ArticlePloS one2011
LIS1 regulates osteoclast formation and function through its interactions with dynein/dynactin and Plekhm1.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
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- Tcirg1 deficiency delays osteoarthritis progression by impairing lysosome acidification and peripheral accumulation in osteoclasts.Frontiers in cell and developmental biology · 2025Article
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- RUFY4 deletion prevents pathological bone loss by blocking endo-lysosomal trafficking of osteoclasts.Bone research · 2024Article
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- Identification of combined biomarkers for predicting the risk of osteoporosis using machine learning.Aging · 2022Article
- GPR125 positively regulates osteoclastogenesis potentially through AKT-NF-κB and MAPK signaling pathways.International journal of biological sciences · 2022Article
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- Aesculetin Inhibits Osteoclastic Bone Resorption through Blocking Ruffled Border Formation and Lysosomal Trafficking.International journal of molecular sciences · 2020Article
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- Membrane trafficking in osteoclasts and implications for osteoporosis.Biochemical Society transactions · 2019Review
- Deletion of ferroportin in murine myeloid cells increases iron accumulation and stimulates osteoclastogenesisThe Journal of biological chemistry · 2018Article
- [Effect of lipopolysaccharide on osteoclasts formation and bone resorption function and its mechanism].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2018Article
- Cervical spine fractures in osteopetrosis: a case report and review of the literature.Journal of biomedical research · 2018Article
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- Osteoclasts-Key Players in Skeletal Health and Disease.Microbiology spectrum · 2016Review
- LIS1 Regulates Osteoclastogenesis through Modulation of M-SCF and RANKL Signaling Pathways and CDC42.International journal of biological sciences · 2016Article
- Ubiquitin E3 Ligase LNX2 is Critical for Osteoclastogenesis In Vitro by Regulating M-CSF/RANKL Signaling and Notch2.Calcified tissue international · 2015Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Microtubule organization and lysosomal secretion are both critical for the activation and function of osteoclasts, highly specialized polykaryons that are responsible for bone resorption and skeletal homeostasis. Here, we have identified a novel interaction between microtubule regulator LIS1 and Plekhm1, a lysosome-associated protein implicated in osteoclast secretion. Decreasing LIS1 expression by shRNA dramatically attenuated osteoclast formation and function, as shown by a decreased number of mature osteoclasts differentiated from bone marrow macrophages, diminished resorption pits formation, and reduced level of CTx-I, a bone resorption marker. The ablated osteoclast formation in LIS1-depleted macrophages was associated with a significant decrease in macrophage proliferation, osteoclast survival and differentiation, which were caused by reduced activation of ERK and AKT by M-CSF, prolonged RANKL-induced JNK activation and declined expression of NFAT-c1, a master transcription factor of osteoclast differentiation. Consistent with its critical role in microtubule organization and dynein function in other cell types, we found that LIS1 binds to and colocalizes with dynein in osteoclasts. Loss of LIS1 led to disorganized microtubules and aberrant dynein function. More importantly, the depletion of LIS1 in osteoclasts inhibited the secretion of Cathepsin K, a crucial lysosomal hydrolase for bone degradation, and reduced the motility of osteoclast precursors. These results indicate that LIS1 is a previously unrecognized regulator of osteoclast formation, microtubule organization, and lysosomal secretion by virtue of its ability to modulate dynein function and Plekhm1.
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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.