Rik Derynck, PhD

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
Rik Derynck, PhD

Professor, Departments of Cell/Tissue Biology and Anatomy, UCSF

derynck@itsa.ucsf.edu

Phone: (415) 476-7322, 476-6081 (voice)
Box 0640, UCSF
San Francisco, CA 94143-0640

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Cancer Center Membership

Program Member » Developmental Therapeutics

Research Summary

My research goes back to the early days of recombinant DNA, when it was discovered that cDNA could be made in vitro using mRNA as template, when the first restriction enzymes were had to be purified (and exchanged) before starting your research, and when one did not yet have scenarios on how to express a foreign gene from a plasmid in bacteria. As a graduate student, I initiated research that deviated from the overall scope of the host lab and led to the cDNA cloning and bacterial expression of fibroblast interferon, now known as interferon-β. The impact of this research was very substantial, and occurred at the time that cDNA cloning of some proteins with therapeutic potential led to the formation of the first biotechnology companies. This interferon was then developed as a therapy by Biogen and is now clinically used. I moved in 1981 into Genentech, where I started research that led to the characterization of transforming growth factors, i.e. TGF-α and TGF-β, which rapidly became prototypes for their respective families. TGF-α is a transmembrane growth factor, as are the other growth factors in that family, and was originally thought to only act in carcinomas. My lab had a research program on the biology of TGF-α for more than 20 years. I also showed through cDNA cloning that TGF-β was very different from TGF-α. TGF-β, now known as TGF-β1, is the founding member of a large family of differentiation factors of high relevance in developmental and cancer biology, and immunology.

During the last 30 years, my lab made many key contributions to this now extensive research area on the biology of the TGF-β family. My lab was instrumental in identifying the TGF-β receptors and Smads and the mechanisms of Smad signaling and transcriptional control, and has also been playing a key role in the characterization of non-Smad mechanisms of TGF-β signaling. My lab also discovered that TGF-β induces epithelial-mesenchymal differentiation (which was initially highly controversial), and has been pursuing underlying mechanisms after the TGF-β signaling mediators were identified and starting to be characterized. My lab is seen as a leader in the TGF-β field, having contributed in major ways since its inception. Many mechanistic and conceptual advances in the field originate from my lab.

Education

University of Louvain, Belgium, Lic.Sc.(M.Sc.), 1974, Zoology
University of Ghent, Belgium, Ph.D., 1981, Molecular Biology


Professional Experience

  • 1973-1974
    Undergraduate thesis with Dr. Henri Koch, Catholic University, Louvain, Belgium
  • 1974-1981
    Predoctoral Fellow/Research Associate with Dr. Walter Fiers, State University, Ghent, Belgium
  • 1981-1985
    Scientist, Dept. of Molecular Biology, Genentech Inc., South San Francisco
  • 1985-1990
    Senior Scientist, Departments of Molecular and Developmental Biology, Genentech Inc., South San Francisco
  • 1991-present
    Professor, Department of Cell and Tissue Biology and Department of Anatomy, University of California San Francisco
  • 2002-present
    Director, UCSF Program in Craniofacial and Mesenchymal Biology, University of California San Francisco
  • 2002-present
    Co-Director, UCSF Institute for Regeneration Medicine

Selected Publications

  1. Morikawa M, Derynck R, Miyazono K. TGF-ß and the TGF-ß Family: Context-Dependent Roles in Cell and Tissue Physiology. Cold Spring Harb Perspect Biol. 2016; 8(5).
    View on PubMed
  2. Budi EH, Xu J, Derynck R. Regulation of TGF-ß Receptors. Methods Mol Biol. 2016; 1344:1-33.
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  3. Muthusamy BP, Budi EH, Katsuno Y, Lee MK, Smith SM, Mirza AM, Akhurst RJ, Derynck R. ShcA Protects against Epithelial-Mesenchymal Transition through Compartmentalized Inhibition of TGF-ß-Induced Smad Activation. PLoS Biol. 2015 Dec; 13(12):e1002325.
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  4. Budi EH, Muthusamy BP, Derynck R. The insulin response integrates increased TGF-ß signaling through Akt-induced enhancement of cell surface delivery of TGF-ß receptors. Sci Signal. 2015; 8(396):ra96.
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  5. Xu P, Bailey-Bucktrout S, Xi Y, Xu D, Du D, Zhang Q, Xiang W, Liu J, Melton A, Sheppard D, Chapman HA, Bluestone JA, Derynck R. Innate Antiviral Host Defense Attenuates TGF-ß Function through IRF3-Mediated Suppression of Smad Signaling. Mol Cell. 2014 Dec 18; 56(6):723-37.
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  6. Derynck R, Muthusamy BP, Saeteurn KY. Signaling pathway cooperation in TGF-ß-induced epithelial-mesenchymal transition. Curr Opin Cell Biol. 2014 Dec; 31:56-66.
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  7. Kehrl JH, Wakefield LM, Roberts AB, Jakowlew S, Alvarez-Mon M, Derynck R, Sporn MB, Fauci AS. Pillars Article: production of transforming growth factor ß by human T lymphocytes and its potential role in the regulation of T cell growth. J Exp Med. 1986. 163: 1037-1050. J Immunol. 2014 Apr 1; 192(7):2939-52.
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  8. Xu J, Derynck R. Does Smad6 methylation control BMP signaling in cancer? Cell Cycle. 2014 Apr 15; 13(8):1209-10.
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  9. Lamouille S, Xu J, Derynck R. Molecular mechanisms of epithelial-mesenchymal transition. Nat Rev Mol Cell Biol. 2014 Mar; 15(3):178-96.
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  10. Derynck R, Akhurst RJ. BMP-9 balances endothelial cell fate. Proc Natl Acad Sci U S A. 2013 Nov 19; 110(47):18746-7.
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  11. Xu J, Wang AH, Oses-Prieto J, Makhijani K, Katsuno Y, Pei M, Yan L, Zheng YG, Burlingame A, Brückner K, Derynck R. Arginine Methylation Initiates BMP-Induced Smad Signaling. Mol Cell. 2013 Jul 11; 51(1):5-19.
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  12. Sakaki-Yumoto M, Liu J, Ramalho-Santos M, Yoshida N, Derynck R. Smad2 is essential for maintenance of the human and mouse primed pluripotent stem cell state. J Biol Chem. 2013 Jun 21; 288(25):18546-60.
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  13. Lamouille S, Subramanyam D, Blelloch R, Derynck R. Regulation of epithelial-mesenchymal and mesenchymal-epithelial transitions by microRNAs. Curr Opin Cell Biol. 2013 Apr; 25(2):200-7.
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  14. Katsuno Y, Lamouille S, Derynck R. TGF-ß signaling and epithelial-mesenchymal transition in cancer progression. Curr Opin Oncol. 2013 Jan; 25(1):76-84.
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  15. Sakaki-Yumoto M, Katsuno Y, Derynck R. TGF-ß family signaling in stem cells. Biochim Biophys Acta. 2013 Feb; 1830(2):2280-96.
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  16. Xu P, Liu J, Derynck R. Post-translational regulation of TGF-ß receptor and Smad signaling. FEBS Lett. 2012 Jul 4; 586(14):1871-84.
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  17. Xu P, Liu J, Sakaki-Yumoto M, Derynck R. TACE activation by MAPK-mediated regulation of cell surface dimerization and TIMP3 association. Sci Signal. 2012 May 1; 5(222):ra34.
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  18. Lamouille S, Connolly E, Smyth JW, Akhurst RJ, Derynck R. TGF-ß-induced activation of mTOR complex 2 drives epithelial-mesenchymal transition and cell invasion. J Cell Sci. 2012 Mar 1; 125(Pt 5):1259-73.
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  19. Upadhyay G, Yin Y, Yuan H, Li X, Derynck R, Glazer RI. Stem cell antigen-1 enhances tumorigenicity by disruption of growth differentiation factor-10 (GDF10)-dependent TGF-beta signaling. Proc Natl Acad Sci U S A. 2011 May 10; 108(19):7820-5.
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  20. Subramanyam D, Lamouille S, Judson RL, Liu JY, Bucay N, Derynck R, Blelloch R. Multiple targets of miR-302 and miR-372 promote reprogramming of human fibroblasts to induced pluripotent stem cells. Nat Biotechnol. 2011 May; 29(5):443-8.
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