Deborah J. Veis (Novack), M.D., Ph.D.

Internal Medicine
Bone & Mineral Diseases
Pathology and Immunology

Molecular Cell Biology Program
Immunology Program

  • 314-454-8472

  • 314-454-5975

  • 314-454-5047

  • 8301

  • BJC Institute of Health, 11th floor



  • bone biology, osteoclast, arthritis, cancer, NF-KB, metastasis, osteoporosis, microenvironment, mitochondria, osteoblast

  • Role of NF-KB signalling in bone loss, during bone metastasis, arthritis, and osteoporosis

Research Abstract:

Bone is a dynamic and complex organ whose integrity is controlled by the interaction of many cell types, including osteoclasts which remove bone and osteoblasts which build it. Normally, activity of bone cells is coordinated, and many bone cells use similar signaling pathways for different purposes. My laboratory studies NF-kB signaling pathways in bone cells, particularly in the context of pathological bone loss, such as in osteoporosis, inflammatory arthritis, and cancer metastasis to bone. A major focus is on the role of the alternative/non-canonical NF-kB pathway in osteoclasts, where it controls both differentiation and activity. We recently showed that new anti-cancer drugs (IAP antagonists) activate alternative NF-kB in osteoclasts, causing an increase in tumor growth specifically in bone. Ongoing projects address specific molecular pathways downstream of this pathway in osteoclasts and other bone cells, and how modulation of NF-kB modulates the bone microenvironment. Recently, we have also begun to investigate the role of mitochondria in bone cells. We are using many transgenic mouse models as well as pharmacological approaches, combining in vivo disease modeling with in vitro cell cultures.

Selected Publications:

Krauss JL, Zeng R, Hickman-Brecks CL, Wilson JE, Ting JP-Y, Novack DV. NLPR12 provides a critical checkpoint for osteoclast differentiation. Proc. Natl. Acad. Sci., 2015, doi:10.1073/pnas.1500196112 [ePub ahead of print]

Zeng R, Faccio R, Novack DV. Alternative NF-B regulates RANKL-induced osteoclast differentiation and mitochondrial biogenesis via independent mechanisms. J Bone Miner Res. 2015. doi: 10.1002/jbmr.2584.

Yang C and Novack DV. (2013). Anti-cancer IAP antagonists promote bone metastasis: a cautionary tale. J. Bone Miner. Metab. 2013 June 6. J. Bone Miner. Metab. 2013 31(5):496-506.

Chang Yang, Jennifer L Davis, Rong Zeng, Paras Vora, Xinming Su, Lynne Collins, Suwanna Vangveravong, Robert H. Mach, David Piwnica-Worms, Katherine N. Weilbaecher, Roberta Faccio, Deborah Veis Novack. (2013). Antagonism of Inhibitor of Apoptosis Proteins Increases Bone Metastasis via Unexpected Osteoclast. Cancer Discovery; 3(2):212-223.

Cremasco V, Decker CE, Stumpo D, Blackshear PJ, Nakayama KI, Nakayama K, Lupu TS, Graham DB, Novack DV, Faccio R. (2012). PKCδ deficiency perturbs bone homeostasis by selective uncoupling of cathepsin K secretion and ruffled border formation in osteoclasts. J Bone Miner Res.; 27:2452-2463.PMCID: PMC3498518.

Bonar SL, Brydges SD, Mueller JL, McGeough MD, Pena C, Chen D, Grimston SK, Hickman-Brecks CL, Ravindran S, McAlinden A, Novack DV, Kastner DL, Civitelli R, Hoffman HM, Mbalaviele G. (2012). Constitutively activated NLRP3 inflammasome causes inflammation and abnormal skeletal development in mice. PLoS One. 7(4):e35979. Epub 2012 Apr 27. PMCID: PMC3338787

Novack DV. (2011) Role of NF-κB in the skeleton. Cell Res. 21(1): 169-82.

Yang C, McCoy K, Davis JL, Schmidt-Supprian M, Sasaki Y, Faccio R, Novack DV. (2010). NIK Stabilization in Osteoclasts Results in Osteoporosis and Enhanced Inflammatory Osteolysis. PLoS ONE 5(11): e15383. doi:10.1371/journal.pone.0015383. PMCID: PMC2975662

Vaira S, Alhawagri M, Anwisye I, Kitaura H, Faccio R, and Novack DV. (2008). RANKL activates an apoptotic JNK pathway opposed by RelA/p65. J Clin Invest 118: 2088-2097. PMCID: PMC2373419

Vaira S, Johnson T, Hirbe AC, Alhawagri M, Anwisye I, Sammut B, O’Neal J, Zou W, Weilbaecher KN, Faccio R, and Novack DV. (2008). RelB is the NF-kappaB subunit downstream of NIK responsible for osteoclast differentiation. Proc. Natl. Acad. Sci 105: 3897-3902. PMCID: PMC2268780

Last Updated: 12/11/2017 10:54:36 AM

Antagonism of IAP proteins increases bone metastasis via unexpected osteoclast activation. Cancer Discovery 2013;3:212-223.
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