The kinesin KIF1Bβ acts downstream from EglN3 to induce apoptosis and is a potential 1p36 tumor suppressor

Susanne Schlisio, Rajappa S. Kenchappa, Liesbeth C.W. Vredeveld, Rani E. George, Rodney Stewart, Heidi Greulich, Kristina Shahriari, Nguyen V. Nguyen, Pascal Pigny, Patricia L. Dahia, Scott L. Pomeroy, John M. Maris, A. Thomas Look, Matthew Meyerson, Daniel S. Peeper, Bruce D. Carter, William G. Kaelin

Research output: Contribution to journalArticlepeer-review

254 Scopus citations


VHL, NF-1, c-Ret, and Succinate Dehydrogenase Subunits B and D act on a developmental apoptotic pathway that is activated when nerve growth factor (NGF) becomes limiting for neuronal progenitor cells and requires the EglN3 prolyl hydroxylase as a downstream effector. Germline mutations of these genes cause familial pheochromocytoma and other neural crest-derived tumors. Using an unbiased shRNA screen we found that the kinesin KIF1Bβ acts downstream from EglN3 and is both necessary and sufficient for neuronal apoptosis when NGF becomes limiting. KIF1Bβ maps to chromosome 1p36.2, which is frequently deleted in neural crest-derived tumors including neuroblastomas. We identified inherited loss-of-function KIF1Bβ missense mutations in neuroblastomas and pheochromocytomas and an acquired loss-of-function mutation in a medulloblastoma, arguing that KIF1Bβ is a pathogenic target of these deletions.

Original languageEnglish (US)
Pages (from-to)884-893
Number of pages10
JournalGenes and Development
Issue number7
StatePublished - Apr 1 2008


  • Apoptosis
  • Kinesin
  • Neuroblastoma
  • Pheochromocytoma
  • Prolyl hydroxylase

ASJC Scopus subject areas

  • General Medicine


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