Yi-Ping Li, PhD

Dean’s Endowed Chair Professor

Director, Division in Cellular and Molecular Medicine
Phone
504-988-0475
School or College
School of Medicine
Yi-Ping Li, PhD

Education & Affiliations

1990-1993 Postdoc Fellow, The Forsyth Institute. Harvard University affiliate
1989-1990 Postdoc Fellow, The Population Council's Center for Biomedical Research (CBR), Rockefeller University affiliate
1988 Ph.D., Molecular Genetics, Shanghai Institution of Biochemistry, The Academy of Sciences of China
1979 B.S., Department of Chemistry, Zhejiang University, China

Biography

Go To Yi-Ping Li's Laboratory

At UAB, Dr. Yi-Ping Li was the Jay M McDonald Endowed Professor, Senior vice Director of the Center for Metabolic Bone Disease, Co-Director of Global Center for Craniofacial, Oral and Dental Diseases, and Associate Director of their NIH T32 "Training Program in Rheumatic and Musculoskeletal Diseases Research”. He also held a secondary appointment as Professor in UAB’s Dental School. Dr. Li has been an adjunct professor at The Forsyth Institute, which is affiliated with Harvard School of Dental Medicine.

Dr. Li’s research, sponsored by the NIH for 26 years, covers a large scope of topics, including bone biology,  musculoskeletal diseases, immune disorders,  craniofacial development, tumorigenesis and cancer bone metastasis. These varied research interests have proven to be synergistic as there are overlapping themes and techniques. He was one of the first scientists to apply molecular biology approaches to the study of osteoclasts. His work resulted in the publication of a number of seminal papers on the cloning and characterization of the genes that are essential to osteoclast function or differentiation, including Cathepsin K, ATP6i, RGS10A, C/EBPα and Gα13. His work has also resulted in the awarding of 6 patents. The lab has a long history of experience using animal models to study the pathogenesis of human diseases.

Before joining UAB, Dr. Li was Professor, Department of Cytokine Biology, at the Forsyth Institute, Harvard School of Dental Medicine. He received his BS degree in Chemistry from Zhejiang University and his PhD  degree in Molecular Genetics from the Shanghai Institute of Biochemistry, Academy of Sciences of China, P.R. China in 1988 and completed his Post-doctoral Research Training in Medical Genetics at The Forsyth Institute, Department of Immunology, Harvard School of Dental Medicine in 1993.

Google Scholars: https://scholar.google.com/citations?user=RTpI-QYAAAAJ&hl=en
 

Appointment and Position

  • 2021-present Dean’s Endowed Chair Professor, Department of Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA

  • 2010-2021 Jay M. McDonald Endowed Professor, Tenured Full Professor, Department of Pathology, School of Medicine, The University of Alabama at Birmingham,  Alabama

  • 2010-2015 Senior Vice Director for Research, Center for Metabolic Bone Disease, The University of Alabama at Birmingham, Alabama

  • 2010-2018 Adjunct Senior Research Investigator, Department of Cytokine Biology, The Forsyth Institute, Harvard University.

  • 2007- 2010 Tenured Senior Member of the Staff (equivalent to tenured full professor). Department of Cytokine Biology, The Forsyth Institute, Harvard University.

  • 1998-2007 Associate Member of the Staff (equivalent to Associate Professor), Department of Cytokine Biology, The Forsyth Institute, Harvard University.

  • 1995-2008 Assistant Member of the Staff (equivalent to Assistant Professor), Department of Cytokine Biology, The Forsyth Institute, Harvard University.

  • 1994-1995 Instructor, Department of Developmental Biology, Harvard School of Dental Medicine

Research

Dr. Yi-Ping Li’s research, continuously sponsored by the NIH for 27 years’, covers a large scope of topics, including bone biology, musculoskeletal diseases, immune disorders, skeletal and craniofacial development, oral diseases, inflammatory diseases, tumorigenesis and cancer bone metastasis. These varied research interests have proven to be synergistic as there are overlapping themes and techniques. Dr. Li was one of the first scientists to apply molecular biology approaches to the study of osteoclasts. Dr. Li’s work resulted in the publication of a number of seminal papers on the cloning and characterization of the genes that are essential to osteoclast function or differentiation, including Cathepsin K, ATP6i, RGS10A, C/EBPα and Gα13. Dr. Li’s work has also resulted in the awarding of 6 patents. Dr. Li’s lab has a long history of experience using animal models to study the pathogenesis of human diseases. Dr. Yi-Ping Li has published many papers in high quality, peer-reviewed journals, such as Nature Genetics; Nature Communications; Genes & Development; PNAS; Journal of Cell Science; Development; Molecular and Cellular Biology; Journal of Immunology; Journal of Bone and Mineral Research; Molecular Endocrinology; Developmental Biology; Journal of Pathology; Human Molecular Genetics; Nucleic Acids Research and PLOS Genetics. 

Please see the detailed research projects at both https://medicine.tulane.edu/yi-ping-li-laboratories and Lab Webpage: https://www.yi-ping-li-lab.org

Current Research Interests

  1. To characterize molecular mechanisms of tumorgenesis and cancer bone metastasis, and utilize immunotherapy to development new diagnostic and therapeutic alternatives to suppress cancer growth and metastasis. We have defined ATP6i as T cell activation regulator and Cathepsin K as dendritic cell maturation regulator and as a tumor suppressing gene and its role of mutation in prostate cancer metastasis. We have developed AAV mediated gene knockdown system for therapeutic alternatives for human breast cancer bone metastasis. We have also demonstrated that whole-body Ctsk knockdown or a small molecule inhibitor of Ctsk enhance the efficacy of immunotherapy by improving anti-tumor immunity and promoting dendritic cell maturation, and that osteoclast proton pump regulator Atp6v1c1 enhances breast cancer growth by activating the mTORC1 pathway and bone metastasis by increasing V-ATPase activity.

    Publications

    1. *Matthew McConnell, Shengmei Feng, Wei Chen, Guochun Zhu,  Dejun Shen,  Selvarangan Ponnazhagan,  Lianfu Deng,, and Li YP. Osteoclast proton pump regulator Atp6v1c1 enhances breast cancer growth by activating the mTORC1 pathway and bone metastasis by increasing V-ATPase activity. Oncotarget. 2017 May 2. PMID: 28504970;   PMCID: PMC5564597

    2. *Feng S, Guochun Zhu, Matthew McConnell, Lianfu Deng, Qiang Zhao, Mengrui Wu, Qi Zhou, Jinshen Wang, Jin Qi, Li Y-P,* and Wei Chen. Silencing of Atp6v1c1 Prevents Breast Cancer Growth and Bone Metastasis. International Journal of Biological Sciences 2013; 9(8): 853-862. PMCID: PMC3805834.

    3. Tu Q, Zhang J, Fix A, Brewer E, Li YP, Zhang ZY, Chen J. Targeted overexpression of BSP in osteoclasts promotes bone metastasis of breast cancer cells. J Cell Physiol 2008;218:135-45. PMCID: PMC2666312.

    4. Ping Z, Siegal GP, Harada S, Eltoum IE, Youssef M., Shen T, He J, Huang Y, Chen D, Li YP, Bland KI, Chang HR, Shen D. ERBB2 mutation is associated with a worse prognosis in patients with CDH1 altered invasive lobular cancer of the breast. Oncotarget. 2016, 7(49), PMID: 27811364;  PMCID: PMC5340256.

       

  2. To seek selectively shut off Immune responses and Specifically Activate immune responses.  AAV mediated gene therapy to prevent bone loss and inflammatory Diseases such as Rheumatoid arthritis (RA) and periodontitis, osteoarthritis (OA) and aging related diseases such as osteoarthritis (OA). We have applied my findings in osteoclast biology to translational medicine through a novel AAV mediated gene silencing tool targeting crucial osteoclast proteins (e.g. ATP6i, RGS10, C1, AC45 and Cathepsin K), which have the capacity to reduce bone loss and inflammation associated with oral diseases in mouse models of periodontal and endodontic diseases. My lab has investigated the therapeutic effect of AAV-sh-Apt6i, AAV-sh-Cathepsin K, and AAV-sh-RGS10. This groundbreaking work investigates the therapeutic potential of targeting ATP6i, RGS10, and Cathepsin K as treatments for immune-mediated oral inflammatory diseases and has led to numerous insights on the roles of these genes in osteoimmunology. Importantly, this work has shown that a number of critical osteoclast genes also have important roles in the immune system.

    Publications:

    1. *Hao L, Chen J, Zhu Z, Reddy MS, Mountz JD, Li Y-P*, Chen W. Odanacatib, Cathepsin K Specific Inhibitor, Inhibits Inflammation and Bone Loss Caused by Periodontal Diseases. J Periodontol. 2015 Apr 16:1-18. PMCID: PMC4648620

    2. *Liang Hao, Wei Chen, Matthew McConnell, Zheng Zhu, Sheng Li, Michael Reddy, Paul D. Eleazer4, Min Wang, Yi-Ping Li. A small molecule, Odanacatib, inhibits inflammation and bone loss caused by endodontic disease. Infection and Immunity. 2015, Apr;83(4):1235-45. PMCID: PMC4363442.

    3. *Zheng Zhu, Wei Chen, Liang Hao, Guochun Zhu, Yun Lu, Sheng Li, Lin Wang*, Yi-Ping Li*. Ac45 silencing mediated by    AAV-sh-Ac45-RNAi prevents both bone loss and inflammation caused by periodontitis. Journal of Clinical Periodontology. J Clin Periodontol. 2015 Jul;42(7):599-608. PMCID: PMC4620917.

    4. *Ma, J, Chen W, Zhang L, Tucker B, Zhu G, Sasaki H, Hao L, Wang L, Ci H, Jiang H, Stashenko P, and Li Y-P*. RNAi mediated silencing of Atp6i prevents both periapical bone erosion and periapical inflammation in the mouse model of endodontic disease. Infection and Immunity. 2013; 81 (4): 1021–1030. PMCID: PMC3639609.

  3. To define the negative signaling in dendritic cells and macrophages to attenuate inflammation and bone destruction in Rheumatoid arthritis and autoimmune diseases. The proposed study will provide important insights into the negative regulation of the cells of the immune system to target inflammation and bone destruction in RA by elucidating the underlying mechanism of Gα13 signaling. Knowledge gained from this study may generate potential therapeutic means for treating RA and other inflammatory bone diseases. We also characterizing the mechanism by which endogenous negative regulators of osteoclasts control bone homeostasis under physiological and pathological conditions in mouse models. This study endeavors to understand how osteoclast (OC) differentiation is negatively regulated and to characterize the mechanism by which endogenous negative regulators of osteoclasts control bone homeostasis under physiological and pathological conditions.

    Publications:

    1. *Mengrui Wu, Wei Chen, Yun Lu, Guochun Zhu, Liang Hao and Li YP, Gα13 negatively controls osteoclastogenesis through regulation of the RhoA/Akt/GSK3β/NFATc1 signaling pathway. Nature Communications, 2017 Jan 19;8:13700, PMID: 28102206; PMCID: PMC5253683

    2. *Wu M, Wang Y, Deng LF, Chen W, Li Y-P. TRAF Family Member-Associated NF-κB Activator (TANK) Induced By RANKL Negatively Regulates Osteoclasts Survival and Function. Int J Biol Sci 2012; 8(10):1398-1407. PMCID: PMC3492797.

    3. *Wenbin Yang,  Zheng Zhu1, Longjiang Li,  Ning Gao, Abigail McVicar,  Lin Wang, Yi-Ping Li,  Wei Chen AAV-sh-Ac45 simultaneously inhibits bone resorption and attenuates inflammation through impairing acidification, Cathepsin K secretion, TLRs signaling activation, and the dendritic cell maturation pathway Infection and Immunity, 2020 Dec 15;89(1):e00436-20

    4. *Wang Y, Chen W, Hao L, McVicar A, Wu J, Gao N, Liu Y, and Li YP. C1 silencing attenuates inflammation and alveolar bone resorption in endodontic disease.  Journal of Endodontics 2019 Jul;45(7):898-906 

  4. To characterize Znf9/CNBP as Myotonic dystrophy type II (DM2) disease gene and key regulators in craniofacial and skeletal development. Our research has had a major impact on the field of muscle disease and has expanded our understanding of the pathogenesis of DM2 disease. Prior to my findings, it was unknown that Znf9 haploinsufficiency was related to the pathogenesis of DM2 (Chen et al, JMB, 2007). I have also identified Cnbp for the first time as a key regulator in craniofacial development by using the mouse gene knockout system. My research has had a major impact on the field of craniofacial development, has expanded our understanding of the biological and molecular basis of craniofacial morphogenesis, and has provided much needed insights into human congenital birth defects which affect the development of the head, face, and neck. 

    Publications:

    1. *Chen W, Liang Y, Deng W, Shimizu K, Ashique AM, Li E, Li Y-P*. The zinc-finger protein, CNBP, is required for forebrain formation in the mouse. Development 2003; 130:1367-79. 

    2. *Abe Y#, Chen W#, Huang W, Li Y-P*. CNBP regulates forebrain formation at organogenesis stage in chick embryos. Dev Biol 2006; 295:116-27.

    3. *Chen W, Wang Y, Abe Y, Cheney L, Udd B, Li Y-P*. Haploinsuffciency for Znf9 in Znf9+/- mice is associated with multiorgan abnormalities resembling myotonic dystrophy. J Mol Biol 2007; 368(1):8-17. 

    4. *Shimizu K, Chen W, Ashique AM, Moroi R, Li Y-P*. Molecular cloning, developmental expression, promoter analysis and functional characterization of the mouse CNBP gene. Gene 2003; 307:51-62. 

  5. To determine how osteoclasts resorb bone and which molecules are responsible to the bone resorption process. I am the major investigator who discovered the role of subunits of the osteoclast proton pump in osteoclast function at a time when the role of osteoclasts in bone resorption and mechanism of action of proton pumps was still largely unknown. We discovered that Cathepsin K is a major osteoclast-specific protease responsible for matrix protein degradation, that RGS10 transduces RANKL signaling to control osteoclast differentiation by regulating [Ca2+]i oscillation and activation of NFATc1. Furthermore, I made the novel discoveries that ATP6i (TCIRG1) is an osteoclast-specific subunit of the proton pump responsible for dissolving the mineral phase of bone. Based our work, ATP6i has been identified as a human osteopetrosis disease gene. These two molecules have been listed as major osteoclast function genes in the current model of osteoclast differentiation in the Principles of Bone Biology textbook (edited by Bilezikian JP et al., 2008).

    Publications:

    1. Li Y-P, Alexander M, Wucherpfennig AL, Yelick P, Chen W, Stashenko P. Cloning and complete coding sequence of a novel human cathepsin expressed in giant cells of osteoclastomas. J Bone Miner Res 1995;10:1197-1202.

    2. *Li Y-P, Chen W, Liang Y, Li E, Stashenko P. Atp6i-deficient mice exhibit severe osteopetrosis due to loss of osteoclast-mediated extracellular acidification. Nat Genet 1999;23:447-51. 

    3. *Chen W, Yang S, Abe Y, Li M, Wang Y, Shao J, Li E, Li Y-P*. Novel pycnodysostosis mouse model uncovers cathepsin K function as a potential regulator of osteoclast apoptosis and senescence. Hum Mol Genet 2007;16:410-23. PMCID: PMC3578583

    4. *Yang S, Chen W, Stashenko P, Li Y-P*. Specificity of RGS10A as a key component in the RANKL signaling mechanism for osteoclast differentiation. J Cell Sci 2007;120:3362-71. PMCID: PMC3587975.

  6. To characterize mechanisms underlying how transcription factors and epigenetic factors regular osteoclast differentiation and activation. We have done novel works in investigating the mechanism underlying transcription factors specifying osteoclast lineage commitment from monocyte/macrophages and characterizing osteoclast genes and promoters. The studies have established C/EBPα as the key transcriptional regulator of osteoclast lineage commitment, providing a unique therapeutic target for diseases of excessive bone resorption (e.g. osteoporosis and arthritis) and leading the way for future exploratory studies. We have also demonstrated that C/EBPα controls osteoclast terminal differentiation, activation, function, and postnatal bone homeostasis through direct regulation of Nfatc1. The function of osteoclast proteins makes them ideal targets for bone resorption related diseases, such as bone cancer metastasis, osteoporosis, periodontitis, and rheumatoid arthritis. Recently, we revealed that Gα13 is a master endogenous negative switch for osteoclastogenesis through regulation of the RhoA/Akt/GSK3β/NFATc1 signalling pathway.

    Publications:

    1. *Chen W, Zhu G, Hao L, Wu M, Ci HL, and Li Y-P*. C/EBPa is the Key Regulator of Osteoclast Lineage Commitment. Proc Natl Acad Sci U S A. PNAS. 2013; 110(18):7294-9. PMCID: PMC3645589.

    2. *Kamolmatyakul S, Chen W, Yang S, Abe Y, Moroi R, Ashique AM, Li Y-P*. IL-1α stimulates cathepsin K expression in osteoclasts via the tyrosine kinase-NF-κB pathway. J Dent Res 2004;83:791-6. PMCID: PMC3966556.

    3. *Mengrui Wu, Wei Chen, Yun Lu, Guochun Zhu, Liang Hao and Li YP*, Gα13 negatively controls osteoclastogenesis through regulation of the RhoA/Akt/GSK3β/NFATc1 signaling pathway. Nature Communications, 2017 Jan 19;8:13700, PMCID: PMC5253683.

    4. *Chen W, Zhu G, Tang J, Zhou HD, Li YP. C/ebpalpha controls osteoclast terminal differentiation, activation, function, and postnatal bone homeostasis through direct regulation of Nfatc1. J Pathol. 2018 Mar;244(3):271-282. doi: 10.1002/path.5001. PubMed PMID: 29083488.

  7. To characterize the function of transcription factors and epigenetic factors in bone and revealed its crucial roles in the development of osteoblasts, bone and cartilage. My lab has recently published several papers exploring the underlying mechanism by which Cbfβ, a key binding factor for Runx proteins, regulates cartilage and bone development. We have investigated the pathogenesis of cleidocranial dysplasia (CCD) and revealed that CCD may result from functional defects of the Runx2/Cbfβ heterodimeric complex in various skeletal cells. Cbfβ has been found to play an indispensable role in postnatal skeletal development and homeostasis in various skeletal cell types by up-regulating the expression of Atf4 and Osterix. We have  characterized the mechanism by which Cbfβ regulates chondrogenesis and osteoblastogenesis and revealed that Cbfβ controls the balance of chondrocyte proliferation and differentiation by upregulating Indian hedgehog expression and inhibiting parathyroid hormone-related protein receptor expression in postnatal cartilage and bone formation. 

    Publications:

    1. *Tian F, Wu M, Deng L, Zhu G, Ma J, Gao B, Wang L, Li YP*, Chen W*. Core binding factor beta (Cbfb) controls the balance of chondrocyte proliferation and differentiation by up-regulating Indian hedgehog (Ihh) expression... J Bone Miner Res. 2014 Jul;29 (7):1564-74. PMID: 24821091. PMCID: PMC4644666 

    2. *Wu M, Li YP, Zhu G, Lu Y, Wang Y, Jules J, McConnell M, Serra R, Shao JZ, Chen W*. Chondrocyte-specific knockout of Cbfβ reveals the indispensable function of Cbfβ in chondrocyte maturation, growth plate development and trabecular bone formation in mice. Int J Biol Sci. 2014 Jul 29;10(8):861-72.  PMID: 25170300, PMCID: PMC4147220

    3. *Wu M, Li C, Zhu G, Wang Y, Jules J, Lu Y, McConnell M, Wang YJ, Shao JZ, Li YP*, Chen W*. Deletion of core-binding factor β (Cbfβ) in mesenchymal progenitor cells provides new insights into Cbfβ/Runxs complex function in cartilage and bone development. Bone. 2014 Aug; 65:49-59. PMID: 24798493, PMCID: PMC4644668

    4. *Chen W, Ma J, Zhu G, Jules J, Wu M, McConnell M, Zhou X, Tain F,  Paulson C, Wang L, and Li YP*. Cbfb Deletion in Mice Recapitulates Cleidocranial Dysplasia and Reveals Multiple Functions of Cbfb; Required for Skeletal Development. Proc Natl Acad Sci U S A. (PNAS). 2014; 111(23): 8482-7. PMID: 24850862, PMCID: PMC4060659

*Indicates that the PI (Dr. Yi-Ping Li) is the correspondence author

RESEARCH FUNDING

Grant Name                     R01 AR074954

Role in Project:                  Principal Investigator
Year (Inclusive):                02/15/20-02/14/25
Source:                              NIH;NIAMS

 

Grant Name                      R01 DE023813

Role in Project:                  Principal Investigator
Year (Inclusive):                03/20/19-04/30/24
Source:                             NIH; NIDCR

 

Grant Name                     R01 DE028264

Role in Project:                  Principal Investigator
Year (Inclusive):                09/01/18 - 08/31/23
Source:                             NIH; NIDCR

 

Grant Name                     R01 AR075735

Role in Project:                  Principal Investigator
Year (Inclusive):                08/01/19 - 07/31/24
Source:                             NIH; NIAMS

Publications

(Last 5 years)
Articles

  1. Tang CY, Wu M, Zhao D, Edwards D, McVicar A, Luo Y, Zhu G, Wang Y, Zhou HD, Chen W, Li YP. Runx1 is a central regulator of osteogenesis for bone homeostasis by orchestrating BMP and WNT signaling pathways. PLoS Genet. 2021 Jan 21;17(1):e1009233. doi: 10.1371/journal.pgen.1009233. PMID: 33476325; PMCID: PMC7819607.

  2. Tang J, Xie J, Chen W, Tang C, Wu J, Wang Y, Zhou XD, Zhou HD, Li YP. Runt-related transcription factor 1 is required for murine osteoblast differentiation and bone formation. J Biol Chem. 2020 Aug 14;295(33):11669-11681. doi: 10.1074/jbc.RA119.007896. Epub 2020 Jun 22. PubMed PMID: 32571873; PubMed Central PMCID: PMC7450143.

  3. Tang CY, Chen W, Luo Y, Wu J, Zhang Y, McVicar A, McConnell M, Liu Y, Zhou HD, Li YP. Runx1 up-regulates chondrocyte to osteoblast lineage commitment and promotes bone formation by enhancing both chondrogenesis and osteogenesis. Biochem J. 2020 Jul 17;477(13):2421-2438. doi: 10.1042/BCJ20200036. PubMed PMID: 32391876.

  4. Wang Y, Chen W, Hao L, McVicar A, Wu J, Gao N, Liu Y, Li YP. C1 Silencing Attenuates Inflammation and Alveolar Bone Resorption in Endodontic Disease. J Endod. 2019 Jul;45(7):898-906. doi: 10.1016/j.joen.2019.02.024. Epub 2019 May 16. PubMed PMID: 31104818.

  5. Li Z, Liu T, Gilmore A, Gómez NM, Fu C, Lim J, Yang S, Mitchell CH, Li YP, Oursler MJ, Yang S. Regulator of G Protein Signaling Protein 12 (Rgs12) Controls Mouse Osteoblast Differentiation via Calcium Channel/Oscillation and Gαi-ERK Signaling. J Bone Miner Res. 2019 Apr;34(4):752-764. doi: 10.1002/jbmr.3645. Epub 2019 Jan 28. PubMed PMID: 30489658; PubMed Central PMCID: PMC7675783.

  6. Guo S, Zhang Y, Zhou T, Wang D, Weng Y, Chen Q, Ma J, Li YP, Wang L. GATA4 as a novel regulator involved in the development of the neural crest and craniofacial skeleton via Barx1. Cell Death Differ. 2018 Nov;25(11):1996-2009. doi: 10.1038/s41418-018-0083-x. Epub 2018 Mar 9. PubMed PMID: 29523871; PubMed Central PMCID: PMC6219484.

  7. Chen J, Deng L, Porter C, Alexander G, Patel D, Vines J, Zhang X, Chasteen-Boyd D, Sung HJ, Li YP, Javed A, Gilbert S, Cheon K, Jun HW. Angiogenic and Osteogenic Synergy of Human Mesenchymal Stem Cells and Human Umbilical Vein Endothelial Cells Cocultured on a Nanomatrix. Sci Rep. 2018 Oct 24;8(1):15749. doi: 10.1038/s41598-018-34033-2. PubMed PMID: 30356078; PubMed Central PMCID: PMC6200728.

  8. Huang H, Wang J, Zhang Y, Zhu G, Li YP, Ping J, Chen W. Bone resorption deficiency affects tooth root development in RANKL mutant mice due to attenuated IGF-1 signaling in radicular odontoblasts. Bone. 2018 Sep;114:161-171. doi: 10.1016/j.bone.2017.12.026. Epub 2017 Dec 29. PubMed PMID: 29292230.

  9. Chen W, Zhu G, Jules J, Nguyen D, Li YP. Monocyte-Specific Knockout of C/ebpα Results in Osteopetrosis Phenotype, Blocks Bone Loss in Ovariectomized Mice, and Reveals an Important Function of C/ebpα in Osteoclast Differentiation and Function. J Bone Miner Res. 2018 Apr;33(4):691-703. doi: 10.1002/jbmr.3342. Epub 2018 Jan 26. PubMed PMID: 29149533; PubMed Central PMCID: PMC6240465.

  10. Chen W, Zhu G, Tang J, Zhou HD, Li YP. C/ebpα controls osteoclast terminal differentiation, activation, function, and postnatal bone homeostasis through direct regulation of Nfatc1. J Pathol. 2018 Mar;244(3):271-282. doi: 10.1002/path.5001. Epub 2018 Jan 29. PubMed PMID: 29083488; PubMed Central PMCID: PMC6240466.

  11. Jules J, Li YP, Chen W. C/EBPα and PU.1 exhibit different responses to RANK signaling for osteoclastogenesis. Bone. 2018 Feb;107:104-114. doi: 10.1016/j.bone.2017.05.009. Epub 2017 Oct 12. PubMed PMID: 29032174; PubMed Central PMCID: PMC6240464.

  12. Jules J, Chen W, Feng X, Li YP. C/EBPα transcription factor is regulated by the RANK cytoplasmic 535IVVY538 motif and stimulates osteoclastogenesis more strongly than c-Fos. J Biol Chem. 2018 Jan 26;293(4):1480-1492. doi: 10.1074/jbc.M116.736009. Epub 2017 Nov 9. PubMed PMID: 29122885; PubMed Central PMCID: PMC5787821.

  13. Wu M, Wang Y, Shao JZ, Wang J, Chen W, Li YP. Cbfβ governs osteoblast-adipocyte lineage commitment through enhancing β-catenin signaling and suppressing adipogenesis gene expression. Proc Natl Acad Sci U S A. 2017 Sep 19;114(38):10119-10124. doi: 10.1073/pnas.1619294114. Epub 2017 Sep 1. PubMed PMID: 28864530; PubMed Central PMCID: PMC5617241.

  14. McConnell M, Feng S, Chen W, Zhu G, Shen D, Ponnazhagan S, Deng L, Li YP. Osteoclast proton pump regulator Atp6v1c1 enhances breast cancer growth by activating the mTORC1 pathway and bone metastasis by increasing V-ATPase activity. Oncotarget. 2017 Jul 18;8(29):47675-47690. doi: 10.18632/oncotarget.17544. PubMed PMID: 28504970; PubMed Central PMCID: PMC5564597.

  15. Pan J, Wang J, Hao L, Zhu G, Nguyen DN, Li Q, Liu Y, Zhao Z, Li YP, Chen W. The Triple Functions of D2 Silencing in Treatment of Periapical Disease. J Endod. 2017 Feb;43(2):272-278. doi: 10.1016/j.joen.2016.07.014. PubMed PMID: 28132712.

  16. Wu M, Chen W, Lu Y, Zhu G, Hao L, Li YP. Gα13 negatively controls osteoclastogenesis through inhibition of the Akt-GSK3β-NFATc1 signalling pathway. Nat Commun. 2017 Jan 19;8:13700. doi: 10.1038/ncomms13700. PubMed PMID: 28102206; PubMed Central PMCID: PMC5253683.

  17. Ping Z, Siegal GP, Harada S, Eltoum IE, Youssef M, Shen T, He J, Huang Y, Chen D, Li Y, Bland KI, Chang HR, Shen D. ERBB2 mutation is associated with a worse prognosis in patients with CDH1 altered invasive lobular cancer of the breast. Oncotarget. 2016 Dec 6;7(49):80655-80663. doi: 10.18632/oncotarget.13019. PubMed PMID: 27811364; PubMed Central PMCID: PMC5340256.

  18. Chen W, Gao B, Hao L, Zhu G, Jules J, MacDougall MJ, Wang J, Han X, Zhou X, Li YP. The silencing of cathepsin K used in gene therapy for periodontal disease reveals the role of cathepsin K in chronic infection and inflammation. J Periodontal Res. 2016 Oct;51(5):647-60. doi: 10.1111/jre.12345. Epub 2016 Jan 11. PubMed PMID: 26754272; PubMed Central PMCID: PMC5482270.

  19. Jules J, Chen W, Feng X, Li YP. CCAAT/Enhancer-binding Protein α (C/EBPα) Is Important for Osteoclast Differentiation and Activity. J Biol Chem. 2016 Jul 29;291(31):16390-403. doi: 10.1074/jbc.M115.674598. Epub 2016 Apr 20. PubMed PMID: 27129246; PubMed Central PMCID: PMC4965585.

  20. Wu M, Chen G, Li YP. TGF-β and BMP signaling in osteoblast, skeletal development, and bone formation, homeostasis and disease. Bone Res. 2016;4:16009. doi: 10.1038/boneres.2016.9. eCollection 2016. Review. PubMed PMID: 27563484; PubMed Central PMCID: PMC4985055.

  21. Yuan X, Cao J, Liu T, Li YP, Scannapieco F, He X, Oursler MJ, Zhang X, Vacher J, Li C, Olson D, Yang S. Regulators of G protein signaling 12 promotes osteoclastogenesis in bone remodeling and pathological bone loss. Cell Death Differ. 2015 Dec;22(12):2046-57. doi: 10.1038/cdd.2015.45. Epub 2015 Apr 24. PubMed PMID: 25909889; PubMed Central PMCID: PMC4816106.

  22. Hao L, Chen J, Zhu Z, Reddy MS, Mountz JD, Chen W, Li YP. Odanacatib, A Cathepsin K-Specific Inhibitor, Inhibits Inflammation and Bone Loss Caused by Periodontal Diseases. J Periodontol. 2015 Aug;86(8):972-83. doi: 10.1902/jop.2015.140643. Epub 2015 Apr 16. PubMed PMID: 25879791; PubMed Central PMCID: PMC4648620.

  23. Zhu Z, Chen W, Hao L, Zhu G, Lu Y, Li S, Wang L, Li YP. Ac45 silencing mediated by AAV-sh-Ac45-RNAi prevents both bone loss and inflammation caused by periodontitis. J Clin Periodontol. 2015 Jul;42(7):599-608. doi: 10.1111/jcpe.12415. Epub 2015 Jun 11. PubMed PMID: 25952706; PubMed Central PMCID: PMC4620917.

  24. Jules J, Yang S, Chen W, Li YP. Role of Regulators of G Protein Signaling Proteins in Bone Physiology and Pathophysiology. Prog Mol Biol Transl Sci. 2015;133:47-75. doi: 10.1016/bs.pmbts.2015.02.002. Epub 2015 Apr 27. Review. PubMed PMID: 26123302; PubMed Central PMCID: PMC4817727.

  25. Hao L, Chen W, McConnell M, Zhu Z, Li S, Reddy M, Eleazer PD, Wang M, Li YP. A small molecule, odanacatib, inhibits inflammation and bone loss caused by endodontic disease. Infect Immun. 2015 Apr;83(4):1235-45. doi: 10.1128/IAI.01713-14. Epub 2015 Jan 12. PubMed PMID: 25583522; PubMed Central PMCID: PMC4363442.