Now showing items 1-6 of 6

    • A Cross-Species Study of PI3K Protein-Protein Interactions Reveals the Direct Interaction of P85 and SHP2 

      Breitkopf, Susanne B.; Yang, Xuemei; Begley, Michael J.; Kulkarni, Meghana; Chiu, Yu-Hsin; Turke, Alexa B.; Lauriol, Jessica; Yuan, Min; Qi, Jie; Engelman, Jeffrey A.; Hong, Pengyu; Kontaridis, Maria I.; Cantley, Lewis C.; Perrimon, Norbert; Asara, John M. (Nature Publishing Group, 2016)
      Using a series of immunoprecipitation (IP) – tandem mass spectrometry (LC-MS/MS) experiments and reciprocal BLAST, we conducted a fly-human cross-species comparison of the phosphoinositide-3-kinase (PI3K) interactome in a ...
    • Developmental SHP2 dysfunction underlies cardiac hypertrophy in Noonan syndrome with multiple lentigines 

      Lauriol, Jessica; Cabrera, Janel Rodriguez; Roy, Ashbeel; Keith, Kimberly; Hough, Sara M.; Damilano, Federico; Wang, Bonnie; Segarra, Gabriel C.; Flessa, Meaghan E.; Miller, Lauren E.; Das, Saumya; Bronson, Roderick Terry; Lee, Kyu-Ho; Kontaridis, Maria Irene (American Society for Clinical Investigation, 2016)
      Hypertrophic cardiomyopathy is a common cause of mortality in congenital heart disease (CHD). Many gene abnormalities are associated with cardiac hypertrophy, but their function in cardiac development is not well understood. ...
    • PTPN11-Associated Mutations in the Heart: Has LEOPARD Changed Its RASpots? 

      Lauriol, Jessica; Kontaridis, Maria Irene (Elsevier BV, 2011)
      In this review, we focus on elucidating the cardiac function of germline mutations in the PTPN11 gene, encoding the Src homology-2 (SH2) domain-containing protein tyrosine phosphatase SHP2. PTPN11 mutations cause LEOPARD ...
    • Rapamycin reverses hypertrophic cardiomyopathy in a mouse model of LEOPARD syndrome–associated PTPN11 mutation 

      Marin, Talita M.; Keith, Kimberly; Davies, Benjamin Ivor; Conner, David Atwater; Guha, Prajna; Kalaitzidis, Demetrios; Wu, Xue; Lauriol, Jessica; Wang, Bo; Bauer, Michael; Bronson, Roderick Terry; Franchini, Kleber G.; Neel, Benjamin G.; Kontaridis, Maria Irene (American Society for Clinical Investigation, 2011)
      LEOPARD syndrome (LS) is an autosomal dominant “RASopathy” that manifests with congenital heart disease. Nearly all cases of LS are caused by catalytically inactivating mutations in the protein tyrosine phosphatase (PTP), ...
    • Rapidly progressive hypertrophic cardiomyopathy in an infant with Noonan syndrome with multiple lentigines: Palliative treatment with a rapamycin analog 

      Hahn, Andreas; Lauriol, Jessica; Thul, Josef; Behnke-Hall, Kachina; Logeswaran, Tushiha; Schänzer, Anne; Bögürcü, Nuray; Garvalov, Boyan K.; Zenker, Martin; Gelb, Bruce D.; von Gerlach, Susanne; Kandolf, Reinhard; Kontaridis, Maria Irene; Schranz, Dietmar (Wiley-Blackwell, 2015)
      Noonan syndrome with multiple lentigines (NSML) frequently manifests with hypertrophic cardiomyopathy (HCM). Recently, it was demonstrated that mTOR inhibition reverses HCM in NSML mice. We report for the first time on the ...
    • RhoA signaling in cardiomyocytes protects against stress-induced heart failure but facilitates cardiac fibrosis 

      Lauriol, J; Keith, K.; Jaffre, Fabrice; Couvillon, A.; Saci, A.; Goonasekera, S. A.; McCarthy, Jason; Kessinger, Chase; Wang, J; Ke, Q; Kang, Peter Myung-Hoon; Molkentin, J. D.; Carpenter, C.; Kontaridis, Maria Irene (American Association for the Advancement of Science (AAAS), 2014)
      The Ras-related guanosine triphosphatase RhoA mediates pathological cardiac hypertrophy, but also promotes cell survival and is cardioprotective after ischemia/reperfusion injury. To understand how RhoA mediates these ...