File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1111/j.1582-4934.2007.00014.x
- Scopus: eid_2-s2.0-33947306609
- PMID: 17367500
- WOS: WOS:000245458200005
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: PIKE GTPase are phosphoinositide-3-kinase enhancers, suppressing programmed cell death
Title | PIKE GTPase are phosphoinositide-3-kinase enhancers, suppressing programmed cell death |
---|---|
Authors | |
Keywords | Akt PIKE PI3K GTPase Apoptosis |
Issue Date | 2007 |
Citation | Journal of Cellular and Molecular Medicine, 2007, v. 11, n. 1, p. 39-53 How to Cite? |
Abstract | Phosphoinositide-3-kinase enhancers (PIKE) are GTP-binding proteins that posses anti-apoptotic functions. The PIKE family includes three members, PIKE-L, PIKE-S and PIKE-A, which are originated from a single gene (CENTG1) through alternative splicing or differential transcription initiation. Both PIKE-S and PIKE-L bind to phosphoinositide-3-kinase (PI3K) and enhance its activity. PIKE-A does not interplay with PI3K. Instead, it interacts with the downstream effector Akt and promotes its activity. These actions are mediated by their GTPase activity. Because both PI3K and Akt are important effectors in the growth factor-mediated signaling which triggers cellular growth and acts against apoptosis, PIKEs therefore serve as the molecular switch that their activation are crucial for growth factors to exert their physiological functions. In this review, the current understanding of different PIKE isoforms in growth factors-induced anti-apoptotic function will be discussed. Moreover, the role of PIKE in the survival and invasion activity of cancer cells will also be introduced. © 2007 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd. |
Persistent Identifier | http://hdl.handle.net/10722/225031 |
ISSN | 2023 Impact Factor: 4.3 2023 SCImago Journal Rankings: 1.207 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Chan, Chi Bun | - |
dc.contributor.author | Ye, Keqiang | - |
dc.date.accessioned | 2016-04-18T11:16:34Z | - |
dc.date.available | 2016-04-18T11:16:34Z | - |
dc.date.issued | 2007 | - |
dc.identifier.citation | Journal of Cellular and Molecular Medicine, 2007, v. 11, n. 1, p. 39-53 | - |
dc.identifier.issn | 1582-1838 | - |
dc.identifier.uri | http://hdl.handle.net/10722/225031 | - |
dc.description.abstract | Phosphoinositide-3-kinase enhancers (PIKE) are GTP-binding proteins that posses anti-apoptotic functions. The PIKE family includes three members, PIKE-L, PIKE-S and PIKE-A, which are originated from a single gene (CENTG1) through alternative splicing or differential transcription initiation. Both PIKE-S and PIKE-L bind to phosphoinositide-3-kinase (PI3K) and enhance its activity. PIKE-A does not interplay with PI3K. Instead, it interacts with the downstream effector Akt and promotes its activity. These actions are mediated by their GTPase activity. Because both PI3K and Akt are important effectors in the growth factor-mediated signaling which triggers cellular growth and acts against apoptosis, PIKEs therefore serve as the molecular switch that their activation are crucial for growth factors to exert their physiological functions. In this review, the current understanding of different PIKE isoforms in growth factors-induced anti-apoptotic function will be discussed. Moreover, the role of PIKE in the survival and invasion activity of cancer cells will also be introduced. © 2007 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Cellular and Molecular Medicine | - |
dc.subject | Akt | - |
dc.subject | PIKE | - |
dc.subject | PI3K | - |
dc.subject | GTPase | - |
dc.subject | Apoptosis | - |
dc.title | PIKE GTPase are phosphoinositide-3-kinase enhancers, suppressing programmed cell death | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1111/j.1582-4934.2007.00014.x | - |
dc.identifier.pmid | 17367500 | - |
dc.identifier.scopus | eid_2-s2.0-33947306609 | - |
dc.identifier.volume | 11 | - |
dc.identifier.issue | 1 | - |
dc.identifier.spage | 39 | - |
dc.identifier.epage | 53 | - |
dc.identifier.isi | WOS:000245458200005 | - |
dc.identifier.issnl | 1582-1838 | - |