Joseph Schlessinger

Summary

Affiliation: Yale University
Country: USA

Publications

  1. Shi X, Mihaylova V, Kuruvilla L, Chen F, Viviano S, Baldassarre M, et al. Loss of TRIM33 causes resistance to BET bromodomain inhibitors through MYC- and TGF-?-dependent mechanisms. Proc Natl Acad Sci U S A. 2016;113:E4558-66 pubmed publisher
    ..These results describe a mechanism for BETi resistance and suggest that combining inhibition of TGF-? signaling with BET bromodomain inhibition may offer new therapeutic benefits. ..
  2. Kuzina E, Ung P, Mohanty J, Tomé F, Choi J, Pardon E, et al. Structures of ligand-occupied β-Klotho complexes reveal a molecular mechanism underlying endocrine FGF specificity and activity. Proc Natl Acad Sci U S A. 2019;116:7819-7824 pubmed publisher
  3. Mo E, Cheng Q, Reshetnyak A, Schlessinger J, Nicoli S. Alk and Ltk ligands are essential for iridophore development in zebrafish mediated by the receptor tyrosine kinase Ltk. Proc Natl Acad Sci U S A. 2017;114:12027-12032 pubmed publisher
  4. Li C, Bonazzoli E, Bellone S, Choi J, Dong W, Menderes G, et al. Mutational landscape of primary, metastatic, and recurrent ovarian cancer reveals c-MYC gains as potential target for BET inhibitors. Proc Natl Acad Sci U S A. 2019;116:619-624 pubmed publisher
    ..01), suggesting that oral BET inhibitors represent a class of personalized therapeutics in patients harboring recurrent/chemotherapy-resistant disease. ..
  5. Reshetnyak A, Opatowsky Y, Boggon T, Folta Stogniew E, Tomé F, Lax I, et al. The strength and cooperativity of KIT ectodomain contacts determine normal ligand-dependent stimulation or oncogenic activation in cancer. Mol Cell. 2015;57:191-201 pubmed publisher
  6. Murray P, Lax I, Reshetnyak A, Ligon G, Lillquist J, Natoli E, et al. Heparin is an activating ligand of the orphan receptor tyrosine kinase ALK. Sci Signal. 2015;8:ra6 pubmed publisher
    ..Thus, heparin and perhaps related glycosaminoglycans function as ligands for ALK, revealing a potential mechanism for the regulation of ALK activity in vivo and suggesting an approach for developing ALK-targeted therapies for cancer. ..
  7. Lee S, Greenlee E, Amick J, Ligon G, Lillquist J, Natoli E, et al. Inhibition of ErbB3 by a monoclonal antibody that locks the extracellular domain in an inactive configuration. Proc Natl Acad Sci U S A. 2015;112:13225-30 pubmed publisher
    ..Given the similarities in the mechanism of ErbB receptor family activation, these findings could facilitate structure-based design of antibodies that inhibit EGFR and ErbB4 by an allosteric mechanism. ..
  8. request reprint
    Schlessinger J. Signal transduction. Autoinhibition control. Science. 2003;300:750-2 pubmed
  9. request reprint
    Schlessinger J. Common and distinct elements in cellular signaling via EGF and FGF receptors. Science. 2004;306:1506-7 pubmed
    ..The differential circuitry of the intracellular networks that are activated by EGFR and FGFR may affect signal specificity and physiological responses. ..

Collaborators

More Information

Publications10

  1. Reshetnyak A, Murray P, Shi X, Mo E, Mohanty J, Tomé F, et al. Augmentor ? and ? (FAM150) are ligands of the receptor tyrosine kinases ALK and LTK: Hierarchy and specificity of ligand-receptor interactions. Proc Natl Acad Sci U S A. 2015;112:15862-7 pubmed publisher
    ..These experiments reveal the hierarchy and specificity of two cytokines as ligands for ALK and LTK and set the stage for elucidating their roles in development and disease states. ..