UCL Cancer Institute Seminar Series

The Class I PI 3-kinases are activated by GPCRs and receptor tyrosine kinases, leading to a complex array of downstream signalling. Given that the four Class I isoforms (P3Kalpha, PI3Kbeta, PI3Kdelta, and PI3Kgamma) all produce the same lipid product, the mechanisms by which they signal in an isoform specific manner has been unclear. We have recently focused on the PI3Kbeta isoform, which has been implicated in thrombosis, spermatogenesis, metabolic regulation, and tumorigenesis. PI3Kbeta is unique in several respects, as compared to other PI3Ks. It is directly activated by both GPCRs and RTKs. Its Ras-binding domain binds Rac/Cdc42 but not Ras. And it directly binds to the endosomal GTPase Rab5. Our laboratory has identified distinct point mutants that specifically disrupt interactions between PI3Kbeta and either Gbeta/gamma or Rab5. We have used these mutants to examine the integration of upstream signalling inputs by PI3Kbeta, and we have identified a novel role for this isoform in tumour invasion and metastasis.

Hosted by: Professor Bart Vanhaesebroeck

Professor Jonathan Backer academic profile

Location

Room G01
UCL Rockefeller Building
London, WC1E 6DE

Contact: Veronica Dominguez v.dominguez@ucl.ac.ukView Map