ArticleCell discovery2020
RGS12 is required for the maintenance of mitochondrial function during skeletal development.
Article in Cell discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
The trial behind it
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Who cites it
11 citing papers in PubMed, 63 citations in OpenAlex.
- Comprehensive Lipidomic Profiling Reveals Distinct Metabolic Remodeling during Differentiation of Human Monocyte-Derived Macrophages.Journal of proteome research · 2026Article
- Vertebral BMSC-EVs under estrogen deficiency drive senescence-related mitochondrial dysfunction in endplate chondrocytes via MRPL1 mRNA delivery.Experimental & molecular medicine · 2026Article
- Role of RGS12 in placental mitochondrial dysfunction and adverse pregnancy outcomes.Cellular and molecular life sciences : CMLS · 2026Article
- The role of RGS12 in tissue repair and human diseases.Genes & diseases · 2025Review
- Regulator of G protein signaling 12 drives inflammatory arthritis by activating synovial fibroblasts through MYCBP2/KIF2A signaling.Molecular therapy. Nucleic acids · 2023Article
- The Potential Role of R4 Regulators of G Protein Signaling (RGS) Proteins in Type 2 Diabetes Mellitus.Cells · 2022Review
- Macrophage RGS12 contributes to osteoarthritis pathogenesis through enhancing the ubiquitination.Genes & diseases · 2022Article
- RGS12 Drives Macrophage Activation and Osteoclastogenesis in Periodontitis.Journal of dental research · 2022Article
- Effect of Regulator of G Protein Signaling Proteins on Bone.Frontiers in endocrinology · 2022Review
- RGS12 Represses Oral Cancer via the Phosphorylation and SUMOylation of PTEN.Journal of dental research · 2021Article
- Macrophage regulator of G-protein signaling 12 contributes to inflammatory pain hypersensitivity.Annals of translational medicine · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial morphology and function are crucial for tissue homeostasis, such as for skeletal development, but the cellular and molecular mechanisms remain unclear. Here, we provide evidence that regulator of G-protein signaling 12 (RGS12) is present in the mitochondria of primary chondrocytes and cartilage tissues. Deletion of RGS12 in type II collagen-positive cells led to a significant decrease in mitochondrial number, membrane potential, and oxidative phosphorylation function. Mechanistically, RGS12 promoted the function of ATP5A as an enhancer of tyrosine phosphorylation. Mice with RGS12 deficiency in the chondrocyte lineage showed serious body retardation, decreased bone mass, and chondrocyte apoptosis due to the defective activity of ATP synthase. To our knowledge, this is the first report that RGS12 is required for maintaining the function of mitochondria, which may allow it to orchestrate responses to cellular homeostasis.
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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.