Evidence map›Paper›PMID 34964999›Full record

ArticleMolecular carcinogenesis2022

Conditional deletion of mTOR discloses its essential role in early B-cell development.

Shuling Zhang, Wendy Dubois, Xingmin Feng, Joe T Nguyen, Neal S Young, Beverly A Mock

Open access · greenAbstract read
In one paragraph

Article in Molecular carcinogenesis, 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
0.1field-weighted citation impact, top 54% 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, 2 citations in OpenAlex.

  1. Medical Aspects of mTOR Inhibition in Kidney Transplantation.International journal of molecular sciences · 2022
    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

6 authors at 1 institution in 1 country.

Shuling ZhangLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Wendy DuboisLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Xingmin FengHematology Branch, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, Maryland, USA.
Joe T NguyenLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Neal S YoungHematology Branch, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, Maryland, USA.
Beverly A MockLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.ORCID 0000-0003-2479-4549
National Institutes of Health · US

Funding

Pathogenesis And Treatment Of Aplastic AnemiaZIAHL002315 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI YOUNG, NEAL S · 2009 to 2025
$60.1M
PATHOGENESIS AND TREATMENT OF APLASTIC ANEMIAZ01HL002315 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI YOUNG, NEAL S · 1985 to 2008
$9.5M
The Genetics of Susceptibility to Mouse Plasma Cell TumorsZIABC010008 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MOCK, BEVERLY · 2009 to 2025
$9.0M
THE GENETICS OF SUSCEPTIBILITY TO MOUSE PLASMA CELL TUMORSZ01BC010008 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MOCK, BEVERLY A. · 1996 to 2008
$1.7M
Intramural NIH HHS Z01 BC010008Intramural NIH HHS Z01 HL002315
6 · The paper itself

Abstract

Mechanistic target of rapamycin (mTOR) is a serine-threonine kinase and central regulator of cell growth, differentiation, and survival. mTOR is commonly hyperactivated in a diverse number of cancers and critical roles for mTOR in regulating immune cell differentiation and function have been demonstrated. However, there is little work investigating the roles of mTOR in early B-cell development. Here we demonstrate that conditional disruption of mTOR in developing mouse B cells results in reduced pre-B-cell proliferation and survival, as well as a developmental block at the pre-B-cell stage, with a corresponding lack of peripheral B cells. Upon immunization with NP-CGG antigen, mice with Mtor conditional disruption in early B cells lost their ability to form germinal centers and produce specific antibodies. In competitive BM repopulation assays, donor BM cells from conditional knock-out mice were completely impaired in their ability to reconstitute B cells. Our data reveal the essential role of mTOR in early pre-B-cell development and survival.

Indexed as

Signal TransductionSirolimusAnimalsB-LymphocytesCell DifferentiationLymphocyte ActivationMiceMice, KnockoutTOR Serine-Threonine KinasesmTOR protein, mouseSirolimusTOR Serine-Threonine Kinasesantibody productionB-cell developmentcompetitive BM transplantationMb1-Cre micemTOR

Identifiers

PMID34964999
PMCPMC8930614
OpenAlexW4200209815

What OpenQuestion holds

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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.