Evidence map›Paper›PMID 35732702›Full record

ArticleScientific reports2022

SILAC kinase screen identifies potential MASTL substrates.

Kamila A Marzec, Samuel Rogers, Rachael McCloy, Benjamin L Parker, David E James, D Neil Watkins, Andrew Burgess

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

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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

7 authors at 5 institutions in 2 countries.

Kamila A Marzec *ANZAC Research Institute, Concord Hospital, Concord, NSW, 2139, Australia.
Samuel Rogers *Children's Medical Research Institute, The University of Sydney, Westmead, Australia.
Rachael McCloyThe Kinghorn Cancer Centre, Garvan Institute of Medical Research, Sydney, NSW, 2010, Australia.
Benjamin L ParkerDepartment of Anatomy and Physiology, University of Melbourne, Melbourne, VIC, 3010, Australia.
David E JamesCharles Perkins Centre, School of Life and Environmental Sciences, The University of Sydney, Sydney, NSW, 2006, Australia.
D Neil WatkinsDepartment of Internal Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, R3E 0W2, Canada.
Andrew BurgessANZAC Research Institute, Concord Hospital, Concord, NSW, 2139, Australia. andrew.burgess1@health.nsw.gov.au.
University of Sydney · AUConcord Repatriation General Hospital · AUResearch Institute in Oncology and Hematology · CAThe Kinghorn Cancer Centre · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microtubule-associated serine/threonine kinase-like (MASTL) has emerged as a critical regulator of mitosis and as a potential oncogene in a variety of cancer types. To date, Arpp-19/ENSA are the only known substrates of MASTL. However, with the roles of MASTL expanding and increased interest in development of MASTL inhibitors, it has become critical to determine if there are additional substrates and what the optimal consensus motif for MASTL is. Here we utilized a whole cell lysate in vitro kinase screen combined with stable isotope labelling of amino acids in cell culture (SILAC) to identify potential substrates and the residue preference of MASTL. Using the related AGC kinase family members AKT1/2, the kinase screen identified several known and new substrates highly enriched for the validated consensus motif of AKT. Applying this method to MASTL identified 59 phospho-sites on 67 proteins that increased in the presence of active MASTL. Subsequent in vitro kinase assays suggested that MASTL may phosphorylate hnRNPM, YB1 and TUBA1C under certain in vitro conditions. Taken together, these data suggest that MASTL may phosphorylate several additional substrates, providing insight into the ever-increasing biological functions and roles MASTL plays in driving cancer progression and therapy resistance.

Indexed as

Microtubule-Associated ProteinsNeoplasmsProtein Serine-Threonine KinasesCell Culture TechniquesHumansIsotope LabelingMitosisPhosphorylationMASTL protein, humanMicrotubule-Associated ProteinsProtein Serine-Threonine Kinases

Identifiers

PMID35732702
PMCPMC9217955
OpenAlexW4283262824

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.