Evidence map›Paper›PMID 27957526›Full record

ArticleeNeuro

Mammalian FMRP S499 Is Phosphorylated by CK2 and Promotes Secondary Phosphorylation of FMRP.

Christopher M Bartley, Rachel A O'Keefe, Anna Blice-Baum, Mihaela-Rita Mihailescu, Xuan Gong, Laura Miyares, Esra Karaca, Angélique Bordey

Open access · goldAbstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 38 citations in OpenAlex.

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  14. Protein phase separation: A novel therapy for cancer?British journal of pharmacology · 2020
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  20. Kinase pathway inhibition restores PSD95 induction in neurons lacking fragile X mental retardation protein.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
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

8 authors at 3 institutions in 2 countries.

Christopher M BartleyDepartments of Neurosurgery, and Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510; Department of Neurobiology, Yale University School of Medicine, New Haven, CT 06510.ORCID 0000-0002-1391-4130
Rachel A O'KeefeDepartments of Neurosurgery, and Cellular and Molecular Physiology, Yale University School of Medicine , New Haven, CT 06510.
Anna Blice-BaumDepartment of Chemistry and Biochemistry, Duquesne University , Pittsburgh, PA 15282.
Mihaela-Rita MihailescuDepartment of Chemistry and Biochemistry, Duquesne University , Pittsburgh, PA 15282.ORCID 0000-0002-1162-7699
Xuan GongDepartments of Neurosurgery, and Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510; Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha 410008, China.
Laura MiyaresDepartments of Neurosurgery, and Cellular and Molecular Physiology, Yale University School of Medicine , New Haven, CT 06510.ORCID 0000-0002-1698-6199
Esra KaracaDepartments of Neurosurgery, and Cellular and Molecular Physiology, Yale University School of Medicine , New Haven, CT 06510.
Angélique BordeyDepartments of Neurosurgery, and Cellular and Molecular Physiology, Yale University School of Medicine , New Haven, CT 06510.ORCID 0000-0003-3496-3385
Yale University · USDuquesne University · USCentral South University · CN

Funding

TSC-mTOR on neuron developmentR01NS086329 · NINDS · YALE UNIVERSITY · PI BORDEY, ANGELIQUE · 2013 to 2017
$1.8M
Fragile X Mental Retardation Protein translation regulator function: interactionsR15HD078017 · NICHD · DUQUESNE UNIVERSITY · PI MIHAILESCU, MIHAELA R · 2013 to 2013
$394k
NICHD NIH HHS R15 HD078017NINDS NIH HHS R01 NS086329
6 · The paper itself

Abstract

The fragile X mental retardation protein (FMRP) is an mRNA-binding regulator of protein translation that associates with 4-6% of brain transcripts and is central to neurodevelopment. Autism risk genes' transcripts are overrepresented among FMRP-binding mRNAs, and FMRP loss-of-function mutations are responsible for fragile X syndrome, the most common cause of monogenetic autism. It is thought that FMRP-dependent translational repression is governed by the phosphorylation of serine residue 499 (S499). However, recent evidence suggests that S499 phosphorylation is not modulated by metabotropic glutamate receptor class I (mGluR-I) or protein phosphatase 2A (PP2A), two molecules shown to regulate FMRP translational repression. Moreover, the mammalian FMRP S499 kinase remains unknown. We found that casein kinase II (CK2) phosphorylates murine FMRP S499. Further, we show that phosphorylation of FMRP S499 permits phosphorylation of additional, nearby residues. Evidence suggests that these nearby residues are modulated by mGluR-I and PP2A pathways. These data support an alternative phosphodynamic model of FMRP that is harmonious with prior studies and serves as a framework for further investigation.

Indexed as

AnimalsBlotting, WesternCasein Kinase IICells, CulturedCerebral CortexFragile X Messenger Ribonucleoprotein 1HEK293 CellsHumansMass SpectrometryMiceNaphthyridinesPhenazinesPhosphorylationProtein BiosynthesisProtein Kinase InhibitorsReceptors, Metabotropic GlutamateCasein Kinase IIFMR1 protein, humanFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1metabotropic glutamate receptor type 1NaphthyridinesPhenazinesProtein Kinase InhibitorsReceptors, Metabotropic GlutamateRecombinant Proteinssilmitasertibcasein kinaseFMRPfragile XmTORphosphorylationtranslation

Identifiers

PMID27957526
PMCPMC5116651
OpenAlexW2546792091

What OpenQuestion holds

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LicenceCC BY
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.