Evidence map›Paper›PMID 37905069›Full record

ArticlebioRxiv : the preprint server for biology2023

Identification of the KIF18A alpha-4 helix as a therapeutic target for chromosomally unstable tumor cells.

Katherine Schutt, Katelyn A Queen, Kira Fisher, Olivia Budington, Weifeng Mao, Wei Liu, Yisong Xiao, Fred Aswad, James Joseph, Jason Stumpff

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Katherine SchuttDepartment of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT.
Katelyn A QueenDepartment of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT.
Kira FisherDepartment of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT.
Olivia BudingtonDepartment of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT.
Weifeng MaoApeiron Therapeutics, Shanghai, CN.
Wei LiuApeiron Therapeutics, Shanghai, CN.
Yisong XiaoApeiron Therapeutics, Shanghai, CN.
Fred AswadApeiron Therapeutics, Burlingame, CA.
James JosephApeiron Therapeutics, Burlingame, CA.
Jason StumpffDepartment of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT.
University of Vermont · USApeiron Biologics (Austria) · AT

Funding

Mechanisms of microtubule motors and chromosome segregationR35GM144133 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI JASON K STUMPFF · 2022 to 2026
$2.4M
Tuning Mitotic Kinesins Through Motor Domain Post Translational ModificationsR01GM130556 · NIGMS · MAYO CLINIC JACKSONVILLE · PI GROSS, STEVEN P, MURETTA, JOSEPH M. · 2019 to 2022
$2.4M
NIGMS NIH HHS R01 GM130556NIGMS NIH HHS R35 GM144133
6 · The paper itself

Abstract

The mitotic kinesin, KIF18A, is required for proliferation of cancer cells that exhibit chromosome instability (CIN), implicating it as a promising target for treatment of a subset of aggressive tumor types. Determining regions of the KIF18A protein to target for inhibition will be important for the design and optimization of effective small molecule inhibitors. In this study, we investigated the effects of mutating S284 within the alpha-4 helix of KIF18A, which was previously identified as a phosphorylated residue. Mutations in S284 cause relocalization of KIF18A from the plus-ends of spindle microtubules to the spindle poles. Furthermore, KIF18A S284 mutants display loss of KIF18A function and fail to support proliferation in CIN tumor cells. Interestingly, similar effects on KIF18A localization and function were seen after treatment of CIN cells with KIF18A inhibitory compounds that are predicted to interact with residues within the alpha-4 helix. These data implicate the KIF18A alpha-4 helix as an effective target for inhibition and demonstrate that small molecules targeting KIF18A selectively limit CIN tumor cell proliferation and result in phenotypically similar effects on mitosis at the single cell level compared to genetic perturbations.

Identifiers

PMID37905069
PMCPMC10614886
OpenAlexW4387779424

What OpenQuestion holds

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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.