ArticleCell reports2015
ASXL2 Regulates Glucose, Lipid, and Skeletal Homeostasis.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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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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
51 citing papers in PubMed, 65 citations in OpenAlex.
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- Tumor suppressor BAP1 emerges as a key regulator of metabolism and cell death in tumors.Frontiers in cell and developmental biology · 2026Review
- Environmental Insults to Glucose Metabolism: The Role of Pollutants in Insulin Resistance.International journal of molecular sciences · 2025Review
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- Genetic diversity and dietary adaptations of the Central Plains Han Chinese population in East Asia.Communications biology · 2025Article
- Integrative analysis of ASXL family genes reveals ASXL2 as an immunoregulatory molecule in head and neck squamous cell carcinoma.Scientific reports · 2024Article
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- Novel Insights into Osteoclast Energy Metabolism.Current osteoporosis reports · 2023Review
- Identification of a de novo variant in the ASXL2 gene related to Shashi-Pena syndrome.Molecular genetics & genomic medicine · 2023Article
- BAP1 promotes osteoclast function by metabolic reprogramming.Nature communications · 2023Article
- The role of TRPV2 as a regulator on the osteoclast differentiation during orthodontic tooth movement in rats.Scientific reports · 2023Article
- A Zeb1/MtCK1 metabolic axis controls osteoclast activation and skeletal remodeling.The EMBO journal · 2023Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
ASXL2 is an ETP family protein that interacts with PPARγ. We find that ASXL2-/- mice are insulin resistant, lipodystrophic, and fail to respond to a high-fat diet. Consistent with genetic variation at the ASXL2 locus and human bone mineral density, ASXL2-/- mice are also severely osteopetrotic because of failed osteoclast differentiation attended by normal bone formation. ASXL2 regulates the osteoclast via two distinct signaling pathways. It induces osteoclast formation in a PPARγ/c-Fos-dependent manner and is required for RANK ligand- and thiazolidinedione-induced bone resorption independent of PGC-1β. ASXL2 also promotes osteoclast mitochondrial biogenesis in a process mediated by PGC-1β but independent of c-Fos. Thus, ASXL2 is a master regulator of skeletal, lipid, and glucose 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.