la vamp est associee a la membrane presynaptique. Ces resultats suggerent qu'en plus d'une localisation vesiculaire, la vamp est localisee au niveau de la membrane presynaptique. Cette localisation n'est pas due a une fusion des vesicules synaptiques avec la membrane presynaptique puisque la presence de la vamp n'est pas correlee avec celle d'autres marqueurs vesiculaires tels que la synaptophysine, sv2 ou vacht. Sur la preparation de membrane presynaptique, on peut mettre en evidence un complexe sds-resistant entre la vamp, la syntaxine et la snap 25. Suite a ce travail nous nous sommes demandes si des la sortie du trans golgi network, la vamp est cotransportee vers la terminaison nerveuse avec les autres proteines vesiculaires ou s'il y a deja eu une etape de tri. En immunopurifiant le precurseur des vesicules synaptiques via un anticorps anti-sv2, nous mettons en evidence la presence de proteines vesiculaires mais pas de la vamp (ni des t-snares). Toujours dans la logique de l'etude du trafic intracellulaire, nous nous sommes interesses a la kif 1a, proteine moteur impliquee dans le transport du precurseur des vesicules synaptiques vers la terminaison nerveuse. Nous avons tout d'abord clone le gene de la kif 1a. Apres avoir determiner la repartition cellulaire et subcellulaire de la kif 1a, notre problematique a ete de savoir comment est regulee l'accrochage/decrochage de la kif 1a a son cargo et aussi qu'elle est l'identite du recepteur responsable de la specificite d'accrochage.
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Ygge, Nicklas, and Robin Hagberg. "Kontroll eller fria tyglar? : En fallstudie om organisationskontroll inom konsultbranschen ur ett organisatoriskt perspektiv." Thesis, Linköpings universitet, Företagsekonomi, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-149668.
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Bakgrund: Då utvecklingen i det företagsekonomiska samhället har gått från ett industrisamhälle till ett kunskapssamhälle efterfrågas extern expertis från kunskapsintensiva företag. Många konsultföretag är goda exempel på den postbyråkratiska organisationsformen, som karaktäriseras av relativt få skikt av hierarki, flexibilitet, delaktighet i beslutsfattande och lösa karriärstrukturer, där identiteten blir svårmanövrerad. Identitet är av särskild betydelse när det kommer till KIF:er av olika skäl. Det blir allt mer framträdande för ledare att försöka forma individerna själva. Det är viktigt för ledningen att influera anställda via strategier för att exempelvis uppnå organisationskontroll, säkerställa lojalitet och behållning, och förebygga existentiell osäkerhet samt skapa självförtroende och självkänsla i arbetet. Syfte: Syftet med studien är att med hjälp av befintliga teorier och empiriskt underlag bidra med ökad förståelse av hur KIF:er använder identitetsreglering för att erhålla organisationskontroll. Genomförande: Studien har genomförts med en kvalitativ metod via en fallstudiedesign genom intervjuer med anställda inom relevanta företag inom konsultbranschen. Respondenterna har haft varierande befattningar och kunskaper i respektive företag. Slutsats: Resultatet av denna studie visar att kunskapsintensiva företag arbetar med organisationskontroll där identitet spelar en central roll. Flertalet strategier presenteras så som rekrytering, värdeerbjudande, utbildningar, avskalad hierarki, sociala aktiviteter, team, corporate storytelling och värderingar, vilket bidrar till en ökad förståelse för hur KIF:er arbetar med identitetsreglering för att uppnå organisationskontroll.Background: Since the development of business economics has shifted from an industrial society to a knowledge society, external expertise is demanded from knowledge-intensive companies. Many consulting firms are good examples of the post- bureaucratic organization, characterized by relatively few layers of hierarchy, flexibility, decision-making involvement and loose career structures, where the identity becomes difficult to operate. Identity is of particular importance when it comes to KIFs for different reasons. It is becoming increasingly prominent for leaders to try to shape the individuals themselves. It is important for management to influence employees through strategies to achieve organizational control, ensure loyalty and prevent existential uncertainty as well as create self-confidence and self-esteem at work. Purpose: The purpose of the study is to provide, with the help of existing theories and empirical evidence, an increased understanding of how KIFs use identity regulation to obtain organizational control. Empiric: The study has been conducted with a qualitative method through a case study design through interviews with employees in relevant companies in the consulting industry. Respondents have had varying positions and skills in their respective companies. Result: The result of this study shows that knowledge-intensive companies work with organizational control where identity plays a central role. Several strategies are presented such as recruitment, value offerings, educations, scaled-down hierarchy, social activities, teams, corporate storytelling and values, which helps to understand how KIFs work with identity regulation to achieve organizational control.
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Johansson, Andreas, Anton Carlström, and Johan Sonesson. "Varumärkesuppbyggnad och Marknadskommunikation i Svenska Fotbollsklubbar : En fallstudie på BK Forward & KIF Örebro." Thesis, Örebro universitet, Handelshögskolan vid Örebro Universitet, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-29371.
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Background European football has during the past decades seen a fast development towards a more professionalized and commercialized climate. This had led to the fact that a lot of clubs are run like any other company, and the focus on marketing and market shares has increased. To be able to create a strong brand clubs have to put a lot of work into marketing, not only of their own brand, but of their sponsors and partners as well. Purpose The purpose of this study is to (in step 1) analyze how two smaller Swedish football clubs build their brand and work with their marketing communication. In step 2, the purpose is to create a model of how these clubs may work to develop their brand and marketing communication. Method With a qualitative approach, the authors of this paper have analyzed text and documents as well as performed two in-depth interviews. Findings Both clubs lack a well-developed strategy regarding their work with their brand and marketing communication. However, there are in both cases factors that, if developed correctly, could help build a stronger brand and better the marketing communication. One of these factors is the clubs’ work with social responsibility. Conclusion There is an importance of creating a strong internal identity in order to be able to position the club and define the offer towards different segments. Through this comes the possibility to create a strong strategy for marketing communication.
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Becher, Alexander [Verfasser]. "The armadillo protein p0071 controls directionality of kinesin-2 driven transport by mediating KIF3 motor complex stability / Alexander Becher." Ulm : Universität Ulm, 2019. http://d-nb.info/1183099479/34.
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Yazid, Zaleha Binti. "Exploring the effects of conflict towards the social dynamics of the self-managed project team (SMPT) in small and medium sized knowledge intensive firms (KIFs)." Thesis, University of Strathclyde, 2012. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=17008.
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This study focuses on exploring the effect of conflict towards the social dynamics of the self-managed project team (SMPT) in small and medium sized knowledgeintensive firms (KIFs). Literature suggests that the implementation of SMPTs not only increases productivity in organisations but also contributes towards increasing employees’ involvement as the team is being managed by the team members rather than a formal leader who exists within the team. The team process involves people in different areas of expertise working together resulting in different opinions and views that are likely to cause conflicts. Thus, it is crucial for organisations to create understanding on the role of conflict and how it is managed within the SMPT in order to ensure the successfulness of this particular type of team. This study contributes to the understanding of how the SMPT is being influenced by different types of conflict and their management strategies as well as the extent of external leader involvement in conflict situations. This longitudinal study comprises of evidence collected through semi-structured interviews involving face-to-face interviews and weekly telephone interviews for twelve weeks with the managements and team members from six SMPTs in three small and medium sized KIFs in Malaysia. The in-depth exploration of conflict occurrences in SMPTs reveals the interrelatedness between different types of conflict as well as different approaches of conflict management strategies being adapted by SMPTs. The evidence suggests that over time, the positioning of external leaders in SMPTs change as a result of how conflict is managed. These empirical findings are developed into proposed models of the transformation of SMPTs.
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Chen, Feng-Tian. "Transport de l'enzyme lysosomale alpha-L-iduronidase dans les prolongements neuronaux." Paris 7, 2005. http://www.theses.fr/2005PA077178.
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Cavallin, Mara. "Physiopathologie moléculaire et cellulaire des anomalies du développement du cortex cérébral : le syndrome d'Aicardi WDR81 mutations cause extreme microcephaly and impair mitotic progression in human fibroblasts and Drosophila neural stem cells TLE1, a key player in neurogenesis, a new candidate gene for autosomal recessive postnatal microcephaly Mutations in TBR1 gene leads to cortical malformations and intellectual disability Aicardi syndrome: Exome, genome and RNA-sequencing of a large cohort of 19 patients failed to detect the genetic cause Recurrent RTTN mutation leading to severe microcephaly, polymicrogyria and growth restriction Recurrent KIF2A mutations are responsible for classic lissencephaly Recurrent KIF5C mutation leading to frontal pachygyria without microcephaly Rare ACTG1 variants in fetal microlissencephaly De novo TUBB2B mutation causes fetal akinesia deformation sequence with microlissencephaly: An unusual presentation of tubulinopathy A novel recurrent LIS1 splice site mutation in classic lissencephaly Further refinement of COL4A1 and COL4A2 related cortical malformations Prenatal and postnatal presentations of corpus callosum agenesis with polymicrogyria caused By EGP5 mutation Delineating FOXG1 syndrome from congenital microcephaly to hyperkinetic encephalopathy Delineating FOXG1 syndrome: From congenital microcephaly to hyperkinetic encephalopathy." Thesis, Sorbonne Paris Cité, 2019. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2213&f=18201.
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Les malformations du cortex cérébral (MDC) représentent une cause importante de handicap et d'épilepsie pharmaco-résistante. Le séquençage à haut débit a permis une amélioration considérable de l'identification des bases moléculaires des MDC non syndromiques. Toutefois, certaines formes, notamment les MDC complexes, demeurent inexpliquées. Mon projet de thèse a pour objectif de progresser dans la compréhension des MDC complexes en utilisant deux modèles : les microlissencéphalies (MLIS) et le syndrome d'Aicardi (AIC), une forme syndromique particulière associant des malformations de l'oeil et du cerveau uniquement rapporté chez les filles. L'étude par séquençage d'exome en trios de 16 familles MLIS m'a permis d'identifier et de caractériser un nouveau gène, WDR81, impliqué dans le cycle cellulaire. Par la même stratégie, j'ai pu identifier un variant homozygote pathogène dans TLE1, un partenaire majeur de FOXG1 dans la balance prolifération/différenciation de progéniteurs neuronaux, dans une famille consanguine de microcéphalie postnatale dont le phénotype est proche du syndrome FOXG1. En parallèle, mes travaux ont permis de préciser les spectres phénotypiques associés à RTTN, EPG5, COL4A1, COL4A2, TBR1, KIF5C, KIF2A et FOXG1. La deuxième partie de mon projet avait pour objet l'identification des bases moléculaires du syndrome d'Aicardi à partir d'une cohorte internationale de 19 patientes. Après avoir exclu un biais d'inactivation du chromosome X et la présence de microremaniements chromosomiques, j'ai réalisé un séquençage d'exome en trio. Aucun variant récurrent n'a été retrouvé dans les séquences codantes. Dans un second temps, j'ai testé une approche combinant les données du séquençage de génome et l'analyse du transcriptome (RNA-Seq) sur fibroblastes, me permettant d'identifier des transcrits dérégulés qui étaient impliqués dans le développement du cerveau et de l'oeil. J'ai comparé les résultats de cette analyse avec ceux de l'analyse du génome dans le but d'identifier des variants dans ces gènes candidats. En conclusion, mon travail de thèse a permis d'améliorer la connaissance des bases moléculaires des MDC complexes et d'ouvrir des perspectives de nouveaux mécanismes tels que ceux engageant les gènes WDR81 et EPG5, et le rôle des endosomes et de l'autophagie dans les MDC, et aussi TLE1 comme nouvelle cause de microcéphalies postnatales. Mes travaux ont également permis de générer une collection de données de séquençage haut débit (WES, WGS et RNA-Seq) qui seront mises en commun dans le cadre d'un consortium international afin de développer des nouvelles stratégies d'analyse en particulier pour les séquences non codantes. Cette approche permettra également d'ouvrir la voie vers la compréhension des mécanismes cellulaires impliqués dans la formation du cerveau et de l' œilMalformations of cortical development (MCD) are a major cause of intellectual disability and drug-resistant epilepsy. Next Generation Sequencing (NGS) has considerably improved the identification of the molecular basis of non-syndromic MCD. However, certain forms, including complex MCD, remain unexplained. My PhD project aimed to improve the understanding of complex MCD using two disorders: Microlissencephaly (MLIS) and Aicardi Syndrome (AIC), the latter associating brain and eye malformations and only reported in girls. Trio Whole Exome Sequencing (WES) performed in 16 MLIS families allowed me to identify and functionally characterize a new MLIS gene, WDR81, in which mutations lead to cell cycle alteration. Moreover, using the same strategy, I was able to identify a pathogenic homozygous variant in TLE1 in a patient from consanguineous family with a postnatal microcephaly, suggestive of a FOXG1-like presentation. Interestingly, TLE1 is a major partner of FOXG1, a gene involved in maintaining the balance between progenitor proliferation and differentiation. In parallel, my work allowed me to redefine the phenotypic spectrum associated with RTTN, EPG5, COL4A1 and COL4A2, TBR1, KIF5C, KIF2A and FOXG1. The second part of my PhD program was aimed at identifying the genetic basis of AIC in an international cohort of 19 patients. After excluding a skewed X chromosome inactivation and the presence of chromosomal rearrangements, I performed WES in trios. The analysis of the data from WES did not allow me to identify any recurrent variants. I therefore tested a new approach combining Whole Genome Sequencing (WGS) and RNA-Sequencing (RNA-Seq) on fibroblast cells. I identified a number of deregulated transcripts implicated in brain and eye development. I compared the results of this analysis with the WGS analysis in order to find variants in these candidate genes. In conclusion, these studies have improved the knowledge of the molecular basis of complex MCD, such as TLE1 in postnatal microcephaly, and revealed the pathogenic mechanisms such as WDR81 in cell cycle progression and EPG5 in endosomes and autophagy. My work has also generated a collection of NGS data (WES, WGS and RNA-Seq) that will be shared in an international consortium to develop new analytical strategies, in particular for the non-coding DNA regions. This novel strategy provides opportunities to improve understanding of the cellular mechanisms involved in brain and eye development
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Röhlk, Christian [Verfasser]. "Characterization of conventional kinesins Kif3 and Kif5 from Dictyostelium discoideum / vorgelegt von Christian Röhlk." 2007. http://d-nb.info/985849983/34.
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Schmidt, Michael. "Regulation of recycling endosomal membrane traffic by a γ-BAR/ kinesin KIF5 complex." Doctoral thesis, 2007. http://hdl.handle.net/11858/00-1735-0000-0006-B375-8.
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Schmidt, Michael [Verfasser]. "Regulation of recycling endosomal membrane traffic by a γ-BAR [gamma-BAR], kinesin KIF5 complex / submitted by Michael Schmidt." 2008. http://d-nb.info/988980355/34.
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Hou, Jen-Tzu, and 侯恁慈. "Ectopic ATP Synthase trafficking via KIF5B and Drp1 interaction." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/75hyss.
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碩士國立臺灣大學
分子與細胞生物學研究所
106
Adenosine triphosphate (ATP) synthase, an inner membrane enzyme of mitochondria, is essential for ATP production in many cell biological processes. Our previous studies have shown that ATP synthases not only existed on mitochondrial inner membrane but also plasma membrane (ectopic ATP synthases) in several cancer cell lines. However, the trafficking mechanism of ATP synthase to cell surface is still required further investigation. According to our previous gene set enrichment analysis (GSEA) results, we inferred ectopic ATP synthases transported to cell surface through the microtubule-mediated mitochondria trafficking. To examine whether this presumption is correct, we conducted flow cytometry and immunocytochemistry (ICC) after treating nocodazole, a microtubule-depolymerizing agent, in cancer cells. The results revealed that microtubule disruption reduced ectopic ATP synthase expression level. In addition, silencing kinesin family member 5B (KIF5B), a microtubule motor protein, with small interfering RNA showed the similar trend with the results of microtubule disruption. On the other hand, we also found that mitochondria dynamic related to ectopic ATP synthase expression. Both flow cytometry and ICC demonstrated that mitochondrial fission protein, dynamic-related protein 1 (Drp1), knockdown and overexpression resulted in low and high ectopic ATP synthase expression respectively. In addition, Drp1 C-terminus was showed more significant than N-terminus in ectopic ATP synthase expression in overexpression experiments. Moreover, we used protein-protein interaction database and docking web server to predict whether KIF5B bound with Drp1 directly. Taken together, these findings suggest that KIF5B-Drp1 complex-mediated mitochondrial trafficking via microtubule may play a crucial role in ectopic ATP synthases transport.
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Hartel, Michaela [Verfasser]. "Molecular cloning and functional studies of Neurospora crassa KIF1, a new member of the UNC-104, KIF1 family of kinesin-like proteins / vorgelegt von Michaela Hartel." 2004. http://d-nb.info/971612161/34.
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Hsu, Shu-Hsuan Claire. "Regulators of Hedgehog Signaling in Chondrocytes: Sufu, Kif7, and Primary Cilium." Thesis, 2012. http://hdl.handle.net/1807/32739.
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The Hedgehog (Hh) signaling pathway has received attention regarding its important role in embryonic development, however the mechanism by which pathway regulators, such as Suppressor of fused (Sufu), Kinesin family member 7 (Kif7), and primary cilium, mediate Hh signaling transduction is not entirely understood. The work presented here examines the roles of Sufu and Kif7 in regulating Hh signaling in growth plate chondrocytes, as well as how they mediate parathyroid hormone-like hormone (Pthlh) signaling during chondrocyte development. I show here that Sufu and Kif7 are essential regulators of Indian hedgehog (Ihh) signaling. While Sufu negatively regulates Gli transcription factors, Kif7 functions both positively and negatively in chondrocytes. Kif7 plays a role in Sufu protein degradation and the exclusion of Sufu-Gli complexes from the primary cilium. Importantly, halving the dosage of Sufu restores normal Hh pathway activity and chondrocyte development in Kif7-null mice, demonstrating that the positive role of Kif7 is to restrict the inhibitory function of Sufu. Furthermore, Kif7 exerts inhibitory function on Gli transcriptional activity in chondrocytes when Sufu function is absent. Therefore, Kif7 regulates the activity of Gli transcription factors through both Sufu-dependent and Sufu-independent mechanisms. I show that Sufu is crucial for mediating the negative effect of Pthlh on Gli transcriptional activity and chondrocyte hypertrophic differentiation, whereas Kif7 and primary cilium are dispensable in this process. Although primary cilium is required for Hh ligand-mediated activation of Gli transcription, Pthlh negatively controls Gli transcriptional activity in a cilia-independent manner. The results of this work provide insight into how Hh signaling is regulated by Sufu and Kif7 in the context of primary cilium, but also suggest Sufu serves as an important link between Ihh and Pthlh signaling during growth plate chondrocyte development.
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Schäfer, Barbara [Verfasser]. "KIF5C, ein neuer Bindungspartner für die Proteinkinase CK2 / vorgelegt von Barbara Schäfer." 2008. http://d-nb.info/996155791/34.
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Chen, Chien-Yu, and 陳芊伃. "KIF9 Recombinant protein fragment is not suitable as a diagnostic autoantibody marker of gynecological diseases." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/94798540411092292385.
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碩士中山醫學大學
生化暨生物科技研究所
99
Gynecological diseases such as adenomyosis, myoma, and endometriosis, although are not diseases with high mortality rates, if the symptoms are too severe, they will not only affect the patients` quality of life, but also result in infertility of the patients. Even after the patients have received treatment, the recurrence rate is still high. Currently, the only available clinical diagnostic examination of these three diseases is the highly invasive procedure-laparoscopy. References reflect the SEREX (Serological identification of antigens by recombinant expression cloning) experimental method, which identifies TAAs by screening the patient`s sera, produces auto-antibodies by the tumorgenesis process. It would be helpful in diagnosis and treatment if we can detect the autoantibodies in the patients` serum as diagnostic or prognosis markers for gynecological diseases. Previously, in our laboratory, it has been found that the use of IMP1 and cyclin B1 autoantibody coordination can aid the detection of endometrioma. The sensitivity and specificity was 83.9% and 72.7%. Because of the above results, we hope to find other specific TAAs to use as autoantiboby diagnostic markers for adenomyosis, myoma and endometriosis. By using ELISA and the Western blot experiment to screen KIF9 autoantiboby, we have found that pET32a vector recombinant protein expressions would produce false positive results by inducing thioredoxin protein influence. Through the usage of pET30a vector instead of pET32a to express KIF9 tumor associated protein, out of 84 patients with gynecological diseases, only 1.2% of tested serum showed positive reactions. This indicates KIF9 recombinant protein fragment is not suitable as a diagnostic autoantibody marker of gynecological diseases.
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Chien-Yu and 陳芊伃. "KIF9 Recombinant protein fragment is not suitable as a diagnostic autoantibody marker of gynecological diseases." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/85875064077801210473.
Full textAbstract:
碩士中山醫學大學
生化暨生物科技研究所
99
Gynecological diseases such as adenomyosis, myoma, and endometriosis, although are not diseases with high mortality rates, if the symptoms are too severe, they will not only affect the patients` quality of life, but also result in infertility of the patients. Even after the patients have received treatment, the recurrence rate is still high. Currently, the only available clinical diagnostic examination of these three diseases is the highly invasive procedure-laparoscopy. References reflect the SEREX (Serological identification of antigens by recombinant expression cloning) experimental method, which identifies TAAs by screening the patient`s sera, produces auto-antibodies by the tumorgenesis process. It would be helpful in diagnosis and treatment if we can detect the autoantibodies in the patients` serum as diagnostic or prognosis markers for gynecological diseases. Previously, in our laboratory, it has been found that the use of IMP1 and cyclin B1 autoantibody coordination can aid the detection of endometrioma. The sensitivity and specificity was 83.9% and 72.7%. Because of the above results, we hope to find other specific TAAs to use as autoantiboby diagnostic markers for adenomyosis, myoma and endometriosis. By using ELISA and the Western blot experiment to screen KIF9 autoantiboby, we have found that pET32a vector recombinant protein expressions would produce false positive results by inducing thioredoxin protein influence. Through the usage of pET30a vector instead of pET32a to express KIF9 tumor associated protein, out of 84 patients with gynecological diseases, only 1.2% of tested serum showed positive reactions. This indicates KIF9 recombinant protein fragment is not suitable as a diagnostic autoantibody marker of gynecological diseases.
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Sye, Ko-Wei, and 謝克威. "Study of the physiological role of KIF3A and KIF5B–using PC12 cell as a model system." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/mm67q3.
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碩士國立陽明大學
生命科學暨基因體科學研究所
97
Kinesins constitute a superfamily of microtubule-based motor proteins. Some of them regulate polarized transport of organelles and proteins in nerve system to result in differential morphology and functions in subcellular regions of neurons. Because nerve growth factor (NGF) induces na��ve PC12 cells to acquire neuronal-like differential morphology and functions among cell body and neurites. Therefore, KIFs seem to play a role in NGF-mediated differentiation of PC12 cells. This study is to understand whether KIF3 and KIF5, which possibly regulate transport calcium pools and vesicles, involves in the effects of NGF on calcium homeostasis and exocytotic activity of PC12 cells. Overexpression of shKIF5B instead of shKIF3A or DN-KIF3A-EGFP reduced NGF-induced neurite outgrowth. NGF-differentiated PC12 cells overexpressing either EGFP as control, or DN-KIF3A or shKIF5B were stimulated by ATP to evoke [Ca2+]i increase, and changes of [Ca2+]i in cell body and neurites of these cells were visualized by calcium imaging. DN-KIF3A and shKIF3A reduced resting [Ca2+]i in cell bodies and neurites of NGF-differentiated PC12 cells, but difference of resting calcium among cell bodies and neurites is not affected, i.e. higher resting [Ca2+]i in neurite than in cell body. To test whether mitochondria may be re-distributed by DN-KIF3A to affect calcium homeostasis in PC12 cells, subcellular distribution of mitochondria was visualized by DsRed-Mito. There is no significant difference between control and DN-KIF3A-overexpressing cells. Moreover, only TG (thapsigargin, ER calcium pump inhibitor) instead of CCCP (carbonyl cyanide m-chlorophenylhydrazone, inhibitor to deplete mitochondrial calcium pool) reduces differential resting [Ca2+]i among neuritis and cell bodies and the effects of DN-KIF3A on resting [Ca2+]i, and support that KIF3A regulates resting [Ca2+]i is not mediated by mitochondria calcium pools. Such reduction of resting [Ca2+]i by shKIF3A results in decreased LDCVs (Large dense core vesicle) exocytosis. Similar to shKIF3A, shKif5B reduces resting calcium level only in NGF-treated cells instead of na��ve cells, even morphology of NGF-treated and na��ve KIF5B knock down cells are similar. In conclusion, KIF3A and KIF5B play a role in calcium homeostasis only in NGF-treated PC12 cells. But the mechanism in how KIFs regulate calcium homeostasis and exocytosis needs to be further studied.
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Liao, Yi-Hua. "Characterization of the biological functions of ARMS (ankyrin repeat-rich membrane spanning) in melanoma tumorigenesis and KIF3-mediated axonal transport and neurite outgrowth." 2007. http://www.cetd.com.tw/ec/thesisdetail.aspx?etdun=U0001-2612200715413500.
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Nedvědová, Jana. "Popis interakcí mezi histondeacetylasou 6 a kinesinem." Master's thesis, 2019. http://www.nusl.cz/ntk/nusl-397037.
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Intracellular transport is provided by two major types of molecular motors kinesins and cytoplasmic dynein. Kinesin-1 is a molecular motor that transports molecules and organelles along microtubule tracks anterogradely. Specific protein-protein interactions are required to activate kinesin-1 as the free kinesin exist in an autoinhibited state. The activation of kinesin-1 induces its conformational change, enables microtubule binding and ATP hydrolysis necessary for the directional cargo transport. HDAC6 is a multifunctional protein composed of several domains. It plays an important role in many microtubule dependent processes as HDAC6 is a major tubulin deacetylase. It has been shown that HDAC6 manipulation (inhibition/genetic ablation) affects transport along microtubules but the exact mechanisms are unknown. The effect can be caused either by deacetylation microtubules or direct interaction with molecular motors. This thesis is focused on characterization of interactions between kinesin-1 and HDAC6 that have not been described so far. To this end, we expressed and purified various constructs of kinesin-1 and HDAC6 and tested their interactions by microscale thermophoresis (MST) and hydrogen deuterium exchange (HDX) to determine affinity and interaction sites, respectively. MST data revealed that...