Evidence map›Paper›PMID 16166378›Full record

ArticleGenes & development2005

A c-Rel subdomain responsible for enhanced DNA-binding affinity and selective gene activation.

Shomyseh Sanjabi, Kevin J Williams, Simona Saccani, Liang Zhou, Alexander Hoffmann, Gourisankar Ghosh, Steve Gerondakis, Gioacchino Natoli, Stephen T Smale

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
–field-weighted citation impact
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

80 citing papers in PubMed, 128 citations in OpenAlex.

  1. Trial
  2. Article
  3. Fungal Infections in Disorders of Inborn Errors of Immunity.Clinical reviews in allergy & immunology · 2026
    Review
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  5. Article
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  9. Transcriptional repression by HDAC3 mediates T cell exclusion fromProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Article
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  12. Article
  13. Transient interactions modulate the affinity of NF-κB transcription factors for DNA.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

20 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

9 authors at 4 institutions in 2 countries.

Shomyseh SanjabiHoward Hughes Medical Institute, Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, CA 90095-1662, USA.
Kevin J Williams
Simona Saccani
Liang Zhou
Alexander Hoffmann
Gourisankar Ghosh
Steve Gerondakis
Gioacchino Natoli
Stephen T Smale
University of California, San Diego · USUniversity of California, Los Angeles · USCalifornia Institute of Technology · USHoward Hughes Medical Institute · US

Funding

UCLA Tumor Immunology Training ProgramT32CA009120 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Steven M. Dubinett, MICHAEL A TEITELL · 1985 to 2026
$10.3M
MULTIDISCIPLINARY TRAINING IN MICROBIAL PATHOGENESIST32AI007323 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Peter John Bradley · 1988 to 2026
$8.6M
NCI NIH HHS T32 CA009120NCI NIH HHS T32-CA09120NIAID NIH HHS T32 AI007323NIAID NIH HHS T32-AI07323
6 · The paper itself

Abstract

The NF-kappaB family members p65 (RelA) and c-Rel recognize similar DNA sequences, yet the phenotypes of mutant mice suggest that these proteins regulate distinct sets of genes. Here we demonstrate that 46 unique residues within an 86-residue segment of the Rel homology region (RHR) of c-Rel are responsible for the c-Rel requirement for Il12b gene induction by lipopolysaccharide in bone marrow-derived macrophages. These same residues were responsible for the c-Rel requirement for Il12a induction in dendritic cells, and in both instances, no evidence of c-Rel-specific coactivator interactions was found. Although the residues of c-Rel and p65 that contact specific bases and the DNA backbone within nuclear factor-kappaB (NF-kappaB) recognition sequences are identical, homodimers of c-Rel and of a chimeric p65 protein containing the critical c-Rel residues bound with high affinity to a broader range of NF-kappaB recognition sequences than did wild-type p65 homodimers. These results demonstrate that the unique functions of closely related transcription factor family members can be dictated by differences in the range of DNA sequences recognized at high affinity, despite having similar binding site consensus sequences and DNA contact residues.

Indexed as

Gene Expression RegulationGenes, relAmino Acid SequenceAnimalsBinding SitesConserved SequenceDendritic CellsDNAInterferon-gammaLipopolysaccharidesLysineMacrophagesMiceMice, Mutant StrainsModels, MolecularMolecular Sequence DataDNAInterferon-gammaLipopolysaccharidesLysineNF-kappa BProto-Oncogene Proteins c-relRecombinant Fusion ProteinsTranscription Factor RelA

Identifiers

PMID16166378
PMCPMC1221885
OpenAlexW2148027060

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.