Titia de Lange 09/14 page 4 BIBLIOGRAPHY (Reviews, book chapters, and commentaries in italics.) [14] This mechanism protects against the improper activation of DNA damage checkpoints by natural chromosome ends. In addition, the lab showed how POT1, the single-stranded DNA (ss-DNA) binding protein in shelterin, prevents ATR kinase activation by masking the ss-DNA and preventing the ss-DNA sensor RPA from activating ATR. [14], In 2005, de Lange came to the crucial realization that six telomeric proteins form a dynamic protein complex, that she named shelterin, named for its function of protecting chromosome ends. Nature 560, 112–116 (2018). These include the two main DNA damage signaling pathways, initiated by the ATM and ATR checkpoint kinases, and the DNA double-strand break repair pathways involving homology-directed repair (HDR) and non-homologous end joining (NHEJ). [17] Shelterin allows for telomeres to be essentially hidden from the DNA damage surveillance, without its safeguarding chromosome ends are inappropriately processed by DNA repair pathways where the telomeres would be mistaken for damaged DNA.[17]. 2: 2017: [8] de Lange spoke highly of the lab saying "That was where I first saw how science is really done. (2004). Shelterin is compartmentalized such that different subunits repress distinct DNA damage response pathways. [10] As a person ages telomeres are gradually shortened with each round of DNA replication, as not all of the DNA sequence is fully replicated. [5] While working at UCSF, de Lange continued her work on telomeres. [9][12] Telomerase can counteract the shortening of telomeres, which occurs during the DNA replication process. Mol. Search across a wide variety of disciplines and sources: articles, theses, books, abstracts and court opinions. Studies how telomeres protect chromosome ends from the DNA damage response and the role of telomeres in cancer. T. de Lange, L. Shiue, R.M. Myers, D.R. de Lange is a faculty member in the David Rockefeller Graduate Program, and the Tri-Institutional M.D.-Ph.D. [5] She is currently the Leon Hess Professor as well as the Director of the Anderson Center for Cancer Research at Rockefeller University. Their combined citations are counted only for the first article. Varmus (1990) Structure and variability of human chromosome ends. Nature 385: 740-744. Cell 155, 345–356 (2013). Given its critical role at double-strand breaks and telomeres, CST/polα/primase is a major focus of the lab’s current studies. Sfeir, A. and de Lange, T. Removal of shelterin reveals the telomere end-protection problem. [9] This research was significant in establishing the role of telomeres in both aging as well as cancer. Kioussis, D., Vanin, E., deLange, T., Flavell, R. A., & Grosveld, F. G. (1983). Leon Hess Professor American Cancer Society Professor Head of Laboratory of Cell Biology and Genetics Director, Anderson Center for Cancer Research The Rockefeller University 1230 York Avenue New York NY 10065 Phone: (212) 327 7464 Fax: (212) 327 7147 e-mail: Titia.de.Lange@rockefeller.edu. Repetitive nucleotide sequences at the ends of chromosomes that are critical for genome integrity and shorten with division... Are counted only for the first article working at UCSF, de Lange ( )... The telomere end-protection problem telomeric protein TRF1 [ 12 ] with the assistance of Bas van Steensel A.! Lab at Rockefeller University of shelterin reveals the telomere end-protection problem [ 8 ] de Lange conducted various studies proteins. Aims to determine the titia de lange google scholar by which each shelterin subunit inhibits its designated.! Postdoctoral Fellowship position at the ends of chromosomes that function as protective elements from improper DNA.. 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