Evidence map›Paper›PMID 28787032›Full record

ArticlePloS one2017

Molecular basis of the microtubule-regulating activity of microtubule crosslinking factor 1.

Mohammad Abdul Kader, Tomoko Satake, Masatoshi Yoshida, Ikuko Hayashi, Atsushi Suzuki

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
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  4. Review
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

5 authors at 1 institution in 1 country.

Mohammad Abdul KaderMolecular Cellular Biology Laboratory, Yokohama City University Graduate School of Medical Life Science, Tsurumi-ku, Yokohama, Japan.
Tomoko SatakeMolecular Cellular Biology Laboratory, Yokohama City University Graduate School of Medical Life Science, Tsurumi-ku, Yokohama, Japan.
Masatoshi YoshidaMolecular Cellular Biology Laboratory, Yokohama City University Graduate School of Medical Life Science, Tsurumi-ku, Yokohama, Japan.
Ikuko HayashiMolecular Medical Bioscience Laboratory, Yokohama City University Graduate School of Medical Life Science, Tsurumi-ku, Yokohama, Japan.
Atsushi SuzukiMolecular Cellular Biology Laboratory, Yokohama City University Graduate School of Medical Life Science, Tsurumi-ku, Yokohama, Japan.ORCID http://orcid.org/0000-0002-3026-3026
Yokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The variety of microtubule arrays observed across different cell types should require a diverse group of proteins that control microtubule organization. Nevertheless, mainly because of the intrinsic propensity of microtubules to easily form bundles upon stabilization, only a small number of microtubule crosslinking proteins have been identified, especially in postmitotic cells. Among them is microtubule crosslinking factor 1 (MTCL1) that not only interconnects microtubules via its N-terminal microtubule-binding domain (N-MTBD), but also stabilizes microtubules via its C-terminal microtubule-binding domain (C-MTBD). Here, we comprehensively analyzed the assembly structure of MTCL1 to elucidate the molecular basis of this dual activity in microtubule regulation. Our results indicate that MTCL1 forms a parallel dimer not only through multiple homo-interactions of the central coiled-coil motifs, but also the most C-terminal non-coiled-coil region immediately downstream of the C-MTBD. Among these homo-interaction regions, the first coiled-coil motif adjacent to N-MTBD is sufficient for the MTCL1 function to crosslink microtubules without affecting the dynamic property, and disruption of this motif drastically transformed MTCL1-induced microtubule assembly from tight to network-like bundles. Notably, suppression of the homo-interaction of this motif inhibited the endogenous MTCL1 function to stabilize Golgi-associated microtubules that are essential for Golgi-ribbon formation. Because the microtubule-stabilizing activity of MTCL1 is completely attributed to C-MTBD, the present study suggests possible interplay between N-MTBD and C-MTBD, in which normal crosslinking and accumulation of microtubules by N-MTBD is essential for microtubule stabilization by C-MTBD.

Indexed as

HEK293 CellsHeLa CellsHumansMicrotubule-Associated ProteinsMicrotubulesProtein DomainsProtein MultimerizationProtein StabilityProtein Structure, QuaternaryMicrotubule-Associated ProteinsMTCL1 protein, human

Identifiers

PMID28787032
PMCPMC5546597
OpenAlexW2743494010

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Registered trials

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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.