ArticleEndocrinology2011
KISS1R intracellular trafficking and degradation: effect of the Arg386Pro disease-associated mutation.
Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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.
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Who cites it
28 citing papers in PubMed, 75 citations in OpenAlex.
- Dynamic modulation of LH secretion by continuous kisspeptin infusion in healthy men.Hormones (Athens, Greece) · 2026Article
- Investigation of Radiolabeled KISS1R Ligands as Promising Tools for Diagnosis and Treatment of Triple-Negative Breast Cancer.Molecular pharmaceutics · 2026Article
- Disorders of puberty and neurodevelopment: A shared etiology?Annals of the New York Academy of Sciences · 2024Review
- The Emerging Therapeutic Potential of Kisspeptin and Neurokinin B.Endocrine reviews · 2024Review
- [Gonadotropin-dependent precocious puberty: genetic and clinical characteristics].Problemy endokrinologii · 2023Article
- Effect of CPP-related genes on GnRH secretion and Notch signaling pathway during puberty.Biomedical journal · 2023Review
- Molecular basis of normal and pathological puberty: from basic mechanisms to clinical implications.The lancet. Diabetes & endocrinology · 2023Review
- Genetics of pubertal timing.Best practice & research. Clinical endocrinology & metabolism · 2022Review
- Genetic, epigenetic and enviromental influencing factors on the regulation of precocious and delayed puberty.Frontiers in endocrinology · 2022Review
- A review of the genetics and epigenetics of central precocious puberty.Frontiers in endocrinology · 2022Review
- Kisspeptin Receptor on the Sperm Surface Reflects Epididymal Maturation in the Dog.International journal of molecular sciences · 2021Article
- GENETICS IN ENDOCRINOLOGY: Genetic etiologies of central precocious puberty and the role of imprinted genes.European journal of endocrinology · 2020Review
- 14-3-3 signal adaptor and scaffold proteins mediate GPCR trafficking.Scientific reports · 2019Article
- The matrix protein Fibulin-3 promotes KISS1R induced triple negative breast cancer cell invasion.Oncotarget · 2018Article
- G protein-coupled KISS1 receptor is overexpressed in triple negative breast cancer and promotes drug resistance.Scientific reports · 2017Article
- An update on the genetic causes of central precocious puberty.Annals of pediatric endocrinology & metabolism · 2016Review
- RF9 Acts as a KISS1R Agonist In Vivo and In Vitro.Endocrinology · 2015Article
- Minireview: Spatial Programming of G Protein-Coupled Receptor Activity: Decoding Signaling in Health and Disease.Molecular endocrinology (Baltimore, Md.) · 2015Review
- KISS1R signals independently of Gαq/11 and triggers LH secretion via the β-arrestin pathway in the male mouse.Endocrinology · 2014Article
- Dynamic kisspeptin receptor trafficking modulates kisspeptin-mediated calcium signaling.Molecular endocrinology (Baltimore, Md.) · 2014Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
The goal of this study was to investigate how the Arg386Pro mutation prolongs KiSS-1 receptor (KISS1R) responsiveness to kisspeptin, contributing to human central precocious puberty. Confocal imaging showed colocalization of wild-type (WT) KISS1R with a membrane marker, which persisted for up to 5 h of stimulation. Conversely, no colocalization with a lysosome marker was detected. Also, overnight treatment with a lysosome inhibitor did not affect WT KISS1R protein, whereas overnight treatment with a proteasome inhibitor increased protein levels by 24-fold. WT and Arg386Pro KISS1R showed time-dependent internalization upon stimulation. However, both receptors were recycled back to the membrane. The Arg386Pro mutation did not affect the relative distribution of KISS1R in membrane and internalized fractions when compared to WT KISS1R for up to 120 min of stimulation, demonstrating that this mutation does not affect KISS1R trafficking rate. Nonetheless, total Arg386Pro KISS1R was substantially increased compared with WT after 120 min of kisspeptin stimulation. This net increase was eliminated by blockade of detection of recycled receptors, demonstrating that recycled receptors account for the increased responsiveness of this mutant to kisspeptin. We therefore conclude the following: 1) WT KISS1R is degraded by proteasomes rather than lysosomes; 2) WT and Arg386Pro KISS1R are internalized upon stimulation, but most of the internalized receptors are recycled back to the membrane rather than degraded; 3) the Arg386Pro mutation does not affect the rate of KISS1R trafficking--instead, it prolongs responsiveness to kisspeptin by decreasing KISS1R degradation, resulting in the net increase on mutant receptor recycled back to the plasma membrane.
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What OpenQuestion holds
Registered trials
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.