Evidence map›Paper›PMID 22544702›Full record

ArticleBlood2012

IKKα-mediated signaling circuitry regulates early B lymphopoiesis during hematopoiesis.

Mumtaz Yaseen Balkhi, Jami Willette-Brown, Feng Zhu, Zhisong Chen, Shuang Liu, Denis C Guttridge, Michael Karin, Yinling Hu

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

22 citing papers in PubMed, 27 citations in OpenAlex.

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  7. Lymph node formation and B cell homeostasis require IKK-α in distinct endothelial cell-derived compartments.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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

8 authors at 5 institutions in 1 country.

Mumtaz Yaseen BalkhiCancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, MD 21701, USA.
Jami Willette-Brown
Feng Zhu
Zhisong Chen
Shuang Liu
Denis C Guttridge
Michael Karin
Yinling Hu
Center for Cancer Research · USNational Institutes of Health · USCancer Genetics (United States) · USNational Cancer Institute · USUniversity of California, San Diego · US

Funding

Functions of IKK&945; in Skin Homeostasis and Skin TumorigenesisZIABC011212 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HU, YINLING · 2009 to 2025
$11.0M
Role of IKK alpha in lung squamous cell carcinoma developmentZIABC011391 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HU, YINLING · 2011 to 2025
$9.1M
Role of IKKalpha in lymphoid organ developmentZIABC011422 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HU, YINLING · 2012 to 2025
$4.4M
Intramural NIH HHS ZIA BC011212Intramural NIH HHS ZIA BC011391
6 · The paper itself

Abstract

Multiple transcription factors regulate B-cell commitment, which is coordinated with myeloid-erythroid lineage differentiation. NF-κB has long been speculated to regulate early B-cell development; however, this issue remains controversial. IκB kinase-α (IKKα) is required for splenic B-cell maturation but not for BM B-cell development. In the present study, we unexpectedly found defective BM B-cell development and increased myeloid-erythroid lineages in kinase-dead IKKα (KA/KA) knock-in mice. Markedly increased cytosolic p100, an NF-κB2-inhibitory form, and reduced nuclear NF-κB p65, RelB, p50, and p52, and IKKα were observed in KA/KA splenic and BM B cells. Several B- and myeloid-erythroid-cell regulators, including Pax5, were deregulated in KA/KA BM B cells. Using fetal liver and BM congenic transplantations and deleting IKKα from early hematopoietic cells in mice, this defect was identified as being B cell-intrinsic and an early event during hematopoiesis. Reintroducing IKKα, Pax5, or combined NF-κB molecules promoted B-cell development but repressed myeloid-erythroid cell differentiation in KA/KA BM B cells. The results of the present study demonstrate that IKKα regulates B-lineage commitment via combined canonical and noncanonical NF-κB transcriptional activities to target Pax5 expression during hematopoiesis.

Indexed as

Gene Knock-In TechniquesLymphopoiesisAnimalsB-LymphocytesBone Marrow CellsErythroid CellsGene ExpressionGene Expression RegulationHematopoiesisI-kappa B KinaseInterferon Regulatory Factor-4Interferon Regulatory FactorsMiceMyeloid CellsNF-kappa BPAX5 Transcription FactorI-kappa B KinaseInterferon Regulatory Factor-4Interferon Regulatory FactorsNF-kappa BPAX5 Transcription Factor

Identifiers

PMID22544702
PMCPMC3369682
OpenAlexW2037385668

What OpenQuestion holds

Textmetadata
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.