Evidence map›Paper›PMID 10567549›Full record

ArticleMolecular and cellular biology1999

Massive apoptosis of thymocytes in T-cell-deficient Id1 transgenic mice.

D Kim, X C Peng, X H Sun

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

65 citing papers in PubMed, 132 citations in OpenAlex.

  1. Telomere Maintenance and Oncogenesis.International journal of molecular sciences · 2025
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. ILC Differentiation in the Thymus.Advances in experimental medicine and biology · 2022
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Inhibitor of differentiation 1 transcription factor promotes metabolic reprogramming in hepatocellular carcinoma cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  20. Transcription factors and target genes of pre-TCR signaling.Cellular and molecular life sciences : CMLS · 2015
    Review

5 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

D KimDepartment of Cell Biology, Kaplan Cancer Center, New York University School of Medicine, New York, New York 10016, USA.
X C Peng
X H Sun
New York University · US

Funding

MOLECULAR MECHANISMS OF T CELL LEUKEMOGENESIS BY TALR01CA077553 · NCI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI SUN, XIAO-HONG · 1999 to 2009
$2.5M
REGULATION OF THE ID GENES IN LYMPHOCYE DEVELOPMENTR01AI033597 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI SUN, XIAO-HONG · 1994 to 2005
$1.5M
NCI NIH HHS 1R01CA77553NCI NIH HHS R01 CA077553NIAID NIH HHS 1R01AI33597NIAID NIH HHS R01 AI033597
6 · The paper itself

Abstract

Id1 is an inhibitor of a group of basic helix-loop-helix transcription factors, collectively called E proteins, which includes E12, E47, E2-2, and HEB. We have generated transgenic mice in which Id1 is specifically expressed in T cells. The total number of thymocytes in these mice is less than 4% of that in wild-type mice. The majority of the transgenic thymocytes are CD4 and CD8 double negative and bear the cell surface markers of multipotent progenitor cells. A small number of thymocytes, however, differentiate into CD4 or CD8 single-positive T cells, which also display different characteristics from their wild-type counterparts. More importantly, apoptotic cells constitute about 50% of the total thymocytes. These apoptotic thymocytes have rearranged their T-cell receptor genes, suggesting that they are differentiating T cells. This finding has raised the possibility that the T-cell deficiency in Id1 transgenic mice is the result of a massive apoptosis of differentiating T cells triggered by Id1 expression as opposed to a developmental block at the earliest progenitor stage. The progenitor cells accumulated in the transgenic mice might have survived because they are not susceptible to the apoptotic signals. Despite the massive cell death of the thymocytes at young ages, Id1 transgenic mice frequently develop T-cell lymphoma later in their life span, and lymphomagenesis appears to occur at different stages of T-cell development. Taken together, our data suggest that E proteins, being the targets of Id1, are essential regulators for normal T-cell differentiation and tumor suppression.

Indexed as

ApoptosisRepressor ProteinsAnimalsGene ExpressionGene Rearrangement, T-LymphocyteHelix-Loop-Helix MotifsHumansInhibitor of Differentiation Protein 1MiceMice, TransgenicReceptors, Antigen, T-CellThymus GlandT-LymphocytesTranscription FactorsID1 protein, humanIdb1 protein, mouseInhibitor of Differentiation Protein 1Receptors, Antigen, T-CellRepressor ProteinsTranscription Factors

Identifiers

PMID10567549
PMCPMC84908
OpenAlexW2137931232

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.