ArticleJournal of proteome research2020
Quantitative Proteomics Reveal an Altered Pattern of Protein Expression in Brain Tissue from Mice Lacking GPR37 and GPR37L1.
Article in Journal of proteome research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 14 citations in OpenAlex.
- Role and regulatory mechanism of GPR37 in neurological diseases.Frontiers in cellular neuroscience · 2025Review
- Mapping dynamic molecular changes in hippocampal subregions after traumatic brain injury through spatial proteomics.Clinical proteomics · 2024Article
- GPR37 and its neuroprotective mechanisms: bridging osteocalcin signaling and brain function.Frontiers in cell and developmental biology · 2024Review
- Orphan G Protein-Coupled Receptor GPR37 as an Emerging Therapeutic Target.ACS chemical neuroscience · 2023Review
- Article
- Impaired Aversive Memory Formation in GPR37L1KO Mice.International journal of molecular sciences · 2022Article
- Mouse Mutants ofInternational journal of molecular sciences · 2022Review
- The Effect of Early Life Stress on Emotional Behaviors in GPR37KO Mice.International journal of molecular sciences · 2021Article
- GM1 Is Cytoprotective in GPR37-Expressing Cells and Downregulates Signaling.International journal of molecular sciences · 2021Article
- Combined Inhibition of AKT and KIT Restores Expression of Programmed Cell Death 4 (PDCD4) in Gastrointestinal Stromal Tumor.Cancers · 2021Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
GPR37 and GPR37L1 are glia-enriched G protein-coupled receptors that have been implicated in several neurological and neurodegenerative diseases. To gain insight into the potential molecular mechanisms by which GPR37 and GPR37L1 regulate cellular physiology, proteomic analyses of whole mouse brain tissue from wild-type (WT) versus GPR37/GPR37L1 double knockout (DKO) mice were performed in order to identify proteins regulated by the absence versus presence of these receptors (data are available via ProteomeXchange with identifier PXD015202). These analyses revealed a number of proteins that were significantly increased or decreased by the absence of GPR37 and GPR37L1. One of the most decreased proteins in the DKO versus WT brain tissue was S100A5, a calcium-binding protein, and the reduction of S100A5 expression in KO brain tissue was validated via Western blot. Coexpression of S100A5 with either GPR37 or GPR37L1 in HEK293T cells did not result in any change in S100A5 expression but did robustly increase secretion of S100A5. To dissect the mechanism by which S100A5 secretion was enhanced, cells coexpressing S100A5 with the receptors were treated with different pharmacological reagents. These studies revealed that calcium is essential for the secretion of S100A5 downstream of GPR37 and GPR37L1 signaling, as treatment with BAPTA-AM, an intracellular Ca
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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.