Kinesin-like protein KIF1C is a protein that in humans is encoded by the KIF1Cgene.[5][6]
Kif1C is a fast, plus-end directed microtubule motor.[7] It takes processive 8nm steps along microtubules and can generate forces of up to 5 pN.[8] Kif1C transports α5β1-integrins in human cells.[9] Kif1C has been shown to be non-essential in mouse with other proteins able to perform the same function.[10] However, mutations in KIF1C lead to spastic paraplegia and cerebellar dysfunction in humans.[11][12][13][14] These mutations usually result in a total loss of the protein or (partial) loss of function, such as significant lower force output.[15]
KIF1C has been shown to interact with PTPN21[5] and YWHAG.[16] KIF1C is a dimeric molecule that is held in an autoinhibited state by interaction of its stalk with the microtubule binding interface of the motor domain. Upon binding of PTPN21 or the cargo adapter HOOK3 to the KIF1C stalk, the motor domain is released, engages with microtubules and commences transport.[17]
^Rogers KR, Weiss S, Crevel I, Brophy PJ, Geeves M, Cross R (September 2001). "KIF1D is a fast non-processive kinesin that demonstrates novel K-loop-dependent mechanochemistry". The EMBO Journal. 20 (18): 5101–13. doi:10.1093/emboj/20.18.5101. PMC125638. PMID11566875.5101-13&rft.date=2001-09&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC125638#id-name=PMC&rft_id=info:pmid/11566875&rft_id=info:doi/10.1093/emboj/20.18.5101&rft.aulast=Rogers&rft.aufirst=KR&rft.au=Weiss, S&rft.au=Crevel, I&rft.au=Brophy, PJ&rft.au=Geeves, M&rft.au=Cross, R&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC125638&rfr_id=info:sid/en.wikipedia.org:KIF1C" class="Z3988">
^Caballero Oteyza A, Battaloğlu E, Ocek L, Lindig T, Reichbauer J, Rebelo AP, et al. (June 2014). "Motor protein mutations cause a new form of hereditary spastic paraplegia". Neurology. 82 (22): 2007–16. doi:10.1212/WNL.0000000000000479. PMC4105256. PMID24808017.2007-16&rft.date=2014-06&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4105256#id-name=PMC&rft_id=info:pmid/24808017&rft_id=info:doi/10.1212/WNL.0000000000000479&rft.aulast=Caballero Oteyza&rft.aufirst=A&rft.au=Battaloğlu, E&rft.au=Ocek, L&rft.au=Lindig, T&rft.au=Reichbauer, J&rft.au=Rebelo, AP&rft.au=Gonzalez, MA&rft.au=Zorlu, Y&rft.au=Ozes, B&rft.au=Timmann, D&rft.au=Bender, B&rft.au=Woehlke, G&rft.au=Züchner, S&rft.au=Schöls, L&rft.au=Schüle, R&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4105256&rfr_id=info:sid/en.wikipedia.org:KIF1C" class="Z3988">
^Dor T, Cinnamon Y, Raymond L, Shaag A, Bouslam N, Bouhouche A, et al. (February 2014). "KIF1C mutations in two families with hereditary spastic paraparesis and cerebellar dysfunction". Journal of Medical Genetics. 51 (2): 137–42. doi:10.1136/jmedgenet-2013-102012. PMID24319291. S2CID24214406.137-42&rft.date=2014-02&rft_id=https://api.semanticscholar.org/CorpusID:24214406#id-name=S2CID&rft_id=info:pmid/24319291&rft_id=info:doi/10.1136/jmedgenet-2013-102012&rft.aulast=Dor&rft.aufirst=T&rft.au=Cinnamon, Y&rft.au=Raymond, L&rft.au=Shaag, A&rft.au=Bouslam, N&rft.au=Bouhouche, A&rft.au=Gaussen, M&rft.au=Meyer, V&rft.au=Durr, A&rft.au=Brice, A&rft.au=Benomar, A&rft.au=Stevanin, G&rft.au=Schuelke, M&rft.au=Edvardson, S&rfr_id=info:sid/en.wikipedia.org:KIF1C" class="Z3988">
^Yücel-Yılmaz D, Yücesan E, Yalnızoğlu D, Oğuz KK, Sağıroğlu MŞ, Özbek U, et al. (June 2018). "Clinical phenotype of hereditary spastic paraplegia due to KIF1C gene mutations across life span". Brain & Development. 40 (6): 458–464. doi:10.1016/j.braindev.2018.02.013. PMID29544888. S2CID3892411.458-464&rft.date=2018-06&rft_id=https://api.semanticscholar.org/CorpusID:3892411#id-name=S2CID&rft_id=info:pmid/29544888&rft_id=info:doi/10.1016/j.braindev.2018.02.013&rft.aulast=Yücel-Yılmaz&rft.aufirst=D&rft.au=Yücesan, E&rft.au=Yalnızoğlu, D&rft.au=Oğuz, KK&rft.au=Sağıroğlu, MŞ&rft.au=Özbek, U&rft.au=Serdaroğlu, E&rft.au=Bilgiç, B&rft.au=Erdem, S&rft.au=İşeri, SA&rft.au=Hanağası, H&rft.au=Gürvit, H&rft.au=Özgül, RK&rft.au=Dursun, A&rfr_id=info:sid/en.wikipedia.org:KIF1C" class="Z3988">
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