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I was published in Nature!

Peter Vandenabeele is senior full professor at the Inflammation Research Center (IRC), a VIB department at the Ghent University. He recently published in Nature an original research paper on the regulation of cell survival in vivo (Takahashi et al., 2014). RIPK1 (receptor interacting protein kinase 1) plays an important role both in the survival as well as in the death of epithelial cells. Full knockout mice for the Ripk1 gene are not viable. The team of Vandenabeele managed to make a viable conditional mouse model that lacks Ripk1 only in the intestinal epithelial cells. They also obtained in collaboration with people from GSK (Pennsylvania) a mouse model containing a mutant form of RIPK1 that lacks the kinase activity. Thanks to these genetic mouse models, mechanisms that regulate cell survival and cell death could be explored. Peter Vandenabeele and his team found that the platform function of RIPK lacking the kinase activity is associated with cell survival, while the kinase activity is associated with induction of cell death.  Peter Vandenabeele also published a review paper in Nature about cell death pathways and inflammation in early 2015 (Pasparakis and Vandenabeele, 2015).
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Peter Vandenabeele is senior full professor at the Inflammation Research Center (IRC), a VIB department at the Ghent University. He recently published in Nature an original research paper on the regulation of cell survival in vivo (Takahashi et al., 2014). RIPK1 (receptor interacting protein kinase 1) plays an important role both in the survival as well as in the death of epithelial cells. Full knockout mice for the Ripk1 gene are not viable. The team of Vandenabeele managed to make a viable conditional mouse model that lacks Ripk1 only in the intestinal epithelial cells. They also obtained in collaboration with people from GSK (Pennsylvania) a mouse model containing a mutant form of RIPK1 that lacks the kinase activity. Thanks to these genetic mouse models, mechanisms that regulate cell survival and cell death could be explored. Peter Vandenabeele and his team found that the platform function of RIPK lacking the kinase activity is associated with cell survival, while the kinase activity is associated with induction of cell death.  Peter Vandenabeele also published a review paper in Nature about cell death pathways and inflammation in early 2015 (Pasparakis and Vandenabeele, 2015).