The SPS affair: a complex tale of illicit proliferation.
In this issue of Cancer Cell, Xiao et al. report that PLC-beta3 mutant mice develop myeloprolfierative neoplasms and show that tumor suppressor activity does not require PLC-beta3 catalytic activity. Instead, PLC-beta3 forms a complex with SHP-1 and Stat5 that facilitates Stat5 dephosphorylation. A similar mechanism may be operative in some human leukemias.
Braun
Benjamin S
BS
Department of Pediatrics, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94158, USA.
Shannon
Kevin
K
D000818:Animals; D002454:Cell Differentiation; D049109:Cell Proliferation; D002470:Cell Survival / Q000235:genetics; D008223:Lymphoma / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D009154:Mutation; D009196:Myeloproliferative Disorders / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D054799:Phospholipase C beta / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D010766:Phosphorylation; D053824:Protein Tyrosine Phosphatase, Non-Receptor Type 6 / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D050799:STAT5 Transcription Factor / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D015398:Signal Transduction
D050799:STAT5 Transcription Factor; D053824:Protein Tyrosine Phosphatase, Non-Receptor Type 6; C509248:Ptpn6 protein, mouse; D054799:Phospholipase C beta