Relevant bibliographies by topics / KIF5A

Academic literature on the topic 'KIF5A'

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Published: 11 September 2023

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Journal articles on the topic "KIF5A"

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Rahman, Amena, Adeela Kamal, Elizabeth A. Roberts, and Lawrence S. B. Goldstein. "Defective Kinesin Heavy Chain Behavior in Mouse Kinesin Light Chain Mutants." Journal of Cell Biology 146, no. 6 (September 20, 1999): 1277–88. http://dx.doi.org/10.1083/jcb.146.6.1277.

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Conventional kinesin, kinesin-I, is a heterotetramer of two kinesin heavy chain (KHC) subunits (KIF5A, KIF5B, or KIF5C) and two kinesin light chain (KLC) subunits. While KHC contains the motor activity, the role of KLC remains unknown. It has been suggested that KLC is involved in either modulation of KHC activity or in cargo binding. Previously, we characterized KLC genes in mouse (Rahman, A., D.S. Friedman, and L.S. Goldstein. 1998. J. Biol. Chem. 273:15395–15403). Of the two characterized gene products, KLC1 was predominant in neuronal tissues, whereas KLC2 showed a more ubiquitous pattern of expression. To define the in vivo role of KLC, we generated KLC1 gene-targeted mice. Removal of functional KLC1 resulted in significantly smaller mutant mice that also exhibited pronounced motor disabilities. Biochemical analyses demonstrated that KLC1 mutant mice have a pool of KIF5A not associated with any known KLC subunit. Immunofluorescence studies of sensory and motor neuron cell bodies in KLC1 mutants revealed that KIF5A colocalized aberrantly with the peripheral cis-Golgi marker giantin in mutant cells. Striking changes and aberrant colocalization were also observed in the intracellular distribution of KIF5B and β′-COP, a component of COP1 coatomer. Taken together, these data best support models that suggest that KLC1 is essential for proper KHC activation or targeting.
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Kanai, Yoshimitsu, Yasushi Okada, Yousuke Tanaka, and Nobutaka Hirokawa. "605 Localization of kinesin heavy chains (KIF5A, KIF5B, KIF5C) in nervous system." Neuroscience Research 28 (January 1997): S84. http://dx.doi.org/10.1016/s0168-0102(97)90217-0.

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Tian, Da-Wei, Zhou-Liang Wu, Li-Ming Jiang, Jie Gao, Chang-Li Wu, and Hai-Long Hu. "KIF5A Promotes Bladder Cancer Proliferation In Vitro and In Vivo." Disease Markers 2019 (July 3, 2019): 1–9. http://dx.doi.org/10.1155/2019/4824902.

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Background. Bladder cancer is a common malignancy with uncontrolled and rapid growth. Although lots of the important regulatory networks in bladder cancer have been found, the cancer-relevant genes remain to be further identified. Methods. We examined the KIF5A expression levels in bladder cancer and normal bladder tissue samples via immunohistochemistry and observed the effect of KIF5A on bladder tumor cell proliferation in vitro and in vivo. Additionally, a coexpression between KIF5A and KIF20B in tumor tissues was explored. Results. KIF5A expression level was higher in the bladder cancer tissues than in the adjacent nontumor tissues. Patients with higher KIF5A expression displayed advanced clinical features and shorter survival time than those with lower KIF5A expression. Moreover, KIF5A knockdown inhibited bladder cancer cell proliferation, migration, and invasion demonstrated in vivo and in vitro. In addition, coexpression was found between KIF5A and KIF20B in tumor tissues. Conclusion. The results demonstrated that KIF5A is a critical regulator in bladder cancer development and progression, as well as a potential target in the treatment of bladder cancer.
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Hares, Kelly, Scott Miners, Neil Scolding, Seth Love, and Alastair Wilkins. "KIF5A and KLC1 expression in Alzheimer’s disease: relationship and genetic influences." AMRC Open Research 1 (June 26, 2019): 1. http://dx.doi.org/10.12688/amrcopenres.12861.2.

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Background: Early disturbances in axonal transport, before the onset of gross neuropathology, occur in a spectrum of neurodegenerative diseases including Alzheimer’s disease. Kinesin superfamily motor proteins (KIFs) are responsible for anterograde protein transport within the axon of various cellular cargoes, including synaptic and structural proteins. Dysregulated KIF expression has been associated with AD pathology and genetic polymorphisms within kinesin-light chain-1 (KLC1) have been linked to AD susceptibility. We examined the expression of KLC1 in AD, in relation to that of the KLC1 motor complex (KIF5A) and to susceptibility genotypes. Methods: We analysed KLC1 and KIF5A gene and protein expression in midfrontal cortex from 47 AD and 39 control brains. Results: We found that gene expression of both KIF5A and KLC1 increased with Braak tangle stage (0-II vs III-IV and V-VI) but was not associated with significant change at the protein level. We found no effect of KLC1 SNPs on KIF5A or KLC1 expression but KIF5A SNPs that had previously been linked to susceptibility in multiple sclerosis were associated with reduced KIF5A mRNA expression in AD cortex. Conclusions: Future in vitro and in vivo studies are required to understand the cause of upregulated KIF5A and KLC-1 gene expression in AD and any potential downstream consequences on pathogenesis, including any contribution of genetic polymorphisms within the KIF5A gene locus.
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Hares, Kelly, Scott Miners, Neil Scolding, Seth Love, and Alastair Wilkins. "KIF5A and KLC1 expression in Alzheimer’s disease: relationship and genetic influences." AMRC Open Research 1 (February 19, 2019): 1. http://dx.doi.org/10.12688/amrcopenres.12861.1.

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Background: Early disturbances in axonal transport, before the onset of gross neuropathology, occur in a spectrum of neurodegenerative diseases including Alzheimer’s disease. Kinesin superfamily motor proteins (KIFs) are responsible for anterograde protein transport within the axon of various cellular cargoes, including synaptic and structural proteins. Dysregulated KIF expression has been associated with AD pathology and genetic polymorphisms within kinesin-light chain-1 (KLC1) have been linked to AD susceptibility. We examined the expression of KLC1 in AD, in relation to that of the KLC1 motor complex (KIF5A) and to susceptibility genotypes. Methods: We analysed KLC1 and KIF5A gene and protein expression in midfrontal cortex from 47 AD and 39 control brains. Results: We found that gene expression of both KIF5A and KLC1 increased with Braak tangle stage (0-II vs III-IV and V-VI) but was not associated with significant change at the protein level. We found no effect of KLC1 SNPs on KIF5A or KLC1 expression but KIF5A SNPs that had previously been linked to susceptibility in multiple sclerosis were associated with reduced KIF5A mRNA expression in AD cortex. Conclusions: The findings raise the possibility that genetic polymorphisms within the KIF5A gene locus could contribute to disturbances of axonal transport, neuronal connectivity and function across a spectrum of neurological conditions, including AD.
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Hares, Kelly, K. Kemp, S. Loveless, C. M. Rice, N. Scolding, E. Tallantyre, N. Robertson, and A. Wilkins. "KIF5A and the contribution of susceptibility genotypes as a predictive biomarker for multiple sclerosis." Journal of Neurology 268, no. 6 (January 23, 2021): 2175–84. http://dx.doi.org/10.1007/s00415-020-10373-w.

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AbstractThere is increasing interest in the development of multiple sclerosis (MS) biomarkers that reflect central nervous system tissue injury to determine prognosis. We aimed to assess the prognostic value of kinesin superfamily motor protein KIF5A in MS by measuring levels of KIF5A in cerebrospinal fluid (CSF) combined with analysis of single nucleotide polymorphisms (SNPs; rs12368653 and rs703842) located within a MS susceptibility gene locus at chromosome 12q13–14 region. Enzyme-linked immunosorbent assay was used to measure KIF5A in CSF obtained from two independent biobanks comprising non-inflammatory neurological disease controls (NINDC), clinically isolated syndrome (CIS) and MS cases. CSF KIF5A expression was significantly elevated in progressive MS cases compared with NINDCs, CIS and relapsing–remitting MS (RRMS). In addition, levels of KIF5A positively correlated with change in MS disease severity scores (EDSS, MSSS and ARMSSS), in RRMS patients who had documented disease progression at 2-year clinical follow-up. Copies of adenine risk alleles (AG/AA; rs12368653 and rs703842) corresponded with a higher proportion of individuals in relapse at the time of lumbar puncture (LP), higher use of disease-modifying therapies post LP and shorter MS duration. Our study suggests that CSF KIF5A has potential as a predictive biomarker in MS and further studies into the potential prognostic value of analysing MS susceptibility SNPs should be considered.
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Mahase, Vidhyanand, Adebiyi Sobitan, Christina Johnson, Farion Cooper, Yixin Xie, Lin Li, and Shaolei Teng. "Computational analysis of hereditary spastic paraplegia mutations in the kinesin motor domains of KIF1A and KIF5A." Journal of Theoretical and Computational Chemistry 19, no. 06 (August 5, 2020): 2041003. http://dx.doi.org/10.1142/s0219633620410035.

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Hereditary spastic paraplegias (HSPs) are a genetically heterogeneous collection of neurodegenerative disorders categorized by progressive lower-limb spasticity and frailty. The complex HSP forms are characterized by various neurological features including progressive spastic weakness, urinary sphincter dysfunction, extra pyramidal signs and intellectual disability (ID). The kinesin superfamily proteins (KIFs) are microtubule-dependent molecular motors involved in intracellular transport. Kinesins directionally transport membrane vesicles, protein complexes, and mRNAs along neurites, thus playing important roles in neuronal development and function. Recent genetic studies have identified kinesin mutations in patients with HSPs. In this study, we used the computational approaches to investigate the 40 missense mutations associated with HSP and ID in KIF1A and KIF5A. We performed homology modeling to construct the structures of kinesin–microtubule binding domain and kinesin–tubulin complex. We applied structure-based energy calculation methods to determine the effects of missense mutations on protein stability and protein–protein interaction. The results revealed that the most of disease-causing mutations could change the folding free energy of kinesin motor domain and the binding free energy of kinesin–tubulin complex. We found that E253K associated with ID in KIF1A decrease the protein stability of kinesin motor domains. We showed that the HSP mutations located in kinesin–tubulin complex interface, such as K253N and R280C in KIF5A, can destabilize the kinesin–tubulin complex. The computational analysis provides useful information for understanding the roles of kinesin mutations in the development of ID and HSPs.
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KALCHISHKOVA, NIKOLINA, and KONRAD J. BÖHM. "ON THE RELEVANCE OF THE CORE HELIX ALPHA 6 TO KINESIN ACTIVITY GENERATION." Biophysical Reviews and Letters 04, no. 01n02 (April 2009): 63–75. http://dx.doi.org/10.1142/s1793048009000934.

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KIF5A and Eg5 are plus-end directed motor proteins with conserved motor domains. The catalytic cores of both motors comprise a central β-sheet consisting of eight β-strands surrounded by six α-helices. Notwithstanding the high level of similarity in their structural organization, Eg5 moves significantly slower than KIF5A. Recently, we reported that neck linker and neck elements of KIF5A and Eg5 contribute to velocity regulation. As the neck linker of both motors is known to be connected to the catalytic core via helix α6, the question arises if also helix α6 and strand β8 as the last core elements might be involved in velocity regulation. To elucidate the role these structures in kinesin activity generation we constructed KIF5A- and Eg5-based chimeras in which the β8 strand, helix α6, the neck linker, and the neck were interchanged. Additionally, we studied the role of α6 and β8 in ATP hydrolysis and microtubule binding by expression of truncated KIF5A and Eg5 constructs lacking both strand β8 and helix α6, or α6 only. The results obtained suggest that strand β8 and helix α6 are not involved in microtubule-binding, but α6 is an obligate and kinesin type-specific structure required to generate ATPase activity.
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Filosto, Massimiliano, Stefano Piccinelli, Ilaria Palmieri, Nicola Necchini, Marialuisa Valente, Isabella Zanella, Giorgio Biasiotto, Diego Lorenzo, Cristina Cereda, and Alessandro Padovani. "A Novel Mutation in the Stalk Domain of KIF5A Causes a Slowly Progressive Atypical Motor Syndrome." Journal of Clinical Medicine 8, no. 1 (December 22, 2018): 17. http://dx.doi.org/10.3390/jcm8010017.

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KIF5A encodes the heavy chain A of kinesin; A motor protein involved in motility functions within neuron. Mutations in the KIF5A N-terminal motor domain are known to cause SPG10; An autosomal dominant hereditary spastic paraplegia (HSP), as well as rare Charcot-Marie-Tooth disease 2 (CMT2) cases. Recently C-terminal cargo-binding tail domain mutations have been associated with an amyotrophic lateral sclerosis (ALS) phenotype. Here we describe a subject presenting with an atypical slowly progressive motor syndrome evolving over a period of 4 years; Characterized by walking difficulties; Muscle hypotrophy mainly involving upper limbs and pyramidal signs confined to the lower limbs. Electromyography demonstrated chronic neurogenic damage and active denervation while electroneurography showed slowly worsening axonal damage. We identified the novel heterozygote variant c.2341A>G in the exon 21 of the KIF5A gene resulting in the amino acid change p.Lys781Glu. The residue Lys781 is located within the terminal region of the stalk domain and is highly evolutionary conserved. Our findings confirm that mutations in KIF5A cause ALS-like phenotypes. However, the stalk domain mutation described here appears to result in an “intermediate” slowly progressive phenotype having aspects resembling ALS as well as HSP and axonal neuropathy. We suggest that KIF5A gene should be considered as a candidate gene in all atypical progressive motor syndromes.
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Nakajima, Kazuo, Xiling Yin, Yosuke Takei, Dae-Hyun Seog, Noriko Homma, and Nobutaka Hirokawa. "Molecular Motor KIF5A Is Essential for GABAA Receptor Transport, and KIF5A Deletion Causes Epilepsy." Neuron 76, no. 5 (December 2012): 945–61. http://dx.doi.org/10.1016/j.neuron.2012.10.012.

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Dissertations / Theses on the topic "KIF5A"

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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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Biochemistry
Doctoral
Doctor of Philosophy
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2

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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D'Amico, Eva. "Etude des effets de l'inactivation de Kif3a dans les cellules thyroïdiennes." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209643.

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Afin d’assurer les échanges entre ses différents organites, la cellule eucaryote dispose d’un système ingénieux de trafic vésiculaire intracellulaire. Le transport directionnel de divers cargos tels que des organites membranaires et des complexes protéiques est assuré par des moteurs moléculaires auxquels appartiennent les protéines de la superfamille des kinésines (également appelées KIF pour KInesin Family). Celles-ci se servent des microtubules comme rails et se déplacent vers leur extrémité positive. Parmi elles, la kinésine II est composée de KIF3A et KIF3B, deux protéines motrices et de KAP3, une protéine de liaison au cargo à véhiculer. Ce moteur moléculaire est connu pour participer à l’assemblage du cil primaire à la surface des cellules ainsi qu’au trafic plus conventionnel tel que l’acheminement de protéines à la membrane.

Afin d’étudier le rôle précis de la kinésine II dans la glande thyroïde, nous avons invalidé spécifiquement le gène Kif3a dans cet organe chez la souris. Bien que cette inactivation ait conduit à un développement complet du tissu thyroïdien, les souris invalidées présentent une hypothyroïdie congénitale caractérisée par des concentrations sériques élevées de TSH et basses de T4. Par la suite, nous avons mis en évidence une expression fortement diminuée du transporteur d’iodure NIS chez ces souris, causant une déficience en iodure intracellulaire, une iodation insuffisante de la thyroglobuline et une sécrétion anormale de l’hormone T4 dans la circulation sanguine. De plus, ex vivo, nous avons montré que la réponse à la TSH en terme d’AMPc est altérée dans la thyroïde de ces souris. Ces observations nous ont permis d’émettre l’hypothèse que l’invalidation du gène Kif3a spécifiquement dans la glande thyroïde mène à une anomalie dans la voie de signalisation du récepteur de la TSH, en amont de la production d’AMPc. Finalement, in vitro, par l’utilisation de cellules Kif3a-/-, nous avons analysé l’expression à la membrane plasmique et la réponse à un agoniste du récepteur β2 adrénergique, un membre de la même sous-famille de récepteurs couplés aux protéines G que le récepteur de la TSH. De cette façon, nous avons obtenu des données indiquant que le transport de ce récepteur à la surface cellulaire était altéré en l’absence de Kif3a.

Au vu de ces éléments et de ceux de la littérature, nous suggérons que la kinésine II, et plus particulièrement sa sous-unité KIF3A, joue un rôle important dans le transport du récepteur de la TSH nouvellement synthétisé vers la membrane basale de la cellule de la thyroïde.


Doctorat en Sciences
info:eu-repo/semantics/nonPublished

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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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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.
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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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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.
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Biochemistry
Master
Master of Medical Sciences
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Millington, Grethel. "Primary Cilia-dependent Gli Processing in Neural Crest Cells is Required for Early Tongue Development." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1479815997983138.

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Books on the topic "KIF5A"

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Gerdzhikova, Ina. Plazhnii︠a︡t dnevnik na edna kifla. Plovdiv: Khermes, 2011.

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Boyle, Lia. A Precision Medicine Approach to Understanding KIF1A Associated Neurological Disorder. [New York, N.Y.?]: [publisher not identified], 2021.

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Pravoslavnyĭ Svi͡ato-Tikhonovskiĭ gumanitarnyĭ universitet (Moscow, Russia), ed. Kifa: Patriarshiĭ mestobli︠u︡stitelʹ svi︠a︡shchennomuchenik Petr, mitropolit Krutit︠s︡kiĭ (1862-1937). Moskva: Pravoslavnyĭ Svi︠a︡to-Tikhonovskiĭ gumanitarnyĭ universitet, 2012.

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Böhlke, Christopher. Kif3a guides microtubular dynamics, migration and lumen formation of MDCK cells. Freiburg: Universität, 2013.

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Hu, Daniel Jun-Kit. Roles for Cytoplasmic Dynein and the Unconventional Kinesin, KIF1a, during Cortical Development. [New York, N.Y.?]: [publisher not identified], 2015.

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Laborie, Jean Paul. L' urbanisation de la Mauritanie: Enquête dans trois villes secondaires, Rosso, Kiffa et Aioun-el-Atrouss. Paris: Documentation française, 1988.

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Leloup, Roger. Exiles of Kifa. CineBook, 2022.

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Leloup, Roger. Yoko Tsuno, tome 18 : Les exilés de Kifa. Dupuis, 1991.

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Parker, Philip M. The 2006 Economic and Product Market Databook for Kiffa, Mauritania. ICON Group International, Inc., 2006.

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The 2005 Economic and Product Market Databook for Kiffa, Mauritania. Icon Group International, Inc., 2005.

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Book chapters on the topic "KIF5A"

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Rao, Lu, and Arne Gennerich. "Single-Molecule Studies on the Motion and Force Generation of the Kinesin-3 Motor KIF1A." In Optical Tweezers, 585–608. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2229-2_21.

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Chana, Mundeep S., Brian P. Tripet, and Robert S. Hodges. "The Role of Unstructured Highly Charged Regions on the Stability and Specificity of Dimerization of Two-Stranded α-Helical Coiled-Coils: Neck Region of Kinesin-Like Motor Protein Kif3A." In Peptides: The Wave of the Future, 359–60. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0464-0_165.

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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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Panicker, Saurav, and Satish Ramalingam. "Chromosome 10." In Cancer Genes, 307–43. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815080292123010013.

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Chromosome 10 contains various genes that are significantly involved in tumorigenesis. These genes described herein that play roles in cancer comprise receptor tyrosine kinases (FGFR2), proto-oncogenes (FRAT1, RET), tumor suppressor genes (PTEN, KLF6), and also genes involved in signal transduction (MAPK8), gene fusions (CCDC6, KIF5B, VTI1A), developmental processes (GATA3, NODAL), Epithelial- Mesenchymal transition (ZEB1, VIM) and epigenetic regulation (MLLT10). This chapter provides a compilation of many such genes from Chromosome 10 that are associated with cancer, with vivid delineations of the underlying molecular mechanisms of each gene in its contribution to cancer initiation, progression and metastasis. Genes that are insufficiently investigated but implicated in tumorigenesis have also been described in this chapter.
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Dolley, Shawn, Dan Hartman, Thea Norman, and Ian Hudson. "Wasifu wa Sera Lengwa." In DAC Trials. The Global Health Network, 2021. http://dx.doi.org/10.48060/tghn.15.

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Wakati mwingi, lengo la mwisho la utafiti wa kliniki ni mabadiliko ya sera, lakini mara nyingi kuna pengo kati ya utafiti na pande za sera inayoweza kusababisha kupotezwa kwa fedha na wakati. Kushughulikia haya, kifaa kipya kinachojulikana kama Wasifu wa Sera Lengwa (TPoP) kinaweza kutumika kabla ya kuanza kwa utafiti ili kutambua maswali muhimu ya utafiti, kusaidia maamuzi ya sera au kutumika wakati wa uzalishaji wa ushahidi na usambazaji wake. Wasifu wa Sera Lengwa linasaidia watafiti kuchambua ushahidi uliopo katika sera husika, pengo katika ushahidi huo na asili ya ushahidi utakikanao kujaza haya mapengo. Zaidi ya hayo, inawezesha mazungumzo ya mapema na ya kuendelea baina ya watafiti na wadau. Wakiwa wamejihami na maarifa haya pamoja na mahusiano haya, watafiti wa kliniki huongeza uwezekano waa masomo husika kukidhi mahitaji ili kutengeneza sera bora kwa njia inayofaa.
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Conference papers on the topic "KIF5A"

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Albuquerque Filho, José Marcos Vieira de, Natália Merten Athayde, Alzira Alves de Siqueira Carvalho, Igor Braga Farias, Roberta Ismael Lacerda Machado, and Marco Antônio Troccoli Chieia. "Familial ALS Type 25 – A Brazillian Case Serie." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.186.

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Introduction: Familial Amyotrophic Lateral Sclerosis (fALS) represent 5-10% of ALS patients. Different mutations in the N-terminal motor or coiled-coil domains of the kinesin family member 5A (KIF5A) cause Hereditary Spastic Paraplegia Type 10 (HSP10), Charcot-Marie-Tooth 2 (CMT2), Neonatal Intractable Myoclonus and more recently described fALS Type 25. Previous described phenotypes are very similar to the sporadic type, except from the long course of disease. Methods: We describe four Brazillian patients, under clinical follow-up on two Neuromuscular services with genetic diagnosis of fALS25. Results: Four diferent fALS25 are described. Two brothers and two unrelated patients, with distinct features, three males and one female, age range from 72 to 24; age of onset ranged from 62 to 22. The genetic mutations were the following: simple heterozygous pathogenic variant c.1651C>G (p. Leu551Val), simple heterozygous pathogenic variant c.2953G>A (p. Gly985Ser) and pathogenic variant c.484C>T (p.Arg162Trp); all of KIF5A gene (fALS25). Only one patient presented with similar phenoptype and age of onset as sporadic ALS (sALS), the two brothers presented the symptoms at the ages of 28 and 30, the female patient at 22. All patients still walk without assistence after the diagnosis. All patients showed classic superior and inferior motor neuron involvement signs, but one brother had a mild limb ataxia. The three younger patients had MRI with no specific findings, except from subtle cortical atrophy in one brother, and mild vermis and corpus callosum atrophy on the other brother. Only the female patient had negative familiar history. Conclusions: fALS25 should be suspected in patient with fALS and longer course disease. Mutations KIF5A gene must be remembered either in juvenile form of ALS.
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Dulski, Jaroslaw, Audrey Strongosky, Rana Hanna Al-Shaikh, and Zbigniew Wszolek. "A large kindred with familial ALS due to the KIF5A p.Arg1007Lys mutation (P10-8.004)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000203881.

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Brent, Jonathan, Oliver Sterling-Angus, and Han-Xiang Deng. "ALS Causative Mutations in KIF5A Disrupt Autoinhibition Leading to Toxic Gain of Function (P8-8.002)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000203062.

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Mizuta, C., S. Nakagawa, K. Hiramatsu, A. Miyoshi, E. Kobayashi, T. Kimura, Y. Ueda, and T. Kimura. "379 Downregulating KIF4A significantly suppressed growth of uterine leiomyosarcoma." In ESGO 2021 Congress. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/ijgc-2021-esgo.263.

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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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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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Kim, Minsuh, Yong-Ah Suh, Ju-hee Oh, Bo Ra Lee, Joon Kim, and Se Jin Jang. "Abstract 1176: The role of KIF3A in the suppression of canonical Wnt signaling through the KIF3A and β-arrestin complex, independent of the ciliary mechanism, in non-small cell lung cancer (NSCLC)." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1176.

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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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Huang, Qingling, Valentina E. Schneeberger, Noreen Luetteke, Chengliu Jin, Domenico Coppola, and Jie Wu. "Abstract 2299: Generation and characterization of inducible KIF5B-RET mouse model of non-small cell lung cancer." 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.am2015-2299.

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Hoang-Minh, Lan, Dorit Siebzehnrubl, Loic Deleyrolle, George Ugartemendia, Hunter Futch, Benjamin Griffith, Joshua Breunig, Susan Semple-Rowland, Brent Reynolds, and Matthew Sarkisian. "Abstract 1542: Targeting KIF3a and primary cilia differentially affects sonic hedgehog sensitivity and the rate of glioblastoma progression." 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.am2015-1542.

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