ArticleMolecular and cellular biology2002
Molecular motor KIF1C is not essential for mouse survival and motor-dependent retrograde Golgi apparatus-to-endoplasmic reticulum transport.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 29 citations in OpenAlex.
- The Long Haul: Microtubule Motors as the Essential Supply Line for Neuronal Longevity.Journal of neurochemistry · 2026Review
- Kinesins in Mammalian Spermatogenesis and Germ Cell Transport.Frontiers in cell and developmental biology · 2022Review
- Going Too Far Is the Same as Falling ShortFrontiers in cellular neuroscience · 2019Review
- KIF1C Variants Are Associated with Hypomyelination, Ataxia, Tremor, and Dystonia in Fraternal Twins.Tremor and other hyperkinetic movements (New York, N.Y.) · 2019Article
- Progressive ataxia of Charolais cattle highlights a role of KIF1C in sustainable myelination.PLoS genetics · 2018Article
- Rab6 regulation of the kinesin family KIF1C motor domain contributes to Golgi tethering.eLife · 2015Article
- Modular organization of the mammalian Golgi apparatus.Current opinion in cell biology · 2012Review
- Identification of Orch3, a locus controlling dominant resistance to autoimmune orchitis, as kinesin family member 1C.PLoS genetics · 2012Article
- Expression of kinesin superfamily genes in cultured hippocampal neurons.Cytoskeleton (Hoboken, N.J.) · 2010Article
- The kinesin KIF1C and microtubule plus ends regulate podosome dynamics in macrophages.Molecular biology of the cell · 2006Article
- Fast anterograde transport of herpes simplex virus: role for the amyloid precursor protein of alzheimer's disease.Aging cell · 2003Article
- Kinesin superfamily proteins (KIFs) in the mouse transcriptome.Genome research · 2003Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
KIF1C is a new member of the kinesin superfamily of proteins (KIFs), which act as microtubule-based molecular motors involved in intracellular transport. We cloned full-length mouse kif1C cDNA, which turned out to have a high homology to a mitochondrial motor KIF1Balpha and to be expressed ubiquitously. To investigate the in vivo significance of KIF1C, we generated kif1C(-/-) mice by knocking in the beta-galactosidase gene into the motor domain of kif1C gene. On staining of LacZ, we detected its expression in the heart, liver, hippocampus, and cerebellum. Unexpectedly, kif1C(-/-) mice were viable and showed no obvious abnormalities. Because immunocytochemistry showed partial colocalization of KIF1C with the Golgi marker protein, we compared the organelle distribution in primary lung fibroblasts from kif1C(+/+) and kif1C(-/-) mice. We found that there was no significant difference in the distribution of the Golgi apparatus or in the transport from the Golgi apparatus to the endoplasmic reticulum (ER) facilitated by brefeldin A between the two cells. This retrograde membrane transport was further confirmed to be normal by time-lapse analysis. Consequently, KIF1C is dispensable for the motor-dependent retrograde transport from the Golgi apparatus to the ER.
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