The PI3K-PDK1 connection: more than just a road to PKB.

By B. Vanhaesebroeck, D. Alessi. Biochemical Journal, 2000

1,686 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b037c2bedc5e269c3d0b169a0579080b7c8e3671

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. C. R. Kahn
2. K. Legate
3. A. Brunet
4. R. Fässler
5. S. Wickström
6. B. Vanhaesebroeck

In Molecular Biology

1. L. Diaz
2. Victor E. Velculescu
3. A. Brunet
4. Bert Vogelstein
5. K. Okkenhaug
6. Kenneth W. Kinzler
7. D. Trachootham
8. Peng Huang

Citations in the corpus

• Activation of the PI3K/Akt pathway and chemotherapeutic resistance. (2002, background): “Agonists of protein kinase A (PKA) or -adrenergic receptors, as well as changes in intracellular calcium have all been demonstrated to increase Akt activity in a manner that was resistant to administration of PI3K inhibitors (Datta et al., 1999; Kandel and Hay, 1999; Vanhaesebroeck and Alessi, 2000)”
• Protein Kinase SGK Mediates Survival Signals by Phosphorylating the Forkhead Transcription Factor FKHRL1 (FOXO3a) (2001, background): “Thus, the expression of high levels of dominant-interfering mutants of SGK may lead to inhibition of PDK1 and consequently may prevent the activation of both SGK and Akt (48).”
• 14‐3‐3 suppresses the nuclear localization of threonine 157‐phosphorylated p27Kip1 (2004, background): “The phosphatidylinositol-3 kinase (PI3K)/Akt pathway regulates fundamental cellular functions such as cell prolif- eration, survival and motility (reviewed in Vanhaesebroeck and Alessi, 2000).”
• Genetic and cell biological analysis of integrin outside-in signaling. (2009, background): “This phosphorylation is carried out by PDK1, which is recruited to the plasma membrane by binding to PtdIns-3,4,5-P3 (Vanhaesebroeck and Alessi 2000).”
• From mice to men: insights into the insulin resistance syndromes. (2006, background): “This appears to occur by two means (55, 56).”
• Severe diabetes, age-dependent loss of adipose tissue, and mild growth deficiency in mice lacking Akt2/PKB beta. (2003, background): “Although the three isoforms show broad tissue distribution (3), Akt1 is the most ubiquitously expressed.”
• Redox Regulation of Cell Survival (2008, positive): “PIP3 recruits Akt and 3 (cid:7) -phospho- inositide–dependent kinase-1 (PDK1) to the plasma membrane through its binding with pleckstrin homology (PH) domains of these proteins (315).”