Evidence map›Paper›PMID 36459065›Full record

ArticleThe Journal of cell biology2023

α-Tubulin detyrosination links the suppression of MCAK activity with taxol cytotoxicity.

Danilo Lopes, Alexandre L Seabra, Bernardo Orr, Helder Maiato

Open access · greenAbstract read
In one paragraph

Article in The Journal of cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 21 citations in OpenAlex.

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  6. Peptide-based covalent inhibitor of tubulin detyrosination promotes mesenchymal-to-epithelial transition in lung cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  15. Unveiling the mechanisms and challenges of cancer drug resistance.Cell communication and signaling : CCS · 2024
    Review
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  19. Microtubule detyrosination drives symmetry breaking to polarize cells for directed cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2023
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  20. 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

4 authors at 1 institution in 1 country.

Danilo LopesChromosome Instability & Dynamics Group, i3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.ORCID 0000-0003-2741-1822
Alexandre L SeabraChromosome Instability & Dynamics Group, i3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.ORCID 0000-0002-9474-9148
Bernardo OrrChromosome Instability & Dynamics Group, i3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
Helder MaiatoChromosome Instability & Dynamics Group, i3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.ORCID 0000-0002-6200-9997
Universidade do Porto · PT

Funding

European Research Council 681443
6 · The paper itself

Abstract

α/β-Tubulin posttranslational modifications (PTMs) generate microtubule diversity, but whether they account for cancer cell resistance to microtubule-targeting drugs remains unknown. Here, we performed a pilot dissection of the "cancer tubulin code" using the NCI-60 cancer cell panel. We found that acetylated, detyrosinated, and ∆2-α-tubulin that typically accumulate on stable microtubules were uncoupled in many cancer cells. Acetylated α-tubulin did not affect microtubule dynamics, whereas its levels correlated with, but were not required for, taxol-induced cytotoxicity. In contrast, experimental increase of α-tubulin detyrosination, and/or depletion of the detyrosination-sensitive microtubule-depolymerizing enzyme MCAK, enhanced taxol-induced cytotoxicity by promoting cell death in mitosis and the subsequent interphase, without causing a cumulative effect. Interestingly, only increased detyrosinated α-tubulin aggravated taxol-induced spindle multipolarity. Overall, we identified high α-tubulin acetylation as a potential biomarker for cancer cell response to taxol and uncovered a mechanistic link between α-tubulin detyrosination and the suppression of MCAK activity in taxol-induced cytotoxicity, likely by promoting chromosome missegregation, regardless of spindle defects.

Indexed as

KinesinsMicrotubulesPaclitaxelTubulinCell Line, TumorHumansMitosisProtein Processing, Post-TranslationalKIF2C protein, humanKinesinsPaclitaxelTubulin

Identifiers

PMID36459065
PMCPMC9723805
OpenAlexW4311121618

What OpenQuestion holds

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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.