Evidence map›Paper›PMID 8182138›Full record

ArticleThe Journal of clinical investigation1994

Expression of the mouse corticotropin-releasing hormone gene in vivo and targeted inactivation in embryonic stem cells.

L J Muglia, N A Jenkins, D J Gilbert, N G Copeland, J A Majzoub

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.0field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 113 citations in OpenAlex.

  1. Article
  2. Review
  3. Neuroendocrine control of appetite and metabolism.Experimental & molecular medicine · 2021
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Corticotropin-releasing factor signaling and visceral response to stress.Experimental biology and medicine (Maywood, N.J.) · 2010
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Corticotropin-releasing hormone (CRH) requirement in Clostridium difficile toxin A-mediated intestinal inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  14. Review
  15. Article
  16. Mortality in 7B2 null mice can be rescued by adrenalectomy: involvement of dopamine in ACTH hypersecretion.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  17. Article
  18. Article
  19. Altered stress-induced anxiety in adenylyl cyclase type VIII-deficient mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000
    Article
  20. Circadian rise in maternal glucocorticoid prevents pulmonary dysplasia in fetal mice with adrenal insufficiency.Proceedings of the National Academy of Sciences of the United States of America · 2000
    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

5 authors at 2 institutions in 1 country.

L J MugliaDivision of Endocrinology, Children's Hospital, Boston, Massachusetts 02115.
N A Jenkins
D J Gilbert
N G Copeland
J A Majzoub
National Cancer Institute · USBoston Children's Hospital · US

Funding

PROVIDE BASIC CANCER RESEARCHN01CO074101 · CO · ADVANCED BIOSCIENCE LABORATORIES, INC. · PI VANDE WOUDE, GEORGE F · 1987 to 1994
–
NCI NIH HHS N01-CO-74101
6 · The paper itself

Abstract

Corticotropin-releasing hormone (CRH), one of the primary regulators of the hypothalamic-pituitary-adrenal (HPA) axis, exhibits abnormal regulation in pathologic states such as depression and anorexia nervosa. Analysis of the role of CRH in regulation of the HPA axis would be facilitated by the creation of animal models in which CRH gene structure and function could be manipulated. We have determined the DNA sequence of the mouse CRH gene. Using a highly sensitive reverse transcription-polymerase chain reaction method, we have found expression of CRH mRNA in adrenal, ovary, testis, gut, heart, anterior pituitary, lung, and spleen, in addition to cerebral cortex and hypothalamus. Within the spleen, CRH mRNA is localized specifically to T-lymphocytes. We mapped the chromosomal location of mouse CRH via interspecific mouse backcrosses to chromosome 3, which is not the site of any naturally occurring mutations consistent with CRH deficiency. Because of this, we inactivated a CRH allele in mouse embryonic stem (ES) cells by homologous recombination with a mutant mouse CRH gene lacking the entire coding region of preproCRH. Mice chimeric for each of two ES clones with an inactivated CRH allele are being used to generate animals with complete CRH deficiency.

Indexed as

MutationAnimalsBase SequenceChimeraChromosome MappingCloning, MolecularCorticotropin-Releasing HormoneCrosses, GeneticFemaleGene Expression RegulationMaleMiceMice, Inbred BALB CMice, Inbred C57BLMolecular Sequence DataPolymerase Chain ReactionCorticotropin-Releasing HormoneRNA, Messenger

Identifiers

PMID8182138
PMCPMC294325
OpenAlexW2156629452

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.