The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Evidence That the Diabetes Gene Encodes the Leptin Receptor: Identification of a Mutation in the Leptin Receptor Gene in db/db Mice
Open accessAbstract
OB-R is a high affinity receptor for leptin, an important circulating signal for the regulation of body weight. We identified an alternatively spliced transcript that encodes a form of mouse OB-R with a long intracellular domain. db/db mice also produce this alternatively spliced transcript, but with a 106 nt insertion that prematurely terminates the intracellular domain. We further identified G --> T point mutation in the genomic OB-R sequence in db/db mice. This mutation generates a donor splice site that converts the 106 nt region to a novel exon retained in the OB-R transcript. We predict that the long intracellular domain form of OB-R is crucial for initiating intracellular signal transduction, and as a corollary, the inability to produce this form of OB-R leads to the severe obese phenotype found in db/db mice.
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“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 [26]
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 [26]
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 Chen et al., 1996
Citations
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Metadata
- Authors
- Chen, H., Charlat, O., Tartaglia, L. A., Woolf, E. A., Weng, X., Ellis, S. J., Lakey, N. D., Culpepper, J., More, K. J., Breitbart, R. E., Duyk, G. M., Tepper, R. I., & Morgenstern, J. P.
- Affiliations
- Takeda Oncology (United States) (US)
- Corresponding author
- Tartaglia, Louis A
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1996-02
- Volume
- 84
- Issue
- 3
- Pages
- 491-495
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2051192888
- Cited by
- 2,214
- References
- 17
- Citations by year
- 2026: 16 · 2025: 42 · 2024: 42 · 2023: 46 · 2022: 44 · 2021: 68 · 2020: 54 · 2019: 62 · 2018: 69 · 2017: 75 · 2016: 66 · 2015: 69 · 2014: 95 · 2013: 96 · 2012: 89
- FWCI
- 42.43
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (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, db/db mice, alternative splicing, splice site mutation, obesity, signal transduction, leptin
- MeSH terms
- Amino Acid Sequence, Animals, Base Sequence, Carrier Proteins, Diabetes Mellitus, Type 1, Humans, Mice, Inbred Strains, Mice, Obese, Molecular Sequence Data, Obesity, Phenotype, Proteins, Receptors, Cell Surface, Signal Transduction, Polymerase Chain Reaction, Point Mutation, Sequence Homology, Amino Acid, Alternative Splicing, DNA Primers, DNA, Complementary, Receptors, Cytokine, Leptin, Mice, Receptors, Leptin
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