Research Topics
Genomes and Genes | CARL PETER BLOBELSummaryAffiliation: Hospital for Special Surgery Country: USA Publications
Research Grants
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Publications
ADAMs: key components in EGFR signalling and developmentCarl P Blobel
Arthritis and Tissue Degeneration Program and Cell Biology Program, Hospital for Special Surgery, Weill Medical College of Cornell University, 535 East 70th Street, New York, New York 10021, USA
Nat Rev Mol Cell Biol 6:32-43. 2005..Research on ADAMs and their role in protein ectodomain shedding is emerging as a fertile ground for gathering new insights into the functional regulation of membrane proteins...
The role of protease activity in ErbB biologyCarl P Blobel
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, Department of Medicine, Weil Medical College of Cornell University, New York, NY 10021, USA
Exp Cell Res 315:671-82. 2009..The former are the ADAM proteases and the latter are the gamma-secretase complex and the rhomboid proteases. This review discusses the roles of each of these protease systems within the ErbB system...- A novel regulatory role for stromal-derived factor-1 signaling in bone morphogenic protein-2 osteogenic differentiation of mesenchymal C2C12 cellsWei Zhu
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, New York 10021, USA
J Biol Chem 282:18676-85. 2007..Our data provide the first evidence for a co-requirement of the SDF-1/CXCR4 signaling axis in BMP2-induced osteogenic differentiation of C2C12 and ST2 cells and, thus, uncover a new potential target for modulation of osteogenesis... - Substrate selectivity of epidermal growth factor-receptor ligand sheddases and their regulation by phorbol esters and calcium influxKeisuke Horiuchi
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY 10021, USA
Mol Biol Cell 18:176-88. 2007.... 
Distinct roles for ADAM10 and ADAM17 in ectodomain shedding of six EGFR ligandsUmut Sahin
Cell Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, Box 368, 1275 York Avenue, New York, NY 10021, USA
J Cell Biol 164:769-79. 2004..Identification of EGFR ligand sheddases is a crucial step toward understanding the mechanism underlying ectodomain release, and has implications for designing novel inhibitors of EGFR-dependent tumors...- Metalloprotease-disintegrin ADAM8: expression analysis and targeted deletion in miceKristine Kelly
Cell Biology Program, Sloan Kettering Institute, New York, New York, USA
Dev Dyn 232:221-31. 2005..Examination of Adam8-/- mice, however, revealed no major defects in these or other structures during development or in adult tissues and no evident pathological phenotypes... - Ectodomain shedding of the EGF-receptor ligand epigen is mediated by ADAM17Umut Sahin
Arthritis and Tissue Degeneration Program, Caspary Research Building, Room 426, Hospital for Special Surgery, New York, NY 10021, USA
FEBS Lett 581:41-4. 2007..These results suggest that ADAM17 might be a good target to block the release of bioactive epigen, a highly mitogenic ligand of the EGFR which has been implicated in wound healing and cancer... - A sensitive method to monitor ectodomain shedding of ligands of the epidermal growth factor receptorUmut Sahin
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, Weill Medical College of Cornell University, New York, NY, USA
Methods Mol Biol 327:99-113. 2006..This chapter describes a sensitive and semiquantitative method to measure ectodomain shedding of EGFR ligands that was designed to facilitate studies of this process in cells... - ADAMs 10 and 17 represent differentially regulated components of a general shedding machinery for membrane proteins such as transforming growth factor alpha, L-selectin, and tumor necrosis factor alphaSylvain M Le Gall
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY 10021, USA
Mol Biol Cell 20:1785-94. 2009..These results have general implications for understanding the substrate selectivity of two major cellular sheddases, ADAMs 10 and 17... 
Characterization of the catalytic activity of the membrane-anchored metalloproteinase ADAM15 in cell-based assaysThorsten Maretzky
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery at Weill Medical College of Cornell University, 535 E 70th Street, New York, NY 10021, USA
Biochem J 420:105-13. 2009..A cell-based assay for the catalytic activity of ADAM15 could aid in identifying compounds, which could be used to block the function of ADAM15 in pathological neovascularization and cancer...- Mice lacking the metalloprotease-disintegrin MDC9 (ADAM9) have no evident major abnormalities during development or adult lifeGisela Weskamp
Cellular Biochemistry and Biophysics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
Mol Cell Biol 22:1537-44. 2002.... - Critical function for ADAM9 in mouse prostate cancerLucie Peduto
Department of Pathology, Memorial Sloan Kettering Cancer Center, NY 10021, USA
Cancer Res 65:9312-9. 2005..Taken together, these results suggest that ADAM9 contributes to the pathogenesis of prostate cancer and potentially also other carcinomas, raising the possibility that ADAM9 might be a good target for antitumor drugs... - Evidence for regulation of the tumor necrosis factor alpha-convertase (TACE) by protein-tyrosine phosphatase PTPH1Yufang Zheng
Graduate Program in Physiology, Biophysics and Molecular Medicine, Weill Graduate School of Medical Science of Cornell University, New York, New York 10021, USA
J Biol Chem 277:42463-70. 2002..Taken together, these results suggest that PTPH1 may be a negative regulator of TACE levels and function, and thus provide the first evidence for the regulation of TACE through a cytoplasmic protein... - Catalytic properties of ADAM19Valerie Chesneau
Cellular Biochemistry and Biophysics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
J Biol Chem 278:22331-40. 2003..The identification of potential in vitro substrates offers the basis for further functional studies of ADAM19 in cells and in mice... - Potential role for ADAM15 in pathological neovascularization in miceKeisuke Horiuchi
Cellular Biochemistry and Biophysics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
Mol Cell Biol 23:5614-24. 2003..Since ADAM15 does not appear to be required for developmental angiogenesis or for adult homeostasis, it may represent a novel target for the design of inhibitors of pathological neovascularization... - Evidence for a critical role of the tumor necrosis factor alpha convertase (TACE) in ectodomain shedding of the p75 neurotrophin receptor (p75NTR)Gisela Weskamp
Cell Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
J Biol Chem 279:4241-9. 2004..Because ectodomain shedding of p75NTR releases a soluble ectodomain and could also be a prerequisite for its regulated intramembrane proteolysis, these findings may have important implications for the functional regulation of p75NTR... - Stimulation of platelet-derived growth factor receptor beta (PDGFRbeta) activates ADAM17 and promotes metalloproteinase-dependent cross-talk between the PDGFRbeta and epidermal growth factor receptor (EGFR) signaling pathwaysKaren Mendelson
Arthritis and Tissue Degeneration Program, The Hospital for Special Surgery, New York, New York 10021, USA
J Biol Chem 285:25024-32. 2010..This study identifies the principal sheddase for the PDGFRbeta and provides new insights into the mechanism of PDGFRbeta-dependent signal transduction and cross-talk with the EGFR... - Evaluation of the contributions of ADAMs 9, 12, 15, 17, and 19 to heart development and ectodomain shedding of neuregulins beta1 and beta2Keisuke Horiuchi
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, Weill Medical College of Cornell University, New York, NY 10021, USA
Dev Biol 283:459-71. 2005..These results raise the possibility that ADAMs 9, 17, and 19 contribute to heart development in humans and have implications for understanding the mechanisms underlying congenital heart disease... - ADAM8 is a negative regulator of retinal neovascularization and of the growth of heterotopically injected tumor cells in miceVictor H Guaiquil
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, Caspary Research Building, Room 426, 535 East 70th Street, New York, NY 10021, USA
J Mol Med (Berl) 88:497-505. 2010..On the other hand, blocking ADAM8 could be detrimental in the context of rapidly growing tumors... - Shedding of collagen XVII/BP180 in skin depends on both ADAM10 and ADAM9Claus Werner Franzke
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, New York 10021, USA
J Biol Chem 284:23386-96. 2009..These results provide critical new insights into the identity and regulation of the major sheddases for collagen XVII in keratinocytes and skin and have implications for the treatment of blistering diseases of the skin... - Src stimulates fibroblast growth factor receptor-2 shedding by an ADAM15 splice variant linked to breast cancerThorsten Maretzky
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, and Department of Physiology, Weill Medical College of Cornell University, New York, New York 10021, USA
Cancer Res 69:4573-6. 2009.... - ADAM9 is involved in pathological retinal neovascularizationVictor Guaiquil
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, 535 East 70th Street, New York, NY 10021, USA
Mol Cell Biol 29:2694-703. 2009..Collectively, these results suggest that ADAM9 could be an attractive target for the prevention of proliferative retinopathies, CNV, and cancer... - ADAM10 is a principal 'sheddase' of the low-affinity immunoglobulin E receptor CD23Gisela Weskamp
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery and Department of Medicine, Weill Medical College of Cornell University, New York, New York 10021, USA
Nat Immunol 7:1293-8. 2006..Our findings provide a likely target for the treatment of allergic reactions and set the stage for further studies of the involvement of ADAM10 in CD23-dependent pathologies... - Essential role for ADAM19 in cardiovascular morphogenesisHong Ming Zhou
Cell Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
Mol Cell Biol 24:96-104. 2004..Most adam19(-/-) animals die perinatally, likely as a result of their cardiac defects. These findings raise the possibility that mutations in ADAM19 may contribute to human congenital heart valve and septal defects... - VEGF-A stimulates ADAM17-dependent shedding of VEGFR2 and crosstalk between VEGFR2 and ERK signalingSteven Swendeman
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, Weill Medical College of Cornell University, New York, NY 10021, USA
Circ Res 103:916-8. 2008..Targeting the sheddases of VEGFR2 or NRP-1 might offer new opportunities to modulate VEGF-A signaling, an already-established target for treatment of pathological neovascularization... - ADAM12: a potential target for the treatment of chronic woundsAsheesh Harsha
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery at Weill Medical College of Cornell University, New York, NY, USA
J Mol Med (Berl) 86:961-9. 2008....
Research Grants
- Functional and biochemical studies of ADAM19Carl Blobel; Fiscal Year: 2005....
- ADAMs: Key regulators of EGFR signalingCarl Blobel; Fiscal Year: 2007..Because EGFR-signaling has a crucial role in diseases such as cancer, we hope this work will uncover new targets for the design of drugs that can affect EGFR signaling. ..
- ADAMs: Key regulators of EGFR signalingCarl Blobel; Fiscal Year: 2009..Because EGFR-signaling has a crucial role in diseases such as cancer, we hope this work will uncover new targets for the design of drugs that can affect EGFR signaling. ..
- Role of ADAMs 9 and 15 in Proliferative RetinopathyCarl Blobel; Fiscal Year: 2009..abstract_text> ..
- METALLOPROTEASE DISINTEGRIN MDC9Carl Blobel; Fiscal Year: 2002....