Role of the PAR-3-KIF3 complex in the establishment of neuronal polarity.
Abstract
Neurons polarize to form elaborate multiple dendrites and one long axon. The establishment and maintenance of axon/dendrite polarity are fundamentally important for neurons. Recent studies have demonstrated that the polarity complex PAR-3-PAR-6-atypical protein kinase C (aPKC) is involved in polarity determination in many tissues and cells. The function of the PAR-3-PAR-6-aPKC protein complex depends on its subcellular localization in polarized cells. PAR-3 accumulates at the tip of growing axons in cultured rat hippocampal neurons, but the molecular mechanism of this localization remains unknown. Here we identify a direct interaction between PAR-3 and KIF3A, a plus-end-directed microtubule motor protein, and show that aPKC can associate with KIF3A through its interaction with PAR-3. The expression of dominant-negative PAR-3 and KIF3A fragments that disrupt PAR-3-KIF3A binding inhibited the accumulation of PAR-3 and aPKC at the tip of the neurites and abolished neuronal polarity. These results suggest that PAR-3 is transported to the distal tip of the axon by KIF3A and that the proper localization of PAR-3 is required to establish neuronal polarity.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The asymmetric distribution of Par3 is crucial for the polarization of neurons.
“The asymmetric distribution of Par3 is crucial for the polarization of neurons (Nishimura et al., 2004; Shi et al., 2003).”
From Rassf5 and Ndr kinases act in a novel pathway regulating neuronal polarity through Par3 phosphorylation (2014) · cites this paper as Nishimura et al., 2004
Disruption of Par3 localization by interfering with the kinesin-2-dependent transport of Par3 causes polarity defects in hippocampal neurons, showing that the restricted localization of Par3 to the axon is essential for neuronal polarity.
“Disruption of Par3 localization by interfering with the kinesin-2-dependent transport of Par3 causes polarity defects in hippocampal neurons, showing that the restricted localization of Par3 to the axon is essential for neuronal polarity (Funahashi et al., 2013; Nishimura et al., 2004).”
From Rassf5 and Ndr kinases act in a novel pathway regulating neuronal polarity through Par3 phosphorylation (2014) · cites this paper as Nishimura et al., 2004
In stage 2 neurons, Par3 is present in all neurites but becomes restricted to the axon upon its formation at stage 3.
“In stage 2 neurons, Par3 is present in all neurites but becomes restricted to the axon upon its formation at stage 3.”
From Rassf5 and Ndr kinases act in a novel pathway regulating neuronal polarity through Par3 phosphorylation (2014) · cites this paper as Nishimura et al., 2004
A uniform distribution after overexpression of Par3 or a block of its KIF3A-dependent anterograde transport into the axon disrupts the establishment of neuronal polarity.
“A uniform distribution after overexpression of Par3 or a block of its KIF3A-dependent anterograde transport into the axon disrupts the establishment of neuronal polarity (Nishimura et al., 2004; Shi et al., 2003).”
From Rassf5 and Ndr kinases act in a novel pathway regulating neuronal polarity through Par3 phosphorylation (2014) · cites this paper as Nishimura et al., 2004
No citation lists for this paper
No citation lists for this paper yet — checked again daily.
References 23 · Cited by 289
- Authors
- Nishimura, T., Kato, K., Yamaguchi, T., Fukata, Y., Ohno, S., & Kaibuchi, K.
- Affiliations
- Nagoya University (JP)
- Yokohama City University (JP)
- Corresponding author
- Kaibuchi, Kozo
- Venue
- Nature Cell Biology
- Published
- 2004-03-28
- Volume
- 6
- Issue
- 4
- Pages
- 328-334
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- OpenAlex
- W1964935836
- Cited by
- 289
- References
- 23
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 8 · 2021: 12 · 2020: 9 · 2019: 11 · 2018: 6 · 2017: 9 · 2016: 9 · 2015: 11 · 2014: 10 · 2013: 23 · 2012: 14
- FWCI
- 8.78
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Keywords
- neuronal polarity, Par3, KIF3A, Par6, atypical protein kinase C, microtubule motor proteins, hippocampal neurons, dominant-negative mutant, protein-protein interaction
- MeSH terms
- Animals, Axonal Transport, Carrier Proteins, Cell Differentiation, Cells, Cultured, Chlorocebus aethiops, Fetus, Humans, Nerve Tissue Proteins, Neurons, Protein Kinase C, Kinesins, Cell Polarity, Protein Structure, Tertiary, Molecular Motor Proteins, Growth Cones, Protein Transport, Macromolecular Substances, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
