Evidence map›Paper›PMID 18523151›Full record

ArticleBlood2008

Id2 intrinsically regulates lymphoid and erythroid development via interaction with different target proteins.

Ming Ji, Huajie Li, Hyung Chan Suh, Kimberly D Klarmann, Yoshifumi Yokota, Jonathan R Keller

Open access · greenAbstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

44 citing papers in PubMed, 72 citations in OpenAlex.

  1. Proceedings of the National Academy of Sciences of the United States of America · 2025
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  10. Review
  11. Id2 controls specification of Lgr5The EMBO journal · 2017
    Article
  12. Review
  13. Transcription factor Zeb2 regulates commitment to plasmacytoid dendritic cell and monocyte fate.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  14. Article
  15. Article
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  18. Review
  19. Article
  20. Dendritic cell fate is determined by BCL11A.Proceedings of the National Academy of Sciences of the United States of America · 2014
    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

6 authors at 3 institutions in 2 countries.

Ming JiBasic Research Program, SAIC-Frederick, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA.
Huajie Li
Hyung Chan Suh
Kimberly D Klarmann
Yoshifumi Yokota
Jonathan R Keller
Center for Cancer Research · USNational Cancer Institute · USUniversity of Fukui · JP

Funding

Molecular-Cellular Regulation of Hematopoietic Stem CellsZIABC010001 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KELLER, JONATHAN R · 2009 to 2024
$16.8M
Intramural NIH HHSNCI NIH HHS N01-CO-12 400
6 · The paper itself

Abstract

Inhibitors of DNA binding (Id) family members are key regulators of cellular differentiation and proliferation. These activities are related to the ability of Id proteins to antagonize E proteins and other transcription factors. As negative regulators of E proteins, Id proteins have been implicated in lymphocyte development. Overexpression of Id1, Id2, or Id3 has similar effects on lymphocyte development. However, which Id protein plays a physiologic role during lymphocyte development is not clear. By analyzing Id2 knock-out mice and retroviral transduced hematopoietic progenitors, we demonstrated that Id2 is an intrinsic negative regulator of B-cell development. Hematopoietic progenitor cells overexpressing Id2 did not reconstitute B-cell development in vivo, which resembled the phenotype of E2A null mice. The B-cell population in bone marrow was significantly expanded in Id2 knock-out mice compared with their wild-type littermates. Knock-down of Id2 by shRNA in hematopoietic progenitor cells promoted B-cell differentiation and induced the expression of B-cell lineage-specific genes. These data identified Id2 as a physiologically relevant regulator of E2A during B lymphopoiesis. Furthermore, we identified a novel Id2 function in erythroid development. Overexpression of Id2 enhanced erythroid development, and decreased level of Id2 impaired normal erythroid development. Id2 regulation of erythroid development is mediated via interacting with transcription factor PU.1 and modulating PU.1 and GATA-1 activities. We conclude that Id2 regulates lymphoid and erythroid development via interaction with different target proteins.

Indexed as

Cell LineageAnimalsBasic Helix-Loop-Helix ProteinsB-LymphocytesBone MarrowErythroid CellsErythropoiesisGATA1 Transcription FactorHematopoietic Stem CellsInhibitor of Differentiation Protein 2LymphocytesLymphopoiesisMiceMice, KnockoutProtein BindingProto-Oncogene ProteinsBasic Helix-Loop-Helix ProteinsGata1 protein, mouseGATA1 Transcription FactorIdb2 protein, mouseInhibitor of Differentiation Protein 2Proto-Oncogene ProteinsProto-Oncogene Protein Spi-1Tcf3 protein, mouseTrans-Activators

Identifiers

PMID18523151
PMCPMC2515127
OpenAlexW2083181400

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.