ArticleGenesis (New York, N.Y. : 2000)2013
Mx1-cre mediated Rgs12 conditional knockout mice exhibit increased bone mass phenotype.
Article in Genesis (New York, N.Y. : 2000), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Cell signaling and transcriptional regulation of osteoclast lineage commitment, differentiation, bone resorption and diseases.Cell discovery · 2026Review
- RGS12 represses oral squamous cell carcinoma by driving M1 polarization of tumor-associated macrophages via controlling ciliary MYCBP2/KIF2A signaling.International journal of oral science · 2023Article
- RGS12 polarizes the GPSM2-GNAI complex to organize and elongate stereocilia in sensory hair cells.Science advances · 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
- RGS12 is a novel tumor suppressor in osteosarcoma that inhibits YAP-TEAD1-Ezrin signaling.Oncogene · 2021Article
- Macrophage regulator of G-protein signaling 12 contributes to inflammatory pain hypersensitivity.Annals of translational medicine · 2021Article
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- Regulator of G Protein Signaling Protein 12 (Rgs12) Controls Mouse Osteoblast Differentiation via Calcium Channel/Oscillation and Gαi-ERK Signaling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- Genetic Analysis of Rare Human Variants of Regulators of G Protein Signaling Proteins and Their Role in Human Physiology and Disease.Pharmacological reviews · 2018Review
- The impact of RGS and other G-protein regulatory proteins on Gαi-mediated signaling in immunity.Biochemical pharmacology · 2016Review
- Regulators of G protein signaling 12 promotes osteoclastogenesis in bone remodeling and pathological bone loss.Cell death and differentiation · 2015Article
- Localization and expression profile of Group I and II Activators of G-protein Signaling in the kidney.Journal of molecular histology · 2015Article
- Accessory proteins for heterotrimeric G-proteins in the kidney.Frontiers in physiology · 2015Review
- Notch signaling regulates the phosphorylation of Akt and survival of lipopolysaccharide-activated macrophages via regulator of G protein signaling 19 (RGS19).Immunobiology · 2014Article
- Alveolar bone loss: mechanisms, potential therapeutic targets, and interventions.Advances in dental research · 2014Review
- Deletion of IFT20 in early stage T lymphocyte differentiation inhibits the development of collagen-induced arthritis.Bone research · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Regulators of G-protein Signaling (Rgs) proteins are the members of a multigene family of GTPase-accelerating proteins (GAP) for the Galpha subunit of heterotrimeric G-proteins. Rgs proteins play critical roles in the regulation of G protein couple receptor (GPCR) signaling in normal physiology and human diseases such as cancer, heart diseases, and inflammation. Rgs12 is the largest protein of the Rgs protein family. Some in vitro studies have demonstrated that Rgs12 plays a critical role in regulating cell differentiation and migration; however its function and mechanism in vivo is largely unknown. Here, we generated a floxed Rgs12 allele (Rgs12(flox/flox) ) in which the exon 2, containing both PDZ and PTB_PID domains of Rgs12, was flanked with two loxp sites. By using the inducible Mx1-cre and Poly I:C system to specifically delete Rgs12 at postnatal 10 days in interferon-responsive cells including monocyte and macrophage cells, we found that Rgs12 mutant mice had growth retardation with the phenotype of increased bone mass. We further found that deletion of Rgs12 reduced osteoclast numbers and had no significant effect on osteoblast formation. Thus, Rgs12(flox/flox) conditional mice provide a valuable tool for in vivo analysis of Rgs12 function and mechanism through time- and cell-specific deletion of Rgs12.
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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.