Evidence map›Paper›PMID 16782820›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Inactivation of cardiotrophin-like cytokine, a second ligand for ciliary neurotrophic factor receptor, leads to cold-induced sweating syndrome in a patient.

François Rousseau, Jean-François Gauchat, James G McLeod, Sylvie Chevalier, Catherine Guillet, Florence Guilhot, Isabelle Cognet, Josy Froger, Angelika F Hahn, Per M Knappskog and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
0.5field-weighted citation impact, top 46% 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

29 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. CRLF1 and CLCF1 in Development, Health and Disease.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. Inborn errors of IL-6 family cytokine responses.Current opinion in immunology · 2021
    Review
  12. CRLF1 Is a Key Regulator in the Ligamentum Flavum Hypertrophy.Frontiers in cell and developmental biology · 2020
    Article
  13. Article
  14. Interleukin-6 Family Cytokines.Cold Spring Harbor perspectives in biology · 2018
    Review
  15. Article
  16. Article
  17. Article
  18. Unusual Stüve-Wiedemann syndrome with complete maternal chromosome 5 isodisomy.Annals of clinical and translational neurology · 2014
    Article
  19. Review
  20. 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

12 authors at 6 institutions in 4 countries.

François RousseauInstitut National de la Santé et de la Recherche Médicale U564, F-49033 Angers, France.
Jean-François Gauchat
James G McLeod
Sylvie Chevalier
Catherine Guillet
Florence Guilhot
Isabelle Cognet
Josy Froger
Angelika F Hahn
Per M Knappskog
Hugues Gascan
Helge Boman
Inserm · FRUniversité de Montréal · CAHaukeland University Hospital · NOUniversity of Bergen · NOUniversity of Sydney · AUWestern University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ciliary neurotrophic factor (CNTF) receptor controls a pathway supporting the differentiation and survival of a wide range of neural cell types during development and in adulthood. Cardiotrophin-like cytokine (CLC)-cytokine-like factor 1 (CLF) composite cytokine is a second ligand for the CNTF alpha-component receptor (CNTFRalpha). This composite cytokine is built on the structural model of IL-12, with a complex formed by a four-helix bundle type I cytokine, CLC (also referred to as CLCF1), bound to a soluble receptor subunit, CLF (also known as CRLF1). We have reported mutations in the chaperone soluble receptor CLF, causing cold-induced sweating syndrome (CISS). In this study, we studied the CLC-mutated alleles in a patient suffering from a similar disease. This patient was compound heterozygous for two different CLC mutations. The first allele was inactivated by a stop codon at position 107 (Y107X). In the second allele, a R197L mutation in the CLC-predicted binding site to the CNTFRalpha was detected. Functional analysis of the mutated protein revealed an incapacity for R197L CLC to bind to CNTFRalpha and activate the subsequent signaling events. Structural and docking interaction studies showed that the R197L substitution destabilized the contact site between CLC and CNTFRalpha.

Indexed as

Cold TemperatureAllelesAmino Acid SequenceAmino Acid SubstitutionArginineCodon, TerminatorCytokinesHumansHyperhidrosisLigandsMaleMiddle AgedMolecular Sequence DataMutationReceptor, Ciliary Neurotrophic FactorSweatingArgininecardiotrophin-like cytokineCodon, TerminatorCytokinesLigandsReceptor, Ciliary Neurotrophic Factor

Identifiers

PMID16782820
PMCPMC1502507
OpenAlexW2117732828

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.