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

Internal Medicine
Bone & Mineral Diseases
Pathology and Immunology

Molecular Cell Biology Program
Molecular Microbiology and Microbial Pathogenesis Program
Immunology Program

  • 314-454-8472

  • 314-454-5975

  • 314-454-5047

  • 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:

The Veis lab utilizes a combination of transgenic mouse models and pharmacological approaches to study the molecular regulation of bone mass under basal and diseased conditions, including infection, postmenopausal osteoporosis, and bone metastasis. Our overarching research questions include:
1. How do mitochondrial dynamics impact osteoclast and osteoblast function?
• Bone cells are rich in mitochondria, but the field has yet to investigate other properties of these organelles in bone aside from energy production
• We’re using conditional deletion of mitochondrial fusion and mitophagy protein Mitofusin 2 in bone cells to determine how mitochondrial dynamics affect the bone cells

2. How does the bone microenvironment propagate bacterial insult to the bone by S. aureus?
• Bacterial infection of the bone leads to severe disruption of skeletal integrity that often requires amputation
• We’re using in vitro and in vivo models of osteomyelitis (bone infection) to understand how bone cells interact with S. aureus

3. How does the alternative NF-kB pathway in osteoblasts regulate bone mass and metabolic function?
• The alternative NF-kB pathway is not as well-studied as its classical counterpart, and its role in bone formation is not defined
• By manipulating components of the NF-kB pathway in the osteoblast lineage in mice, we’re discovering unexpected effects on bone formation and bone-driven effects on fat metabolism

4. What accounts for the sex differences in response to anti-cancer drugs in bone?
• Male and female mice respond differently to manipulation of alternative NF-kB signaling in terms of bone mass
• We want to understand how drugs that modulate the pathway may have different effects on bone metastasis in males and females

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 U S A. 2015; 112(33):10455-60. PMCID: PMC4547270.

Zeng R, Faccio R, Novack DV. Alternative NF-kB regulates RANKL-induced osteoclast differentiation and mitochondrial biogenesis via independent mechanisms. J Bone Miner Res. 2015; 30(12):2287-99. PMCID: PMC4834842.

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: 7/30/2018 9:47:48 AM

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