Evidence map›Paper›PMID 18162518›Full record

ArticleEndocrinology2008

Shared and unique susceptibility genes in a mouse model of Graves' disease determined in BXH and CXB recombinant inbred mice.

Sandra M McLachlan, Holly A Aliesky, Pavel N Pichurin, Chun-Rong Chen, Robert W Williams, Basil Rapoport

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Acyloxyacyl hydrolase modulates pelvic pain severity.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  4. Article
  5. Article
  6. Sex, genetics, and the control of thyroxine and thyrotropin in mice.Thyroid : official journal of the American Thyroid Association · 2014
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

6 authors at 3 institutions in 1 country.

Sandra M McLachlanAutoimmune Disease Unit, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. mclachlans@cshs.org
Holly A Aliesky
Pavel N Pichurin
Chun-Rong Chen
Robert W Williams
Basil Rapoport
University of California, Los Angeles · USCedars-Sinai Medical Center · USUniversity of Tennessee Health Science Center · US

Funding

THYROTROPIN RECEPTOR IN HEALTH AND DISEASER01DK019289 · NIDDK · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI RAPOPORT, BASIL · 1986 to 2014
$6.1M
MODULATION OF AN ANIMAL MODEL OF HYPERTHYROIDISMR01DK054684 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI MCLACHLAN, SANDRA M · 1999 to 2017
$5.6M
Informatics Center for Mouse NeurogeneticsP20DA021131 · NIDA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WILLIAMS, ROBERT W. · 2005 to 2009
$5.0M
Systems Genetics of Alcohol Response and Stress Effects in CNSU01AA013499 · NIAAA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WILLIAMS, ROBERT W. · 2002 to 2016
$4.8M
NIAAA NIH HHS U01 AA013499NIAAA NIH HHS U01 AA 13499NIDA NIH HHS P20 DA021131NIDA NIH HHS P20 DA 21131NIDDK NIH HHS DK 19289NIDDK NIH HHS DK 54684NIDDK NIH HHS R01 DK019289NIDDK NIH HHS R01 DK054684
6 · The paper itself

Abstract

Susceptibility genes for TSH receptor (TSHR) antibodies and hyperthyroidism can be probed in recombinant inbred (RI) mice immunized with adenovirus expressing the TSHR A-subunit. The RI set of CXB strains, derived from susceptible BALB/c and resistant C57BL/6 (B6) mice, were studied previously. High-resolution genetic maps are also available for RI BXH strains, derived from B6 and C3H/He parents. We found that C3H/He mice develop TSHR antibodies, and some animals become hyperthyroid after A-subunit immunization. In contrast, the responses of the F1 progeny of C3H/He x B6 mice, as well as most BXH RI strains, are dominated by the B6 resistance to hyperthyroidism. As in the CXB set, linkage analysis of BXH strains implicates different chromosomes (Chr) or loci in the susceptibility to induced TSHR antibodies vs. hyperthyroidism. Importantly, BXH and CXB mice share genetic loci controlling the generation of TSHR antibodies (Chr 17, major histocompatibility complex region, and Chr X) and development of hyperthyroidism (Chr 1 and 3). Moreover, some chromosomal linkages are unique to either BXH or CXB strains. An interesting candidate gene linked to thyroid-stimulating antibody generation in BXH mice is the Ig heavy chain locus, suggesting a role for particular germline region genes as precursors for these antibodies. In conclusion, our findings reinforce the importance of major histocompatibility complex region genes in controlling the generation of TSHR antibodies measured by TSH binding inhibition. Moreover, these data emphasize the value of RI strains to dissect the genetic basis for induced TSHR antibodies vs. their effects on thyroid function in Graves' disease.

Indexed as

Genetic Predisposition to DiseaseAnimalsAutoantibodiesGenetic LinkageGraves DiseaseHyperthyroidismImmunoglobulins, Thyroid-StimulatingMajor Histocompatibility ComplexMiceMice, Inbred C3HMice, Inbred C57BLQuantitative Trait LociRecombination, GeneticX ChromosomeAutoantibodiesImmunoglobulins, Thyroid-Stimulatingthyrotropin-binding inhibitory immunoglobulin

Identifiers

PMID18162518
PMCPMC2276708
OpenAlexW2104587770

What OpenQuestion holds

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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.