-CORE B Core B supports every project within the Program by providing access to state-of-the-art CRISPR-Cas9 and RNAi tools. Short hairpin RNAs (shRNAs) were developed with the support of this program, and ongoing innovations by Core B and Program investigators have helped to make these extremely powerful biological tools. During the past funding period, the Core devised a novel algorithm for predicting shRNA potency, which led to the generation of a 5th version of RNAi libraries corresponding to annotated protein coding genes in humans and mice. Technology has also been developed for using CRISPR-Cas9 screening to expose functionally important protein domains. During the upcoming period of requested support, the Core proposes to aid Program investigators through five general aims. First, the program will continue providing access to state- of-the-art RNAi vectors and CRISPR-Cas9 vectors and procedures for analyzing either single gene knockdowns or for performing pooled RNAi/CRISPR screens. Second, the Core will provide Program investigators with access to the mouse and human version 5 shRNA library and will compile sub-libraries upon request. Third, the Core will construct custom CRISPR-scanning libraries for performing structure-function analysis on genes of interest within each Program. Fourth, the Core will produce custom domain-focused CRISPR libraries to allow for interrogation and discovery cancer drug targets in various contexts. Fifth, the Core will carry on its efforts to improve CRISPR-Cas9 technologies, and make those innovations available to the Program and to the scientific community at large.
- CORE B Core B will provide Program investigators with a suite of newly developed genetic tools for studying basic molecular mechanisms and for exposing novel vulnerabilities in cancer cells. In particular, the CRISPR-Cas9 methodology provided in this Core provides an innovative method for cancer drug target discovery and exposing functional domains of protein and non-coding RNAs.
| Knott, Simon R V; Wagenblast, Elvin; Khan, Showkhin et al. (2018) Asparagine bioavailability governs metastasis in a model of breast cancer. Nature 554:378-381 |
| Shamay, Yosi; Shah, Janki; I??k, Mehtap et al. (2018) Quantitative self-assembly prediction yields targeted nanomedicines. Nat Mater 17:361-368 |
| Tramentozzi, Elisa; Ferraro, Paola; Hossain, Manzar et al. (2018) The dNTP triphosphohydrolase activity of SAMHD1 persists during S-phase when the enzyme is phosphorylated at T592. Cell Cycle 17:1102-1114 |
| Arun, Gayatri; Diermeier, Sarah D; Spector, David L (2018) Therapeutic Targeting of Long Non-Coding RNAs in Cancer. Trends Mol Med 24:257-277 |
| Tarumoto, Yusuke; Lu, Bin; Somerville, Tim D D et al. (2018) LKB1, Salt-Inducible Kinases, and MEF2C Are Linked Dependencies in Acute Myeloid Leukemia. Mol Cell 69:1017-1027.e6 |
| Xu, Yali; Milazzo, Joseph P; Somerville, Tim D D et al. (2018) A TFIID-SAGA Perturbation that Targets MYB and Suppresses Acute Myeloid Leukemia. Cancer Cell 33:13-28.e8 |
| Huang, Yu-Han; Klingbeil, Olaf; He, Xue-Yan et al. (2018) POU2F3 is a master regulator of a tuft cell-like variant of small cell lung cancer. Genes Dev 32:915-928 |
| Livshits, Geulah; Alonso-Curbelo, Direna; Morris 4th, John P et al. (2018) Arid1a restrains Kras-dependent changes in acinar cell identity. Elife 7: |
| Tiriac, Hervé; Belleau, Pascal; Engle, Dannielle D et al. (2018) Organoid Profiling Identifies Common Responders to Chemotherapy in Pancreatic Cancer. Cancer Discov 8:1112-1129 |
| Bhagwat, Anand S; Lu, Bin; Vakoc, Christopher R (2018) Enhancer dysfunction in leukemia. Blood 131:1795-1804 |
Showing the most recent 10 out of 610 publications
