ArticleJournal of molecular graphics & modelling2024
GPR101: Modeling a constitutively active receptor linked to X-linked acrogigantism.
Article in Journal of molecular graphics & modelling, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Comparing models and experimental structures of the GPR101 receptor: Artificial intelligence yields highly accurate models.Journal of molecular graphics & modelling · 2025Article
- Chromatin conformation capture in the clinic: 4C-seq/HiC distinguishes pathogenic from neutral duplications at the GPR101 locus.Genome medicine · 2024Article
- Unlocking the Genetic Secrets of Acromegaly: Exploring the Role of Genetics in a Rare Disorder.Current issues in molecular biology · 2024Review
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
GPR101 is a G protein-coupled receptor (GPCR) implicated in a rare form of genetic gigantism known as X-linked acrogigantism, or X-LAG. In particular, X-LAG patients harbor microduplications in the long arm of the X-chromosome that invariably include the GPR101 gene. Duplications of the GPR101 gene lead to the formation of a new chromatin domain that causes over-expression of the receptor in the pituitary tumors of the patients. Notably, GPR101 is a constitutively active receptor, which stimulates cells to produce the second messenger cyclic AMP (cAMP) in the absence of ligands. Moreover, GPR101 was recently reported to constitutively activate not only the cAMP pathway via G
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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.