Evidence map›Paper›PMID 35469920›Full record

ArticleThe Journal of biological chemistry2022

Identification of a reciprocal negative feedback loop between tau-modifying proteins MARK2 kinase and CBP acetyltransferase.

Zarin Tabassum, Jui-Heng Tseng, Camryn Isemann, Xu Tian, Youjun Chen, Laura E Herring, Todd J Cohen

Open access · goldAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. Neuronal connectivity, behavioral, and transcriptional alterations associated with the loss of MARK2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    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

7 authors at 1 institution in 1 country.

Zarin TabassumDepartment of Neurology, UNC Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Jui-Heng TsengDepartment of Neurology, UNC Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Camryn IsemannDepartment of Neurology, UNC Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Xu TianDepartment of Neurology, UNC Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Youjun ChenDepartment of Neurology, UNC Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Laura E HerringUNC Proteomics Core Facility, Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina, USA.
Todd J CohenDepartment of Neurology, UNC Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina, USA. Electronic address: toddcohen@neurology.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI David Darr · 1985 to 2026
$201.5M
Dual CHIP Functions Control Tau Triage In Alzheimer's DiseaseR01AG061188 · NIA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COHEN, TODD JONATHAN, SCHISLER, JONATHAN C. · 2019 to 2023
$3.1M
Elucidating The Aberrant TDP-43 Species That Promote NeurodegenerationR01NS105981 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COHEN, TODD JONATHAN · 2018 to 2022
$1.7M
Dissecting the Role of HDAC6 in Alzheimer's PathogenesisR21AG058080 · NIA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COHEN, TODD JONATHAN · 2018 to 2019
$428k
NCI NIH HHS P30 CA016086NIA NIH HHS R01 AG061188NIA NIH HHS R21 AG058080NINDS NIH HHS R01 NS105981
6 · The paper itself

Abstract

The posttranslational regulation of the neuronal proteome is critical for brain homeostasis but becomes dysregulated in the aged or diseased brain, in which abnormal posttranslational modifications (PTMs) are frequently observed. While the full extent of modified substrates that comprise the "PTM-ome" are slowly emerging, how the upstream enzymes catalyzing these processes are regulated themselves is not well understood, particularly in the context of neurodegeneration. Here, we describe the reciprocal regulation of a kinase, the microtubule affinity-regulating kinase 2 (MARK2), and an acetyltransferase, CREB-binding protein (CBP), two enzymes known to extensively modify tau proteins in the progression of Alzheimer's disease. We found that MARK2 negatively regulates CBP and, conversely, CBP directly acetylates and inhibits MARK2 kinase activity. These findings highlight a reciprocal negative feedback loop between a kinase and an acetyltransferase, which has implications for how PTM interplay is coordinated on substrates including tau. Our study suggests that PTM profiles occur through the posttranslational control of the master PTM remodeling enzymes themselves.

Indexed as

AcetyltransferasesAlzheimer DiseaseAnimalsCREB-Binding ProteinFeedbackHumansMiceMicrotubulesPhosphorylationProtein Processing, Post-TranslationalProtein Serine-Threonine Kinasestau ProteinsAcetyltransferasesCREB-Binding ProteinCREBBP protein, humanMARK2 protein, humanProtein Serine-Threonine Kinasestau ProteinsacetylationacetyltransferaseaggregationCBPkinaseMARK2neurodegenerationphosphorylationtau

Identifiers

PMID35469920
PMCPMC9136110
OpenAlexW4224279443

What OpenQuestion holds

Textmetadata
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.