The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.
Abnormal splicing of the leptin receptor in diabetic mice
Abstract
Mutations in the mouse diabetes (db) gene result in obesity and diabetes in a syndrome resembling morbid human obesity. Previous data suggest that the db gene encodes the receptor for the obese (ob) gene product, leptin. A leptin receptor was recently cloned from choroid plexus and shown to map to the same 6-cM interval on mouse chromosome 4 as db. This receptor maps to the same 300-kilobase interval as db, and has at least six alternatively spliced forms. One of these splice variants is expressed at a high level in the hypothalamus, and is abnormally spliced in C57BL/Ks db/db mice. The mutant protein is missing the cytoplasmic region, and is likely to be defective in signal transduction. This suggests that the weight-reducing effects of leptin may be mediated by signal transduction through a leptin receptor in the hypothalamus.
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In the citing paper
“It was subsequently shown that leptin receptor RNA was alternatively spliced and that only one of the splice variants, referred to as ObRb at the time (also known as LepR-l), was mutant in C57Bl/Ks db/db mice (25,26).”
From Leptin at 14 y of age: an ongoing story (2009) · cites this paper as [25]
In the citing paper
“ObRb is the only receptor isoform that expresses all the protein motifs required for cytokine receptor signaling.”
From Leptin at 14 y of age: an ongoing story (2009) · cites this paper as [25]
In the citing paper
“These mutant mice show an identical phenotype to animals with null mutations of the leptin receptor or leptin itself (25,26).”
From Leptin at 14 y of age: an ongoing story (2009) · cites this paper as [25]
In the citing paper
“ObRb was highly enriched in the hypothalamus in precisely those nuclei that alter body weight when lesioned (25,27).”
From Leptin at 14 y of age: an ongoing story (2009) · cites this paper as [25]
In the citing paper
“mice that lack only LepRb (e.g. db/db mice) exhibit a phenotype similar to leptin-deficient ob/ob mice (100).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [100]
In the citing paper
“Among the various isoforms of LepR, only the “long”, or “signaling” form, LepRb, appears to be competent for intracellular signal transduction and is critical for energy homeostasis.”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [100]
In the citing paper
“The absence of leptin or leptin receptors in Lepob/ob mice or Leprdb/db mice respectively, results in morbid obesity, hyperphagia, severe hyperglycemia and insulin resistance, and marked hypoactivity (Chen et al., 1996; Coleman, 1978; Lee et al., 1996; Pelleymounter et al., 1995; Tartaglia et al., 1995; Zhang et al., 1994).”
From Leptin-Dependent Control of Glucose Balance and Locomotor Activity by POMC Neurons (2009) · cites this paper as Lee et al., 1996
Citations
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Cited by
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A model for modulation of leptin activity by association with clusterin
Bajari, T. M., Strasser, V., Nimpf, J., & Schneider, W. J. (2003) · The FASEB Journal · doi:10.1096/fj.02-1106fje · Cited by 45
Leptin as a Potential Treatment for Obesity: Progress to Date
Bell-Anderson, K. S., & Bryson, J. M. (2004) · Treatments in Endocrinology · doi:10.2165/00024677-200403010-00002 · Cited by 36
Shimabukuro, M. (2017) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.ed083 · Cited by 34
Robertson, S., Ishida-Takahashi, R., Tawara, I., Hu, J., Patterson, C. M., Jones, J. C., Kulkarni, R. N., & Myers, M. G. (2010) · Diabetes · doi:10.2337/db09-1556 · Cited by 30
ANGPTL4 binds to the leptin receptor to regulate ectopic bone formation
Hu, H., Luo, S., Lai, P., Lai, M., Mao, L., Zhang, S., Jiang, Y., Wen, J., Zhou, W., Liu, X., et al. (2024) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2310685120 · Cited by 18
Elmquist (1998) · doi:10.1002/(sici)1096-9861(19980615)395:4
Metadata
- Authors
- Lee, G.-H., Proenca, R., Montez, J. M., Carroll, K. M., Darvishzadeh, J. G., Lee, J. I., & Friedman, J. M.
- Affiliations
- Howard Hughes Medical Institute (US)
- Rockefeller University (US)
- ORCID
- Friedman, J. M.
- Venue
- Nature
- Published
- 1996-02
- Volume
- 379
- Issue
- 6566
- Pages
- 632-635
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2016994959
- Cited by
- 2,327
- References
- 27
- Citations by year
- 2026: 12 · 2025: 22 · 2024: 17 · 2023: 20 · 2022: 36 · 2021: 46 · 2020: 35 · 2019: 47 · 2018: 38 · 2017: 46 · 2016: 58 · 2015: 62 · 2014: 88 · 2013: 88 · 2012: 83
- FWCI
- 56.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Keywords
- leptin receptor, alternative splicing, db/db mice, obesity, leptin, signal transduction, hypothalamus, obesity-related genes, chromosome 4, cytoplasmic domain, body weight regulation
- MeSH terms
- Amino Acid Sequence, Animals, Base Sequence, Carrier Proteins, Chromosome Mapping, Diabetes Mellitus, Experimental, Mice, Inbred C57BL, Molecular Sequence Data, Mutation, Proteins, Receptors, Cell Surface, Tissue Distribution, Polymerase Chain Reaction, Alternative Splicing, DNA Primers, Leptin, Mice, Receptors, Leptin
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