Prof Ehud Razin
IMRIC, Faculty of Medicine, The Hebrew University of Jerusalem
Prof. Ehud Razin received his B.Sc.in Biology and M.Sc. in Microbiology from the Hebrew University and his Ph.D. in Immunology from the Weizmann Institute of Science, Rehovot, Israel.
Prof. Razin has for many years been a major contributor and leading scientist in the field of mast cell biology. In 1980, while most investigators used rat peritoneal mast cells as a model for study their function, he successfully developed a cultured mouse bone marrow derived system as a mast cells model1. This system still serves as the main tool for studying mast cell function.
Prof. Razin’s long term goal has been to try to ascertain the regulation of gene transcription in mast cells due to their interaction with their growth factors and in response to trigger by immunological stimulus through their surface FCεRI receptors. His team has explored the relationship between aggregation of mast cell surface receptors and AP-1, USF2 and microphthalmia transcription factor (MITF) transcriptional activity. Prof. Razin continued to push the mast cell field ahead by discovering few years ago a new signaling pathway in mast cells and other cells which directly involved in gene regulation. His team observed that in variety of cells LysRS forms a complex with either MITF or USF2, while Ap4A produced by LysRS causes the release of Hint-1 from these two transcription factors. As Hint-1 suppresses the transcriptional activity of MITF and USF2 in these cells, Ap4A could act as a general regulator of the transcriptional activity of transcription factors belonging to the HLH family of proteins2 3. His team also researches the molecular mechanisms of the inhibition of MITF and STAT3 transcriptional activity by PIAS34 5 6.
Other aspects of Prof. Razin’s mast cell research include the dependence of Bcl-2 on its association with HSP90β for its anti-apoptotic function in mast cells7. Recently Prof. Razin has added an exciting new direction to his laboratory’s research by investigating MITF’s functions in the heart8. A role of MITF in cardiac hypertrophy has being demonstrated and the cardiac isoforms of MITF have been characterized.
Prof Razin has been published in top peer-reviewed journals such as Immunity, The Journal of Clinical Investigation and Molecular Cell.
1 Razin, E., C. Cordon-Cardo, and R.A. Good, Growth of a pure population of mouse mast cells in vitro with conditioned medium derived from concanavalin A-stimulated splenocytes. Proc Natl Acad Sci U S A, 1981. 78: p. 2559-61.
2 Lee, Y.N., H. Nechushtan, N. Figov, and E. Razin, The function of lysyl-tRNA synthetase and Ap4A as signaling regulators of MITF activity in FcepsilonRI-activated mast cells. Immunity, 2004. 20: p. 145-51.
3 Yannay-Cohen, N., I. Carmi-Levy, G. Kay, C.M. Yang, J.M. Han, D.M. Kemeny, S. Kim, H. Nechushtan, and E. Razin, LysRS serves as a key signaling molecule in the immune response by regulating gene expression. Mol Cell, 2009. 34: p. 603-11.
4 Levy, C., H. Nechushtan, and E. Razin, A new role for the STAT3 inhibitor, PIAS3: a repressor of microphthalmia transcription factor. J Biol Chem, 2002. 277: p. 1962-6.
5 Levy, C., A. Sonnenblick, and E. Razin, Role played by microphthalmia transcription factor phosphorylation and its Zip domain in its transcriptional inhibition by PIAS3. Mol Cell Biol, 2003. 23: p. 9073-80.
6 Levy, C., Y.N. Lee, H. Nechushtan, O. Schueler-Furman, A. Sonnenblick, S. Hacohen, and E. Razin, Identifying a common molecular mechanism for inhibition of MITF and STAT3 by PIAS3. Blood, 2006. 107: p. 2839-45.
7 Cohen-Saidon, C., I. Carmi, A. Keren, and E. Razin, Antiapoptotic function of Bcl-2 in mast cells is dependent on its association with heat shock protein 90beta. Blood, 2006. 107: p. 1413-20.
8 Tshori, S., D. Gilon, R. Beeri, H. Nechushtan, D. Kaluzhny, E. Pikarsky, and E. Razin, Transcription factor MITF regulates cardiac growth and hypertrophy. J Clin Invest, 2006. 116: p. 2673-81.
SELECTED RECENT PAPERS:
- Levy, C., Nechushtan, H., Razin, E. A new role for the STAT3 inhibitor, PIAS3: a repressor of microphthalmia transcription factor. J Biol Chem 2002; 277: 1962-6.
- Lee, Y.N., Nechushtan, H., Figov, N., Razin, E. The function of lysyl-tRNA synthetase and Ap4A as signaling regulators of MITF activity in FCeRI-activated mast cells. Immunity 2004; 20: 145-51.
- Sonnenblick, A., Levy, C., Razin, E. Interplay between MITF, PIAS3, and STAT3 in Mast Cells and Melanocytes. Mol Cell Biol 2004; 24: 10584-92.
- Sonnenblick, A., Levy, C., Razin, E. Immunological trigger of mast cells by monomeric IgE: Effect on microphthalmia transcription factor, STAT3 network of interactions. J Immunol 2005; 175: 1450-1455.
- Lee, Y,-N, Razin, E. Nonconventional involvement of LysRS in the molecular mechanism of USF2 transcriptional activity in FceRI-activated mast cells. Mol Cell Biol 2005; 25: 8904-8912.
- Nechushtan, H., Razin, E. Mast cells: must they always be different? (Inside Blood) Blood 2006; 107: 1-2
- Cohen-Saidon, C., Carmi, I., Keren, A., Razin, E. Anti-apoptotic function of Bcl-2 in mast cells is dependent on its association with Heat Shock Protein 90b. Blood 2006; 107: 1413-1420.
- Levy, C., Lee, Y.-N., Nechushtan, H., Sonnenblick, A., Hacohen, S., R azin, E. Identifying a common molecular mechanism for inhibition of MITF and STAT3 by PIAS3 Blood 2006; 107: 2839-2845.
- Cohen-Yannay, N., Razin, E. Translation and transcription – the dual functionality of LysRS in mast cells. Mol Cells 2006; 22: 127-32.
- Tshori, S., Gilon, D., Beeri, R., Nechushtan, H., Kaluzhny, D., Pikarsky, E. & Razin, E. Transcription factor MITF regulates cardiac growth and hypertrophy J Clin Invest 2006; 116: 2673-2681.
- Carmi, I. & Razin E. The role played by key transcription factors in activated mast cells Immunol Rev 2007; 217: 280-91.
- Tshori, S., Sonnenblick, A., Yannay-Cohen, N., Nechushtan, H., Kay, G. & Razin, E. The role of microphthalmia transcription factor isoforms in mast cells and in the heart. Mol Cell Biol 2007; 27: 3911-9.
- Carmi-Levy, I., Yannay-Cohen, N., Kay, G., Razin, E., Nechushtan, H. Diadenosine tetraphosphate hydrolase is part of the transcriptional regulation network in immunologically activated mast cells. Mol Cell Biol 2008; 28: 5777-84.
- Yagil, Z., Kay, G., Nechushtan, H., Razin, E. A specific epitope of PIAS3 is responsible for the induction of apoptosis in mast cells. J Immunol 2009; 182: 2168-75.
- Yannay-Cohen, N., Carmi-Levy, I., Kay, G., Yang, C.M., Han, J.M., Kemeny, D.M., Kim, S., Nechushtan, H., Razin, E. LysRS serves as a key signaling molecule in the immune response by regulating gene expression. Mol Cell 2009; 34: 603-11.
- Tshori, S. and Razin, E. Editorial: Mast cell degranulation and calcium entry--the Fyn-calcium store connection. J Leukoc Biol 2010; 88, 837-8.
- Yagil, Z., Nechushtan, H., Kay, G., Yang, C. M., Kemeny, D. M., Razin, E. The enigma of the role of protein inhibitor of activated STAT3 (PIAS3) in the immune response. Trends Immunol 2010; 31, 199-204.
- Carmi-Levy, I., Motzik, A., Ofir-Birin, Y., Yagil, Z., Yang, C. M., Kemeny, D. M., Han, J. M., Kim, S., Kay, G., Nechushtan, H., Suzuki, R., Rivera, J., Razin, E. Importin beta plays an essential role in the regulation of the LysRS-Ap4A pathway in immunologically activated mast cells. Mol Cell Biol 2011, 31, 2111-21.
- Yagil, Z., Hadad-Erlich, T., Ofir-Birin, Y., Tshori, S., Kay, G., Yehktin, Z., Fisher, D.E., Cheng, C., Wong, F.W.S., Hartmann, K., Razin, E. and Nechushtan, H. TFE3, a major regulator of mast cell mediated allergic response. J Allergy Clin Immunol 2012;129:1357-1366 e1355.
- Kim, D.G., J.W. Choi, J.Y. Lee, H. Kim, Y.S. Oh, J.W. Lee, Y.K. Tak, J.M. Song, E. Razin, S.H. Yun, and S. Kim, Interaction of two translational components, lysyl-tRNA synthetase and p40/37LRP, in plasma membrane promotes laminin-dependent cell migration. FASEB Journal, 2012. 26: p. 4142-4159.
- Ofir-Birin Y, Fang P, Bennett SP, Zhang H-M, Wang J, Rachmin I, Shapiro R, Song J, Dagan A, Pozo J, Kim S, Marshall AG, Schimmel P, Yang X-L, Nechushtan H, Razin E*, Guo M. Structural switch of lysyl-tRNA synthetase between translation and transcription. Mol Cell 2013; 49:30-42.