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180Anja Nohe, Ph.D. <p>Associate Professor <br></p>(302) 831-2959 (302) 831-2281 anjanohe@udel.edu 283 DBI242 DBIDepartment of Biological Sciences Wolf Hall University of Delaware Newark, DE 19716 <ul> <li><strong>Diplom.</strong> - University of Würzburg (Germany) </li><li><strong>Ph.D.</strong> - Theodor Boveri Institute, University of Würzburg (Germany) </li><li><strong>Postdoctoral</strong> - University of Western Ontario (Canada) </li></ul><ul> <li><strong>Development of Delivery Techniques.</strong> Current research is limited in tools to transfect proteins into cells, especially the cell nucleus. We recently developed a new very efficient transfection technique for proteins and nanoparticles into the cell nucleus. Our method provides 70-80 percent transfection efficiency of primary cells and cell lines. The uptake is very rapidly, cells stay alive for at least 3 days. Studies show that the method is non invasive, making it a powerful transfection tool. We are currently working on the detailed mechanism of the delivery. </li><li><strong>Development of New Imaging Techniques.</strong> In order to study signal transduction in real time in live cells new imaging tools must be developed. One major goal of my research focuses on the further development of the Family of Image Correlation Spectroscopy (FICS), a powerful tool to measure protein dynamics, aggregation and signalling. </li><li><strong>Differentiation of Stem Cells: Role of Hormones and Growth factors.</strong> In general my laboratory is interested in determining molecular dynamics underlying stem cell differentiation. In detail I am interested in developing new imaging techniques and probes to study real time dynamics of signal transduction mechanisms. We are especially interested to develop new probes and delivery techniques and use these approaches to investigate the influence of nanoscale receptor dynamics underlying diseases such as cancer and osteoporosis. </li></ul><p> </p><p>Project 1. Osteoporosis: One in two women and one in eight men over the age of 50 will have an osteoporosis-related fracture in their lifetime. In 2005, osteoporosis-related fractures were responsible for an estimated $19 billion in costs and are estimated to cost 25.3 billion by 2025. Considering these data, it is surprising that only a limited number of treatment options for osteoporosis exist. These options include a majority of antiresorptive agents that target osteoclasts to reduce bone resorption and one approved anabolic agent, which focus on increasing bone formation. Antiresorptive agents inhibit further loss of bone mass, but the induction of bone formation is very slow. A PTH analog is the only current approved therapeutic agent that enhances osteoblast activity. Often in order to prevent rapid bone turnover and loss of the newly formed bone bisphosphonates are administered to block osteoclasts. New more advanced therapeutics for osteoporosis should drive osteogenesis but also inhibit osteoclastogenesis. Our lab focuses on developing new therapeutics that can drive bone formation.</p><p>Project 2. OA is a major debilitating disease caused by the gradual loss of cartilage, primarily affecting the knees, hips, hands, feet, and spine. OA increases aggregate health care expenditures by $186 billion annually. The Centers for Disease Control and Prevention (CDC) estimates 27 million Americans suffer from OA. Estimates show that by year 2030, 20% of the adult U.S. population, or nearly 67 million people, will have physician-diagnosed arthritis. Unfortunately, optimal, long-term treatment for OA has not yet been discovered and new approaches  for cartilage repair and regeneration are needed. Our laboratory addresses important problems associated with the treatment of OA.</p><p> </p><p><span style="font-family:arial, helvetica, sans-serif;">Linda Sequeira (Research Associate)</span></p> <p><span style="font-family:arial, helvetica, sans-serif;">Nguyen John (PhD student)</span></p> <p><span style="font-family:arial, helvetica, sans-serif;">Weidner Hilary (PhD student)</span></p> <p><span style="font-family:arial, helvetica, sans-serif;">Vrathasha Vrathasha (PhD student)</span></p> <p><span style="font-family:arial, helvetica, sans-serif;">Lora Schell (Master student)</span></p> <p><span style="font-family:arial, helvetica, sans-serif;">Daniel Halloran (Master student)</span></p> <p><span style="font-family:arial, helvetica, sans-serif;">Ryan Wood (Undergraduate research) </span></p> <p><span style="font-family:arial, helvetica, sans-serif;">Semaj Kelly (Undergraduate research)</span></p> <p><span style="font-family:arial, helvetica, sans-serif;">Sabra Mahmoud (Undergraduate research)</span></p> <p><span style="font-family:arial, helvetica, sans-serif;"></span></p><span style="font-size:12pt;"><span id="cke_bm_706S" style="display:none;"> </span><span id="cke_bm_707S" style="display:none;"> </span><span id="cke_bm_708S" style="display:none;"> </span><span id="cke_bm_708E" style="display:none;"> </span><span id="cke_bm_707E" style="display:none;"> </span><span id="cke_bm_706E" style="display:none;"> </span></span> <p> </p><p> </p><em> </em><span aria-hidden="true"></span><span>Durbano, H.W.; Halloran, D.; Nguyen, J.; Stone, V.; McTague, S.; Eskander, M.; <strong>Nohe, A.</strong> Aberrant BMP2 Signaling in Patients Diagnosed with Osteoporosis. Int. J. Mol. Sci. 2020, 21, 6909.<br><br>Halloran D, Vrathasha V, Durbano HW, <strong>Nohe A. </strong>Bone Morphogenetic Protein-2 Conjugated to Quantum Dot®s is Biologically Functional. Nanomaterials (Basel). 2020;10(6):120.<br><br> Nguyen, J.; Kelly, S.; Wood, R.; Heubel, B.; <strong>Nohe, A.</strong> A Synthetic Peptide, CK2.3, Inhibits RANKL-Induced Osteoclastogenesis through BMPRIa and ERK Signaling Pathway. J. Dev. Biol. 2020, 8, 12.<br><br>Sequeira, L.; Nguyen, J.; Wang, L.; <strong>Nohe, A.</strong> A Novel Peptide, CK2.3, Improved Bone Formation in Ovariectomized Sprague Dawley Rats. Int. J. Mol. Sci. 2020, 21, 4874.<br><br>Weidner H, Yuan Goa V, Dibert D, McTague S, Eskander M, Duncan R, Wang L, <strong>Nohe A.</strong> CK2.3, a mimetic peptide of the BMP Type I Receptor Increases Activity in Osteoblasts over BMP2. Int. J.Mol. Sci. 2019; 20(23), 5877.  <a href="https://doi.org/10.3390/ijms20235877">https://doi.org/10.3390/ijms20235877</a>. Epub 2019 Nov 23. PubMed PMID: 31771161; PubMed Central PMCID: PMC6929093 <br><br><a href="https://ascpt.onlinelibrary.wiley.com/action/doSearch?ContribAuthorStored=Forder%2c+James">James Forder</a>, <a href="https://ascpt.onlinelibrary.wiley.com/action/doSearch?ContribAuthorStored=Smith%2c+Mallory">Mallory Smith</a>, <a href="https://ascpt.onlinelibrary.wiley.com/action/doSearch?ContribAuthorStored=Wagner%2c+Margot">Margot Wagner</a>, <a href="https://ascpt.onlinelibrary.wiley.com/action/doSearch?ContribAuthorStored=Schaefer%2c+Rachel+J">Rachel J. Schaefer</a>, <a href="https://ascpt.onlinelibrary.wiley.com/action/doSearch?ContribAuthorStored=Gorky%2c+Jonathon">Jonathon Gorky</a> , <a href="https://ascpt.onlinelibrary.wiley.com/action/doSearch?ContribAuthorStored=Golen%2c+Kenneth+L">Kenneth L. van Golen</a>, <a href="https://ascpt.onlinelibrary.wiley.com/action/doSearch?ContribAuthorStored=Nohe%2c+Anja"><strong>Anja Nohe</strong></a>, <a href="https://ascpt.onlinelibrary.wiley.com/action/doSearch?ContribAuthorStored=Dhurjati%2c+Prasad">Prasad Dhurjati</a>. A Physiologically‐Based Pharmacokinetic Model for Targeting Calcitriol‐Conjugated Quantum Dots to Inflammatory Breast Cancer Cells. Clinical and Translational Science. <a href="https://doi.org/10.1111/cts.12664">https://doi.org/10.1111/cts.12664</a>. <br><br>Vrathasha V, Weidner H, <strong>Nohe A.</strong> <a href="https://www.ncbi.nlm.nih.gov/pubmed/31117181/">Mechanism of CK2.3, a Novel Mimetic Peptide of Bone Morphogenetic Protein Receptor Type IA, Mediated Osteogenesis. </a>Int J Mol Sci. 2019 May 21;20(10). doi: 10.3390/ijms20102500. PubMed PMID: 31117181.<br><br>Nguyen J, Weidner H, Schell LM, Sequeira L, Kabrick R, Dharmadhikari S, Coombs H, Duncan RL, Wang L, <strong>Nohe A.</strong> <a href="https://www.ncbi.nlm.nih.gov/pubmed/30294717">Synthetic Peptide CK2.3 Enhances Bone Mineral Density in Senile Mice.</a> J Bone Res. 2018;6(2). pii: 190. doi: 10.4172/2572-4916.1000190. Epub 2018 Jun 30. PubMed PMID: 30294717; PubMed Central PMCID: PMC6173331. <br><br>Swarup A, Weidner H, Duncan R, <strong>Nohe A.</strong> <a href="https://www.ncbi.nlm.nih.gov/pubmed/29941780">The Preservation of Bone Cell Viability in a Human Femoral Head through a Perfusion Bioreactor.</a> Materials (Basel). 2018 Jun 25;11(7). pii: E1070. doi: 10.3390/ma11071070. PubMed PMID: 29941780; PubMed Central PMCID: PMC6073554. <br><br>Vrathasha V, Booksh K, Duncan RL, <strong>Nohe A.</strong> <a href="https://www.ncbi.nlm.nih.gov/pubmed/29987256">Mechanisms of Cellular Internalization of Quantum Dot® Conjugated Bone Formation Mimetic Peptide CK2.3.</a> Nanomaterials (Basel). 2018 Jul 9;8(7). pii: E513. doi: 10.3390/nano8070513. PubMed PMID: 29987256; PubMed Central PMCID: PMC6071089. <br><br>Lisberg A, Ellis R, Nicholson K, Moku P, Swarup A, Dhurjati P, <strong>Nohe A.</strong> <a href="https://www.ncbi.nlm.nih.gov/pubmed/28181418">Mathematical modeling of the effects of CK2.3 on mineralization in osteoporotic bone.</a> CPT Pharmacometrics Syst Pharmacol. 2017 Mar;6(3):208-215. doi: 10.1002/psp4.12154. Epub 2017 Feb 9. PubMed PMID: 28181418; PubMed Central PMCID: PMC5351412. <br><br>Nguyen J, <strong>Nohe A.</strong> <a href="https://www.ncbi.nlm.nih.gov/pubmed/30123890">Factors that Affect the Osteoclastogenesis of RAW264.7 Cells.</a> J Biochem Anal Stud. 2017;2(1). doi: 10.16966/2576-5833.109. Epub 2017 Aug 28. PubMed PMID: 30123890; PubMed Central PMCID: PMC6097532. <br><br><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Akkiraju%20H%5bAuthor%5d&cauthor=true&cauthor_uid=27312334">Akkiraju H</a>, <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Bonor%20J%5bAuthor%5d&cauthor=true&cauthor_uid=27312334">Bonor J</a>, <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Nohe%20A%5bAuthor%5d&cauthor=true&cauthor_uid=27312334"><strong>Nohe A</strong></a> (2016)  CK2.1, a novel peptide, induces articular cartilage formation in vivo. <a href="https://www.ncbi.nlm.nih.gov/pubmed/27312334">J Orthop Res.</a> 2016 doi: 10.1002/jor.23342. <br><br>Akkiraju H, Bonor H, <strong>Nohe A</strong> (2015). An improved immunostaining and imaging methodology to determine cell and protein distributions within the bone environment. <br><br>Kim HS, Kim JE, Frailey D, <strong>Nohe A</strong>, Duncan R, Czymmek KJ, Kang S (2015).  <a href="http://www.ncbi.nlm.nih.gov/pubmed/26162966">Roles of three Fusarium oxysporum calcium ion (Ca(2+)) channels in generating Ca(2+) signatures and controlling growth.</a> Fungal Genet Biol. 2015 Sep;82:145-57. doi: 10.1016/j.fgb.2015.07.003. <br><br><a href="http://www.ncbi.nlm.nih.gov/pubmed/?term=Gangadharan%20V%5bAuthor%5d&cauthor=true&cauthor_uid=25318104">Gangadharan V</a>, <a href="http://www.ncbi.nlm.nih.gov/pubmed/?term=Nohe%20A%5bAuthor%5d&cauthor=true&cauthor_uid=25318104"><strong>Nohe A</strong></a>, <a href="http://www.ncbi.nlm.nih.gov/pubmed/?term=Caplan%20J%5bAuthor%5d&cauthor=true&cauthor_uid=25318104">Caplan J</a>, <a href="http://www.ncbi.nlm.nih.gov/pubmed/?term=Czymmek%20K%5bAuthor%5d&cauthor=true&cauthor_uid=25318104">Czymmek K</a>, <a href="http://www.ncbi.nlm.nih.gov/pubmed/?term=Duncan%20RL%5bAuthor%5d&cauthor=true&cauthor_uid=25318104">Duncan RL</a>. Caveolin-1 regulates P2X7 receptor signaling in osteoblasts. <a href="http://www.ncbi.nlm.nih.gov/pubmed/25318104">Am J Physiol Cell Physiol.</a> 2015 Jan 1;308(1):C41-50. doi: 10.1152/ajpcell.00037.2014. Epub 2014 Oct 15.<br><br><p>J. Bonor, H. Akkiraju, C. Bowen, B. Bragdon, H. Coombs, L.R. Donahue, R. Duncan, and <strong>A. Nohe</strong>. Systemic injection of CK2.3, a novel peptide acting downstream of Bone Morphogenetic Protein receptor BMPRIa, leads to increased trabecular bone mass. Journal of Orthopedic Research. <a href="http://onlinelibrary.wiley.com/doi/10.1002/jor.v33.2/issuetoc">Volume 33, Issue 2, </a>pages 208–215, February 2015.<br></p></span><img alt="" src="/Images%20Bios/Nohn_Anja-007.png" style="BORDER:0px solid;" />

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