Evidence map›Paper›PMID 34301844›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2021

Protein Kinase CK2 Regulates B Cell Development and Differentiation.

Hairong Wei, Wei Yang, Huixian Hong, Zhaoqi Yan, Hongwei Qin, Etty N Benveniste

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

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  5. Regulation of cancer progression by CK2: an emerging therapeutic target.Medical oncology (Northwood, London, England) · 2024
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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

6 authors at 2 institutions in 1 country.

Hairong WeiDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294; and.
Wei YangDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294; and.
Huixian HongDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294; and.ORCID 0000-0001-7283-8775
Zhaoqi YanDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294; and.
Hongwei QinDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294; and hqin@uab.edu.ORCID 0000-0002-7511-5078
Etty N BenvenisteDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294; and.
University of Alabama at Birmingham · USGladstone Institutes · US

Funding

Therapeutic Intervention of the JAK/STAT Pathway for NeuroinflammationR01NS057563 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENVENISTE, ETTY N · 2008 to 2017
$2.7M
The Role of CK2 in Glioblastoma DevelopmentR01CA194414 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENVENISTE, ETTY N · 2016 to 2020
$1.7M
Targeting the JAK/STAT-3 Pathway Signaling Axis in GliomaR01CA158534 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENVENISTE, ETTY N · 2012 to 2016
$1.5M
NCI NIH HHS R01 CA158534NCI NIH HHS R01 CA194414NINDS NIH HHS R01 NS057563
6 · The paper itself

Abstract

Protein kinase CK2 (also known as Casein Kinase 2) is a serine/threonine kinase composed of two catalytic subunits (CK2α and/or CK2α') and two regulatory CK2β subunits. CK2 is overexpressed and overactive in B cell acute lymphoblastic leukemia and diffuse large B cell lymphomas, leading to inappropriate activation of the NF-κB, JAK/STAT, and PI3K/AKT/mTOR signaling pathways and tumor growth. However, whether CK2 regulates normal B cell development and differentiation is not known. We generated mice lacking CK2α specifically in B cells (using CD19-driven Cre recombinase). These mice exhibited cell-intrinsic expansion of marginal zone B cells at the expense of transitional B cells, without changes in follicular B cells. Transitional B cells required CK2α to maintain adequate BCR signaling. In the absence of CK2α, reduced BCR signaling and elevated Notch2 signaling activation increased marginal zone B cell differentiation. Our results identify a previously unrecognized function for CK2α in B cell development and differentiation.

Indexed as

AnimalsAntigens, CD19B-LymphocytesCasein Kinase IICell DifferentiationCells, CulturedIntegrasesLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutNF-kappa BPrecursor Cells, B-LymphoidReceptors, Antigen, B-CellSignal TransductionAntigens, CD19Casein Kinase IICre recombinaseCsnk2a1 protein, mouseIntegrasesNF-kappa BReceptors, Antigen, B-Cell

Identifiers

PMID34301844
PMCPMC8323969
OpenAlexW3185748560

What OpenQuestion holds

Textmetadata
LicenceTDM
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.