ArticleProceedings of the National Academy of Sciences of the United States of America2013
Lkb1/Stk11 regulation of mTOR signaling controls the transition of chondrocyte fates and suppresses skeletal tumor formation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Molecular insights and therapeutic implications for the tumor suppressor role of LKB1 in non-small cell lung cancer.Cancer letters · 2026Review
- PTC124 promotes mutation site-dependent readthrough of STK11 nonsense mutations and restores tumor suppressor function.BBA advances · 2026Article
- Identification and function of periosteal skeletal stem cells in skeletal development, homeostasis, and disease.Journal of orthopaedic translation · 2025Review
- Compensatory growth and recovery of cartilage cytoarchitecture after transient cell death in fetal mouse limbs.Nature communications · 2024Article
- Growth arrest and DNA damage-inducible alpha regulates muscle repair and fat infiltration through ATP synthase F1 subunit alpha.Journal of cachexia, sarcopenia and muscle · 2023Article
- Cathepsin KFrontiers in cell and developmental biology · 2022Review
- Enchondromatosis and Growth Plate Development.Current osteoporosis reports · 2021Review
- GCN5 acetylation is required for craniofacial chondrocyte maturation.Developmental biology · 2020Article
- Article
- Liver Kinase B1 Fine-Tunes Lineage Commitment of Human Fetal Synovium-Derived Stem Cells.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2020Article
- IDH1 immunohistochemistry reactivity and mosaic IDH1 or IDH2 somatic mutations in pediatric sporadic enchondroma and enchondromatosis.Virchows Archiv : an international journal of pathology · 2019Article
- Lkb1 deletion in periosteal mesenchymal progenitors induces osteogenic tumors through mTORC1 activation.The Journal of clinical investigation · 2019Article
- Rapamycin rescues BMP mediated midline craniosynostosis phenotype through reduction of mTOR signaling in a mouse model.Genesis (New York, N.Y. : 2000) · 2018Article
- Altered paracrine signaling from the injured knee joint impairs postnatal long bone growth.eLife · 2017Article
- Bone Size and Quality Regulation: Concerted Actions of mTOR in Mesenchymal Stromal Cells and Osteoclasts.Stem cell reports · 2017Article
- mTORC1 Plays an Important Role in Skeletal Development by Controlling Preosteoblast Differentiation.Molecular and cellular biology · 2017Article
- Signaling pathways regulating cartilage growth plate formation and activity.Seminars in cell & developmental biology · 2017Review
- mTORC1 regulates PTHrP to coordinate chondrocyte growth, proliferation and differentiation.Nature communications · 2016Article
- Article
- Regulation of Long Bone Growth in Vertebrates; It Is Time to Catch Up.Endocrine reviews · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
Abstract
Liver kinase b1 (Lkb1) protein kinase activity regulates cell growth and cell polarity. Here, we show Lkb1 is essential for maintaining a balance between mitotic and postmitotic cell fates in development of the mammalian skeleton. In this process, Lkb1 activity controls the progression of mitotic chondrocytes to a mature, postmitotic hypertrophic fate. Loss of this Lkb1-dependent switch leads to a dramatic expansion of immature chondrocytes and formation of enchondroma-like tumors. Pathway analysis points to a mammalian target of rapamycin complex 1-dependent mechanism that can be partially suppressed by rapamycin treatment. These findings highlight a critical requirement for integration of mammalian target of rapamycin activity into developmental decision-making during mammalian skeletogenesis.
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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.