Evidence map›Paper›PMID 26323690›Full record

ArticleThe Journal of cell biology2015

TTBK2 with EB1/3 regulates microtubule dynamics in migrating cells through KIF2A phosphorylation.

Takashi Watanabe, Mai Kakeno, Toshinori Matsui, Ikuko Sugiyama, Nariko Arimura, Kenji Matsuzawa, Aya Shirahige, Fumiyoshi Ishidate, Tomoki Nishioka, Shinichiro Taya and 2 more

Abstract read
In one paragraph

Article in The Journal of cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
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  9. Tubulin detyrosination shapesProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. KIF2A deficiency causes early-onset neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Takashi WatanabeDepartment of Cell Pharmacology, Nagoya University Graduate School of Medicine, Showa, Nagoya 466-8550, Japan.
Mai KakenoDepartment of Cell Pharmacology, Nagoya University Graduate School of Medicine, Showa, Nagoya 466-8550, Japan.
Toshinori MatsuiDepartment of Cell Pharmacology, Nagoya University Graduate School of Medicine, Showa, Nagoya 466-8550, Japan.
Ikuko SugiyamaDepartment of Cell Pharmacology, Nagoya University Graduate School of Medicine, Showa, Nagoya 466-8550, Japan.
Nariko ArimuraDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8502, Japan.
Kenji MatsuzawaDepartment of Cell Pharmacology, Nagoya University Graduate School of Medicine, Showa, Nagoya 466-8550, Japan.
Aya ShirahigeDepartment of Cell Pharmacology, Nagoya University Graduate School of Medicine, Showa, Nagoya 466-8550, Japan.
Fumiyoshi IshidateDepartment of Cell Pharmacology, Nagoya University Graduate School of Medicine, Showa, Nagoya 466-8550, Japan.
Tomoki NishiokaDepartment of Cell Pharmacology, Nagoya University Graduate School of Medicine, Showa, Nagoya 466-8550, Japan.
Shinichiro TayaDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8502, Japan.
Mikio HoshinoDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8502, Japan.
Kozo KaibuchiDepartment of Cell Pharmacology, Nagoya University Graduate School of Medicine, Showa, Nagoya 466-8550, Japan kaibuchi@med.nagoya-u.ac.jp.
Nagoya University · JPNational Center of Neurology and Psychiatry · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microtubules (MTs) play critical roles in various cellular events, including cell migration. End-binding proteins (EBs) accumulate at the ends of growing MTs and regulate MT end dynamics by recruiting other plus end-tracking proteins (+TIPs). However, how EBs contribute to MT dynamics through +TIPs remains elusive. We focused on tau-tubulin kinase 2 (TTBK2) as an EB1/3-binding kinase and confirmed that TTBK2 acted as a +TIP. We identified MT-depolymerizing kinesin KIF2A as a novel substrate of TTBK2. TTBK2 phosphorylated KIF2A at S135 in intact cells in an EB1/3-dependent fashion and inactivated its MT-depolymerizing activity in vitro. TTBK2 depletion reduced MT lifetime (facilitated shrinkage and suppressed rescue) and impaired HeLa cell migration, and these phenotypes were partially restored by KIF2A co-depletion. Expression of nonphosphorylatable KIF2A, but not wild-type KIF2A, reduced MT lifetime and slowed down the cell migration. These findings indicate that TTBK2 with EB1/3 phosphorylates KIF2A and antagonizes KIF2A-induced depolymerization at MT plus ends for cell migration.

Indexed as

AnimalsCell Line, TumorCell MovementChlorocebus aethiopsCOS CellsHeLa CellsHumansKinesinsMicrotubule-Associated ProteinsMicrotubulesMolecular Sequence DataPhosphorylationProtein Serine-Threonine KinasesRNA InterferenceRNA, Small InterferingWound HealingKIF2A protein, humanKinesinsMAPRE3 protein, humanMicrotubule-Associated ProteinsProtein Serine-Threonine KinasesRNA, Small Interferingtau-tubulin kinase

Identifiers

PMID26323690
PMCPMC4555816
OpenAlexW2129322844

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.