ArticleThe Journal of clinical investigation2017
Orphan Gpr182 suppresses ERK-mediated intestinal proliferation during regeneration and adenoma formation.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- GPR182 is a lipoprotein receptor for dietary fat absorption.The Journal of clinical investigation · 2026Article
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- Prevention and treatment of peri-implant fibrosis by functionally inhibiting skeletal cells expressing the leptin receptor.Nature biomedical engineering · 2024Article
- Development of a novel tumor microenvironment-related radiogenomics model for prognosis prediction in hepatocellular carcinoma.Quantitative imaging in medicine and surgery · 2023Article
- Atlas of the anatomical localization of atypical chemokine receptors in healthy mice.PLoS biology · 2023Article
- Suppression of CCL2 angiocrine function by adrenomedullin promotes tumor growth.The Journal of experimental medicine · 2023Article
- New pairings and deorphanization among the atypical chemokine receptor family - physiological and clinical relevance.Frontiers in immunology · 2023Review
- GPR182 is a broadly scavenging atypical chemokine receptor influencing T-independent immunity.Frontiers in immunology · 2023Article
- Atypical chemokine receptors: emerging therapeutic targets in cancer.Trends in pharmacological sciences · 2022Review
- GPR182 limits antitumor immunity via chemokine scavenging in mouse melanoma models.Nature communications · 2022Article
- GPR182 is an endothelium-specific atypical chemokine receptor that maintains hematopoietic stem cell homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Deciphering key genes in cardio-renal syndrome using network analysis.Bioinformation · 2021Article
- Article
- The Orphan G-Protein Coupled Receptor 182 Is a Negative Regulator of Definitive Hematopoiesis through Leukotriene B4 Signaling.ACS pharmacology & translational science · 2020Article
- Evidence for a direct effect of the autonomic nervous system on intestinal epithelial stem cell proliferation.Physiological reports · 2018Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Orphan GPCRs provide an opportunity to identify potential pharmacological targets, yet their expression patterns and physiological functions remain challenging to elucidate. Here, we have used a genetically engineered knockin reporter mouse to map the expression pattern of the Gpr182 during development and adulthood. We observed that Gpr182 is expressed at the crypt base throughout the small intestine, where it is enriched in crypt base columnar stem cells, one of the most active stem cell populations in the body. Gpr182 knockdown had no effect on homeostatic intestinal proliferation in vivo, but led to marked increases in proliferation during intestinal regeneration following irradiation-induced injury. In the ApcMin mouse model, which forms spontaneous intestinal adenomas, reductions in Gpr182 led to more adenomas and decreased survival. Loss of Gpr182 enhanced organoid growth efficiency ex vivo in an EGF-dependent manner. Gpr182 reduction led to increased activation of ERK1/2 in basal and challenge models, demonstrating a potential role for this orphan GPCR in regulating the proliferative capacity of the intestine. Importantly, GPR182 expression was profoundly reduced in numerous human carcinomas, including colon adenocarcinoma. Together, these results implicate Gpr182 as a negative regulator of intestinal MAPK signaling-induced proliferation, particularly during regeneration and adenoma formation.
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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.