Evidence map›Paper›PMID 38679165›Full record

ArticleAntiviral research2024

CK1 and PP1 regulate Rift Valley fever virus genome replication through L protein phosphorylation.

Nicole Bracci, Alan Baer, Rafaela Flor, Kaylee Petraccione, Timothy Stocker, Weidong Zhou, Tatiana Ammosova, Rhoel R Dinglasan, Sergei Nekhai, Kylene Kehn-Hall

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Antiviral research, 2024. 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
–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

1 citing paper in PubMed.

  1. 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

10 authors.

Nicole BracciDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Virginia, USA; Center for Emerging, Zoonotic, and Arthropod-borne Pathogens, Virginia Polytechnic Institute and State University, Virginia, USA.
Alan BaerNational Center for Biodefense and Infectious Diseases, School of Systems Biology, George Mason University, Manassas, VA, USA.
Rafaela FlorDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Virginia, USA; Center for Emerging, Zoonotic, and Arthropod-borne Pathogens, Virginia Polytechnic Institute and State University, Virginia, USA.
Kaylee PetraccioneDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Virginia, USA; Center for Emerging, Zoonotic, and Arthropod-borne Pathogens, Virginia Polytechnic Institute and State University, Virginia, USA.
Timothy StockerDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Virginia, USA; Center for Emerging, Zoonotic, and Arthropod-borne Pathogens, Virginia Polytechnic Institute and State University, Virginia, USA.
Weidong ZhouCenter for Applied Proteomics and Molecular Medicine, School of Systems Biology, George Mason University, Manassas, VA, USA.
Tatiana AmmosovaCenter for Sickle Cell Disease, Department of Medicine, Howard University, Washington D.C., USA.
Rhoel R DinglasanEmerging Pathogens Institute, University of Florida, Florida, USA; Department of Infectious Diseases & Immunology, College of Veterinary Medicine, University of Florida, Florida, USA.
Sergei NekhaiCenter for Sickle Cell Disease, Department of Medicine, Howard University, Washington D.C., USA.
Kylene Kehn-HallDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Virginia, USA; Center for Emerging, Zoonotic, and Arthropod-borne Pathogens, Virginia Polytechnic Institute and State University, Virginia, USA. Electronic address: kkehnhall@vt.edu.

Funding

Sleep Disorders in Adults with Sickle Cell Disease: Frequency, Associations with Cardiovascular and Pain Indicators, and Responses to TreatmentU54MD007597 · NIMHD · HOWARD UNIVERSITY · PI GEORGES E. HADDAD · 2019 to 2026
$37.7M
SWG 2: Cure Research Scientific Working GroupP30AI117970 · NIAID · GEORGE WASHINGTON UNIVERSITY · PI Italo Mocchetti · 2015 to 2026
$29.6M
Sickle Cell Disease and Sickle Cell Trait Protection Against HIV-1-infection in Africans and African AmericansR01HL125005 · NHLBI · HOWARD UNIVERSITY · PI MARINA A JEREBTSOVA, SERGEI NEKHAI · 2014 to 2026
$6.7M
Acquisition of Orbitrap mass spectrometerS10OD028681 · OD · HOWARD UNIVERSITY · PI NEKHAI, SERGEI · 2020 to 2020
$869k
NHLBI NIH HHS R01 HL125005NIAID NIH HHS P30 AI117970NIH HHS S10 OD028681NIMHD NIH HHS U54 MD007597
6 · The paper itself

Abstract

Rift Valley fever virus (RVFV) is an arbovirus in the Phenuiviridae family identified initially by the large 'abortion storms' observed among ruminants; RVFV can also infect humans. In humans, there is a wide variation of clinical symptoms ranging from subclinical to mild febrile illness to hepatitis, retinitis, delayed-onset encephalitis, or even hemorrhagic fever. The RVFV is a tri-segmented negative-sense RNA virus consisting of S, M, and L segments. The L segment encodes the RNA-dependent RNA polymerase (RdRp), termed the L protein, which is responsible for both viral mRNA synthesis and genome replication. Phosphorylation of viral RdRps is known to regulate viral replication. This study shows that RVFV L protein is serine phosphorylated and identified Casein Kinase 1 alpha (CK1α) and protein phosphatase 1 alpha (PP1α) as L protein binding partners. Inhibition of CK1 and PP1 through small molecule inhibitor treatment, D4476 and 1E7-03, respectively, caused a change in the phosphorylated status of the L protein. Inhibition of PP1α resulted in increased L protein phosphorylation whereas inhibition of CK1α decreased L protein phosphorylation. It was also found that in RVFV infected cells, PP1α localized to the cytoplasmic compartment. Treatment of RVFV infected cells with CK1 inhibitors reduced virus production in both mammalian and mosquito cells. Lastly, inhibition of either CK1 or PP1 reduced viral genomic RNA levels. These data indicate that L protein is phosphorylated and that CK1 and PP1 play a crucial role in regulating the L protein phosphorylation cycle, which is critical to viral RNA production and viral replication.

Indexed as

Protein Phosphatase 1Rift Valley fever virusVirus ReplicationAnimalsCasein Kinase IalphaCell LineChlorocebus aethiopsGenome, ViralHumansPhosphorylationRift Valley FeverRNA-Dependent RNA PolymeraseRNA, ViralVero CellsViral ProteinsCasein Kinase IalphaProtein Phosphatase 1RNA-Dependent RNA PolymeraseRNA, ViralViral ProteinsAntiviralCK1L proteinPhosphorylationPP1Rift Valley fever virus

Identifiers

PMID38679165
PMCPMC13631916

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.