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Cited by 536

The DOI matches its Crossref record.

A Deletion Truncating the Gonadotropin-Releasing Hormone Gene Is Responsible for Hypogonadism in the hpg Mouse

Mason, Anthony J., Hayflick, Joel S., Zoeller, R. Thomas, Young, W. Scott, Phillips, Heidi S., Nikolics, Karoly, Seeburg, Peter H.·1986·Science
DOI 10.1126/science.3024317
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Abstract

Hereditary hypogonadism in the hypogonadal ( hpg ) mouse is caused by a deletional mutation of at least 33.5 kilobases encompassing the distal half of the gene for the common biosynthetic precursor of gonadotropin-releasing hormone (GnRH) and GnRH-associated peptide (GAP). The partially deleted gene is transcriptionally active as revealed by in situ hybridization histochemistry of hpg hypothalamic tissue sections, but immunocytochemical analysis failed to show the presence of antigen corresponding to any part of the precursor protein.

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Metadata

Authors
Mason, A. J., Hayflick, J. S., Zoeller, R. T., Young, W. S., Phillips, H. S., Nikolics, K., & Seeburg, P. H.
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
1986-12-12
Volume
234
Issue
4782
Pages
1366-1371
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
DOI
10.1126/science.3024317
OpenAlex
W2091095324
Cited by
536
References
0
FWCI
13.19
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: A Deletion Truncating the Gonadotropin-Releasing Hormone Gene Is Responsible for Hypogonadism in the hpg Mouse. https://app.cochat.ai/papers/10.1126/science.3024317
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Mason, A. J., Hayflick, J. S., Zoeller, R. T., Young, W. S., Phillips, H. S., Nikolics, K., & Seeburg, P. H. (1986). A Deletion Truncating the Gonadotropin-Releasing Hormone Gene Is Responsible for Hypogonadism in the hpg Mouse. Science. https://doi.org/10.1126/science.3024317

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.