Christopher J. Carbone, Ph.D.

Affiliations: 
2007 Temple University, Philadelphia, PA, United States 
Area:
Molecular Biology, Genetics
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"Christopher Carbone"

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Dale Haines grad student 2007 Temple University
 (p21 loss cooperates with INK4 inactivation facilitating immortalization and Bcl-2 mediated anchorage independent growth of oncogene-transduced primary mouse fibroblasts.)
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Publications

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Ortiz A, Gui J, Zahedi F, et al. (2019) An Interferon-Driven Oxysterol-Based Defense against Tumor-Derived Extracellular Vesicles. Cancer Cell. 35: 33-45.e6
Katlinski KV, Gui J, Katlinskaya YV, et al. (2017) Inactivation of Interferon Receptor Promotes the Establishment of Immune Privileged Tumor Microenvironment. Cancer Cell. 31: 194-207
Katlinskaya YV, Carbone CJ, Yu Q, et al. (2015) Type 1 interferons contribute to the clearance of senescent cell. Cancer Biology & Therapy. 16: 1214-9
Yu Q, Katlinskaya YV, Carbone CJ, et al. (2015) DNA-damage-induced type I interferon promotes senescence and inhibits stem cell function. Cell Reports. 11: 785-97
Bhattacharya S, Katlinski KV, Reichert M, et al. (2014) Triggering ubiquitination of IFNAR1 protects tissues from inflammatory injury. Embo Molecular Medicine. 6: 384-97
Carbone CJ, Fuchs SY. (2014) Eliminative signaling by Janus kinases: role in the downregulation of associated receptors. Journal of Cellular Biochemistry. 115: 8-16
Zheng H, Gupta V, Patterson-Fortin J, et al. (2013) A BRISC-SHMT complex deubiquitinates IFNAR1 and regulates interferon responses. Cell Reports. 5: 180-93
Carbone CJ, Varghese B, Zheng H, et al. (2013) 33 Cytokine. 63: 251
Carbone CJ, Zheng H, Bhattacharya S, et al. (2012) Protein tyrosine phosphatase 1B is a key regulator of IFNAR1 endocytosis and a target for antiviral therapies. Proceedings of the National Academy of Sciences of the United States of America. 109: 19226-31
Zheng H, Qian J, Carbone CJ, et al. (2011) Vascular endothelial growth factor-induced elimination of the type 1 interferon receptor is required for efficient angiogenesis. Blood. 118: 4003-6
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