ArticleMolecular endocrinology (Baltimore, Md.)2012
Evidence of the importance of the first intracellular loop of prokineticin receptor 2 in receptor function.
Article in Molecular endocrinology (Baltimore, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Genetic Polymorphisms of Prokineticins and Prokineticin Receptors Associated with Human Disease.Life (Basel, Switzerland) · 2024Review
- Additional mutation inBMJ case reports · 2024Article
- Phenotypic and genotypic landscape of PROKR2 in neuroendocrine disorders.Frontiers in endocrinology · 2023Review
- Chimeric GPCRs mimic distinct signaling pathways and modulate microglia responses.Nature communications · 2022Article
- Trafficking-defective mutant PROKR2 cycles between endoplasmic reticulum and Golgi to attenuate endoplasmic reticulum stress.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Prokineticin-Receptor Network: Mechanisms of Regulation.Life (Basel, Switzerland) · 2022Review
- The Clinical and Genetic Characteristics in Children with Idiopathic Hypogonadotropin Hypogonadism.Journal of oncology · 2022Article
- Genetics of congenital hypogonadotropic hypogonadism: peculiarities and phenotype of an oligogenic disease.Human genetics · 2021Review
- Biased signaling in naturally occurring mutations of G protein-coupled receptors associated with diverse human diseases.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- Evidence for a Common Genetic Origin of Classic and Milder Adult-Onset Forms of Isolated Hypogonadotropic Hypogonadism.Journal of clinical medicine · 2019Article
- Modeling mutant/wild-type interactions to ascertain pathogenicity of PROKR2 missense variants in patients with isolated GnRH deficiency.Human molecular genetics · 2018Article
- Sexually dimorphic distribution of Prokr2 neurons revealed by the Prokr2-Cre mouse model.Brain structure & function · 2017Article
- Article
- Digenic Inheritance of PROKR2 and WDR11 Mutations in Pituitary Stalk Interruption Syndrome.The Journal of clinical endocrinology and metabolism · 2017Review
- Tac1 Signaling Is Required for Sexual Maturation and Responsiveness of GnRH Neurons to Kisspeptin in the Male Mouse.Endocrinology · 2017Article
- Genetics of Combined Pituitary Hormone Deficiency: Roadmap into the Genome Era.Endocrine reviews · 2016Review
- Computational Analysis of Missense Variants of G Protein-Coupled Receptors Involved in the Neuroendocrine Regulation of Reproduction.Neuroendocrinology · 2016Article
- FGFR1 and PROKR2 rare variants found in patients with combined pituitary hormone deficiencies.Endocrine connections · 2015Article
- Fertility and fragrance: another cause of Kallmann syndrome.The Journal of clinical investigation · 2015Article
- Prokineticin receptor identified by phage display is an entry receptor for Trypanosoma cruzi into mammalian cells.Parasitology research · 2015Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Prokineticin receptors (PROKR) are G protein-coupled receptors (GPCR) that regulate diverse biological processes, including olfactory bulb neurogenesis and GnRH neuronal migration. Mutations in PROKR2 have been described in patients with varying degrees of GnRH deficiency and are located in diverse functional domains of the receptor. Our goal was to determine whether variants in the first intracellular loop (ICL1) of PROKR2 (R80C, R85C, and R85H) identified in patients with hypogonadotropic hypogonadism interfere with receptor function and to elucidate the mechanisms of these effects. Because of structural homology among GPCR, clarification of the role of ICL1 in PROKR2 activity may contribute to a better understanding of this domain across other GPCR. The effects of the ICL1 PROKR2 mutations on activation of signal transduction pathways, ligand binding, and receptor expression were evaluated. Our results indicated that the R85C and R85H PROKR2 mutations interfere only modestly with receptor function, whereas the R80C PROKR2 mutation leads to a marked reduction in receptor activity. Cotransfection of wild-type (WT) and R80C PROKR2 showed that the R80C mutant could exert a dominant negative effect on WT PROKR2 in vitro by interfering with WT receptor expression. In summary, we have shown the importance of Arg80 in ICL1 for PROKR2 expression and demonstrate that R80C PROKR2 exerts a dominant negative effect on WT PROKR2.
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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.