Carl Blobel

Short CV

Carl P. Blobel is Professor of Medicine and of Physiology, Biophysics and Systems Biology at Weill Cornell Medical College, and Chairman of the Arthritis and Tissue Degeneration Program at the Hospital for Special Surgery in New York City. He received an MD degree from the Justus-Liebig University in Giessen, Germany (1984) and a PhD degree in Biochemistry from the University of California, San Francisco (1991). In 1992 he established his lab at the Sloan-Kettering Institute, and has been at the Hospital for Special Surgery at Weill Cornell Medical College in New York since 2004, where he holds the V.F. and W.R. Salomon endowed Chair in Musculoskeletal Research.

Selected Awards

• 2015, Elected to the Association of American Physicians
• 2012, Bayer Hemophilia Awards Program
• 2009, Chair of the Gordon Research Conference on Matrix Metalloproteinases
• 2004, V.F. and W.R. Salomon Endowed Chair in Musculoskeletal Research (Hospital for Special Surgery)
• 1996, NIH Shannon Director’s Award

Research Interests

Research in Dr. Blobel’s lab is focused on elucidating the function of cell surface metalloproteinases termed ADAMs (a disintegrin and metalloproteinase) in development and disease. ADAMs have emerged as critical modulators of cell-cell interactions through their ability to regulate the bioavailability of membrane proteins such as the pro-inflammatory cytokine TNFα and ligands of the EGF-receptor (EGFR). Moreover, ADAMs are essential for activating cell surface receptors of the Notch family, which control cell fate decisions during the development of specialized cell types in different tissues, but are also involved in the pathogenesis of cancer. Studies in Dr. Blobel’s lab employ a comprehensive combination of biochemical and cell biological approaches as well as mouse models for disease. They have helped establish ADAM17 as a key regulator of the EGFR signaling pathway, which is essential for maintaining the skin and intestinal barrier, but can cause a variety of human pathologies when it is dysregulated. Moreover, his lab has pioneered studies on the newly discovered iRhom1 and 2 as crucial upstream regulators of ADAM17-dependent EGFR and TNFα-signaling. The medical relevance of Dr. Blobel’s work is significant, since it not only helps understand how exactly iRhoms and ADAM17 can promote EGFR-dependent pathologies such as cancer and TNFα-dependent autoimmune disorders such as rheumatoid arthritis, but it has also revealed new and attractive potential targets for treatment of these diseases.

Selected Publications

• Maretzky, Thorsten; McIlwain, David R.; Issuree, Priya Darshinee A; Li, Xue; Malapeira, Jordi; Amin, Sadaf; Lang, Philipp A.; Mak, Tak W.; Blobel, Carl P.: iRhom2 controls the substrate selectivity of stimulated ADAM17-dependent ectodomain shedding. Proceedings of the National Academy of Sciences of the United States of America 110 (28), 2013, 11433-11438.

• Issuree, Priya Darshinee A; Maretzky, Thorsten; McIlwain, David R.; Monette, Sébastien; Qing, Xiaoping; Lang, Philipp A.; Swendeman, Steven L.; Park-Min, Kyung-Hyun; Binder, Nikolaus; Kalliolias, George D.; Yarilina, Anna; Horiuchi, Keisuke; Ivashkiv, Lionel B.; Mak, Tak W.; Salmon, Jane E.; Blobel, Carl P.: iRHOM2 is a critical pathogenic mediator of inflammatory arthritis. The Journal of clinical investigation 123 (2), 2013, 928-932.

• McIlwain, David R.; Lang, Philipp A.; Maretzky, Thorsten; Hamada, Koichi; Ohishi, Kazuhito; Maney, Sathish Kumar; Berger, Thorsten; Murthy, Aditya; Duncan, Gordon; Xu, Haifeng C.; Lang, Karl S.; Häussinger, Dieter; Wakeham, Andrew; Itie-Youten, Annick; Khokha, Rama; Ohashi, Pamela S.; Blobel, Carl P.; Mak, Tak W.: iRhom2 regulation of TACE controls TNF-mediated protection against Listeria and responses to LPS. Science (New York, N.Y.) 335 (6065), 2012, 229-232.

• Franzke, Claus-Werner; Cobzaru, Cristina; Triantafyllopoulou, Antigoni; Löffek, Stefanie; Horiuchi, Keisuke; Threadgill, David W.; Kurz, Thomas; van Rooijen, Nico; Bruckner-Tuderman, Leena; Blobel, Carl P.: Epidermal ADAM17 maintains the skin barrier by regulating EGFR ligand-dependent terminal keratinocyte differentiation. The Journal of experimental medicine 209 (6), 2012, 1105-1119.

• Horiuchi, Keisuke; Kimura, Tokuhiro; Miyamoto, Takeshi; Takaishi, Hironari; Okada, Yasunori; Toyama, Yoshiaki; Blobel, Carl P.: TNF-alpha-converting enzyme (TACE/ADAM17) inactivation in mouse myeloid cells prevents lethality from endotoxin shock. Journal of immunology (Baltimore, Md. : 1950) 179 (5), 2007, 2686-2689.

• Weskamp, Gisela; Ford, Jill W.; Sturgill, Jamie; Martin, Steve; Docherty, Andrew J P; Swendeman, Steven; Broadway, Neil; Hartmann, Dieter; Saftig, Paul; Umland, Shelby; Sehara-Fujisawa, Atsuko; Black, Roy A.; Ludwig, Andreas; Becherer, J. David; Conrad, Daniel H.; Blobel, Carl P.: ADAM10 is a principal 'sheddase' of the low-affinity immunoglobulin E receptor CD23. Nature immunology 7 (12), 2006, 1293-1298.

• Blobel, Carl P.: ADAMs: key components in EGFR signalling and development. Nature reviews. Molecular cell biology 6 (1), 2005, 32-43.

• Sahin, Umut; Weskamp, Gisela; Kelly, Kristine; Zhou, Hong-Ming; Higashiyama, Shigeki; Peschon, Jacques; Hartmann, Dieter; Saftig, Paul; Blobel, Carl P.: Distinct roles for ADAM10 and ADAM17 in ectodomain shedding of six EGFR ligands. The Journal of cell biology 164 (5), 2004, 769-779.

• Blobel, C. P.; Wolfsberg, T. G.; Turck, C. W.; Myles, D. G.; Primakoff, P.; White, J. M.: A potential fusion peptide and an integrin ligand domain in a protein active in sperm-egg fusion. Nature 356 (6366), 1992, 248-252.