KRAS and SKIL mutations synergistically promote pancreatic tumorigenesis through the ubiquitin-proteasome-mediated degradation of Smad4
Pancreatic cancer development requires oncogenic KRAS plus additional genetic hits, yet these cooperating events remain poorly defined. Starting from a germline SKIL A512T mutation discovered in an infant with IPMN, we explored the synergistic role of SKIL and KRAS in tumorigenesis. HEK293T c...