Evidence map›Paper›PMID 21862594›Full record

ArticleThe Journal of biological chemistry2011

Molecular mechanisms for synchronized transcription of three complement C1q subunit genes in dendritic cells and macrophages.

Guobao Chen, Carol Shurong Tan, Boon King Teh, Jinhua Lu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 31% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Targeting C1q signaling in fibro-adipogenic progenitors prevents regenerative fibrosis of aged muscle.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
  6. Article
  7. C1qAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  8. Article
  9. Article
  10. BIN1Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  11. Complement C1q is a key player in tumor-associated macrophage-mediated CD8International journal of biological sciences · 2024
    Article
  12. Causal relationship between complementFrontiers in genetics · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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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

4 authors at 1 institution in 1 country.

Guobao ChenDepartment of Microbiology, Yong Loo Lin School of Medicine and Immunology Programme, National University of Singapore, Block MD4, 5 Science Drive 2, Singapore 117597.
Carol Shurong Tan
Boon King Teh
Jinhua Lu
National University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hereditary homozygous C1q deficiency is rare, but it almost certainly causes systemic lupus erythematosus. On the other hand, C1q levels can decline in systemic lupus erythematosus patients without apparent C1q gene defects and the versatility in C1q production is a likely cause. As an 18-subunit protein, C1q is assembled in a 1:1:1 ratio from three different subunits. The three human C1q genes are closely bundled on chromosome 1 (C1qA-C1qC-C1qB) and their basal and IFNγ-stimulated expression, largely restricted to macrophages and dendritic cells, is apparently synchronized. We cloned the three gene promoters and observed that although the C1qB promoter exhibited basal and IFNγ-stimulated activities consistent with the endogenous C1qB gene, the activities of the cloned C1qA and C1qC promoters were suppressed by IFNγ. To certain extents, these were corrected when the C1qB promoter was cloned at the 3' end across the luciferase reporter gene. A 53-bp element is essential to the activities of the C1qB promoter and the transcription factors PU.1 and IRF8 bound to this region. By chromatin immunoprecipitation, the C1qB promoter was co-precipitated with PU.1 and IRF8. shRNA knockdown of PU.1 and IRF8 diminished C1qB promoter response to IFNγ. STAT1 instead regulated C1qB promoter through IRF8 induction. Collectively, our results reveal a novel transcriptional mechanism by which the expression of the three C1q genes is synchronized.

Indexed as

Transcription, GeneticAnimalsBase SequenceComplement C1qDendritic CellsGene Expression RegulationHomozygoteHumansInterferon-gammaInterferon Regulatory Factor-8Interferon Regulatory FactorsMacrophagesMiceMolecular Sequence DataMutagenesisProto-Oncogene ProteinsComplement C1qInterferon-gammaInterferon Regulatory Factor-8Interferon Regulatory FactorsProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-Activators

Identifiers

PMID21862594
PMCPMC3186423
OpenAlexW2015684766

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.