Evidence map›Paper›PMID 9710627›Full record

ArticleMolecular and cellular biology1998

Id2 promotes apoptosis by a novel mechanism independent of dimerization to basic helix-loop-helix factors.

M Florio, M C Hernandez, H Yang, H K Shu, J L Cleveland, M A Israel

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.4field-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

33 citing papers in PubMed, 110 citations in OpenAlex.

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  16. Id2 is required for specification of dopaminergic neurons during adult olfactory neurogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008
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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 3 institutions in 1 country.

M FlorioPreuss Laboratory for Molecular Neuro-Oncology, Brain Tumor Research Center, Department of Neurological Surgery, University of California, San Francisco, California 94143-0520, USA.
M C Hernandez
H Yang
H K Shu
J L Cleveland
M A Israel
University of California, San Francisco · USSt. Jude Children's Research Hospital · USUniversity of Tennessee Health Science Center · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
The Bcl-2/Bcl-X Pathway in Myc-Induced LymphomagenesisR01CA076379 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CLEVELAND, JOHN L. · 1998 to 2012
$3.5M
TREATMENT OF MALIGNANT BRAIN TUMORSP01CA013525 · NCI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI DEEN, DENNIS F. · 1985 to 1999
–
NCI NIH HHS CA13525NCI NIH HHS CA21765NCI NIH HHS CA76379NCI NIH HHS P30 CA021765NCI NIH HHS R01 CA076379
6 · The paper itself

Abstract

Members of the helix-loop-helix (HLH) family of Id proteins have demonstrated roles in the regulation of differentiation and cell proliferation. Id proteins inhibit differentiation by HLH-mediated heterodimerization with basic HLH transcription factors. This blocks their sequence-specific binding to DNA and activation of target genes that are often expressed in a tissue-specific manner. Id proteins can also act as positive regulators of cell proliferation. The different mechanisms proposed for Id-mediated promotion of entry into S phase also involve HLH-mediated interactions affecting regulators of the G1/S transition. We have found that Id2 augments apoptosis in both interleukin-3 (IL-3)-dependent 32D.3 myeloid progenitors and U2OS osteosarcoma cells. We could not detect a similar activity for Id3. In contrast to the effects of Id2 on differentiation and cell proliferation, Id2-mediated apoptosis is independent of HLH-mediated dimerization. The ability of Id2 to promote cell death resides in its N-terminal region and is associated with the enhanced expression of a known component of the programmed cell death pathway, the proapoptotic gene BAX.

Indexed as

ApoptosisRepressor ProteinsTranscription FactorsAnimalsBone Marrow CellsCell LineCell SurvivalDimerizationDNA-Binding ProteinsGene Expression RegulationHelix-Loop-Helix MotifsInhibitor of Differentiation Protein 2Interleukin-3KineticsMiceRecombinant ProteinsDNA-Binding ProteinsIdb2 protein, mouseInhibitor of Differentiation Protein 2Interleukin-3Recombinant ProteinsRepressor ProteinsTranscription Factors

Identifiers

PMID9710627
PMCPMC109128
OpenAlexW2144264604

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.