Ph.D. Wayne State University. 1990.
D.D.S. University of Michigan. 1980.
My research interests focus on normal and pathological tooth development. My research training was in biochemistry. I expressed the first recombinant amelogenin protein (rM179) and developed a purification method back in 1991. This protein, and the pig version (rP172), is still used by many labs to study amelogenin in vitro along with native amelogenins that we isolate from developing pig teeth. My lab characterized the protein and reported sequence data from a serine protease isolated from developing pig teeth to publish the first cDNA and genomic sequences of what is now known as KLK4. We also fabricated and characterized Klk4 null mice. I am the recognized world expert on this protease and wrote invited chapters on this enzyme in the most recent 2 versions of the Handbook of Proteolytic Enzymes and have twice been an invited to speak on KLK4 at the International Symposium on Kallikreins and Kallikrein-Related Peptidases. Besides the biochemistry of tooth development, I have always been excited about genetics and am course director and principle lecturer for DENT 539 on Tooth Development, Regeneration and Genetics. I work with Dr. Hu to characterize the disease-causing mutations in the families with inherited tooth defects that Dr. Hu recruits. We have identified over 40 disease-causing mutations and were the first to report that FAM83H and ITGB6 mutations cause enamel defects, and that FAM20A mutations cause Enamel Renal Syndrome. Over time I have come to appreciate the great benefits of studying normal tooth development in animals and the genetics of pathological tooth development in humans. I believe that the first step toward improved treatments and cures for inherited conditions is to identify the genes/mutations that cause the disease. Knowing that a gene/protein is critical for normal tooth development in lab animals strongly influences our ability to conclude that an observed mutation in a family with inherited tooth defects is the cause of their disease. There are very few labs, worldwide that combine expertise in tooth development with the genetics of human tooth defects.
Vieira AR, Lee M, Vairo F, Leite JCL, Munerato M, Visioli F, D’Avila AR, Wang SK, Choi M, Simmer JP and Hu JCC. (2015). Root anomalies and dentin dysplasia in autosomal recessive hyperphosphatemic familial tumoral calcinosis (HFTC). Oral Surg Oral Med Oral Pathol Oral Radiol. pii: S2212-4403(15)00918-9.
Bartlett JD and Simmer JP (2015) New Perspectives on Amelotin and Amelogenesis. J Dent Res 94:642-4.
Wang S-H, Hu Y, Yang J, Smith CE, Nunez SM, Richardson AS, Pal S, Samann AC, Hu JC-C, and Simmer JP, (2015) Critical Roles For WDR72 in Calcium Transport and Matrix Protein Removal During Enamel Maturation. Molecular Genetics & Genomic Medicine. 3(4):302-19.
Yang J, Wang S-H, Choi M, Reid BM, Hu Y, Lee Y-L, Herzog CR, Kim-Berman H, Lee M, Benke PJ, Kent Lloyd KC, Simmer JP, Hu JC-C (2015) Taurodontism, Variations in Tooth Number, and Misshapened Crowns in Wnt10a Null Mice and Human Kindreds. Molecular Genetics & Genomic Medicine 3:40–58.
Herzog CR, Reid BM, Seymen F, Koruyucu M, Tuna EB, Simmer JP, Hu JC (2014) Hypomaturation amelogenesis imperfecta caused by a novel SLC24A4 mutation. Oral Surg Oral Med Oral Pathol Oral Radiol 119(2):e77-81.
Suzuki M, Shin M, Simmer JP and Bartlett JD (2014) Fluoride Affects Enamel Protein Content via TGF-beta1-mediated KLK4 Inhibition. J Dent Res 93:1022-7.
Bartlett JD and Simmer JP (2014) Kallikrein-related peptidase-4 (KLK4): role in enamel formation and revelations from ablated mice. Front Physiol 5:240:10.3389/ fphys.2014.00240.
Kawasaki K, Hu JC and Simmer JP (2014) Evolution of Klk4 and enamel maturation in eutherians. Biol Chem 395:1003-13.
Kwak SY, Kim S, Yamakoshi Y, Simmer JP, Beniash E and Margolis HC (2014) Regulation of calcium phosphate formation by native amelogenins in vitro. Connect Tissue Res 55:21-4.
Wang S-K, Choi M, Richardson A, Reid B, Seymen F, Yildirim M, Tuna E, Gencay K, Simmer JP and Hu JC-C (2014) STIM1 and SLC24A4 are critical for enamel maturation. J Dent Res 93:94-100.
Wang SK, Choi M, Richardson AS, Reid BM, Lin BP, Wang SJ, Kim JW, Simmer JP, Hu JC-C (2014) ITGB6 loss-of-function mutations cause autosomal recessive amelogenesis imperfecta. Hum Mol Genet 23:2157-63.
Hu JC, Hu Y, Lu Y, Smith CE, Lertlam R, Wright JT, Suggs C, McKee MD, Beniash E, Kabir ME, Simmer JP (2014) Enamelin is critical for ameloblast integrity and enamel ultrastructure formation. PLoS One 9:e89303.
Wang SK, Reid BM, Dugan SL, Roggenbuck JA, Read L, Aref P, Taheri AP, Yeganeh MZ, Simmer JP, Hu JC-C (2014) FAM20A Mutations Associated with Enamel Renal Syndrome. J Dent Res 93:42-8.