Ten years of protein kinase B signalling: a hard Akt to follow.

By D. Brazil, B. Hemmings. TIBS -Trends in Biochemical Sciences. Regular ed, 2001

1,220 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/04237346b42fcbee52e890dd2fbc986abded1640

How researchers see this paper

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

In Molecular Biology

1. T. Franke
2. D. Komander
3. N. Hay
4. Nahum Sonenberg
5. Tianyan Gao
6. A. Newton
7. A. Goldberg
8. D. Alessi

Citations in the corpus

• The activation of Akt/PKB signaling pathway and cell survival (2005, background): “Over the past decade, Akt/PKB has emerged as a central player in the signal transduction pathways activated in response to growth factors or insulin and is thought to contribute to several cellular functions including nutrient metabolism, cell growth, transcriptional regulation and cell survival [9]”
• Decision making by p53: life, death and cancer (2003, background): “Akt is a well-established antiapoptotic protein, implicated primarily in the normal response to a variety of survival signals, as well as in the aberrant survival of many types of cancer cells.(103,104) Activation of Akt by survival signals is driven through a kinase cascade comprising PI3kinase (PI”
• Severe diabetes, age-dependent loss of adipose tissue, and mild growth deficiency in mice lacking Akt2/PKB beta. (2003, background): “Akt is activated in response to many different growth factors, including insulin and IGF-1 (9).”
• PI3K/Akt: getting it right matters (2008, background): “Numerous studies have since examined oncogenic amplifications of different Akt genes in primary human tumors and cancer cells (for review, see Brazil and Hemmings, 2001; Scheid and Woodgett, 2001).”
• FKBP51 Affects Cancer Cell Response to Chemotherapy by Negatively Regulating Akt (2009, neutral): “PI3K converts phosphatidylinositol-4,5-bisphosphate (PIP2) to phosphatidylinositol3,4,5-trisphosphate (PIP3), which in turn recruits Akt and PDK1 to the plasma membrane (Brazil and Hemmings, 2001).”
• Cisplatin in cancer therapy: molecular mechanisms of action (2014, neutral): “Cisplatin and AKT Akt belongs to a family of serine/threonine kinases which act downstream of phosphoinositide 3-kinase (P13K) and plays a critical role in the cell survival(Brazil and Hemmings, 2001).”
• TRB3, a novel ER stress‐inducible gene, is induced via ATF4–CHOP pathway and is involved in cell death (2005, background): “Akt is known to maintain cell survival, by inhibiting apoptosis, and promote cell cycling (Brazil and Hemmings, 2001).”
• Upstream and downstream of mTOR. (2004, background): “The rate-limiting step in Akt activation is the binding of PIP3 to the pleckstrin homology (PH) domain of Akt and the subsequent translocation of Akt to the plasma membrane (Kandel and Hay 1999; Brazil and Hemmings 2001; Scheid and Woodgett 2001).”