Linked Life Data

11882383

Source:http://linkedlifedata.com/resource/pubmed/id/11882383

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2002-3-7
pubmed:abstractText
Protein kinase B or Akt (PKB/Akt) is a serine/threonine kinase, which in mammals comprises three highly homologous members known as PKBalpha (Akt1), PKBbeta (Akt2), and PKBgamma (Akt3). PKB/Akt is activated in cells exposed to diverse stimuli such as hormones, growth factors, and extracellular matrix components. The activation mechanism remains to be fully characterised but occurs downstream of phosphoinositide 3-kinase (PI-3K). PI-3K generates phosphatidylinositol-3,4,5-trisphosphate (PIP(3)), a lipid second messenger essential for the translocation of PKB/Akt to the plasma membrane where it is phosphorylated and activated by phosphoinositide-dependent kinase-1 (PDK-1) and possibly other kinases. PKB/Akt phosphorylates and regulates the function of many cellular proteins involved in processes that include metabolism, apoptosis, and proliferation. Recent evidence indicates that PKB/Akt is frequently constitutively active in many types of human cancer. Constitutive PKB/Akt activation can occur due to amplification of PKB/Akt genes or as a result of mutations in components of the signalling pathway that activates PKB/Akt. Although the mechanisms have not yet been fully characterised, constitutive PKB/Akt signalling is believed to promote proliferation and increased cell survival and thereby contributing to cancer progression. This review surveys recent developments in understanding the mechanisms and consequences of PKB/Akt activation in human malignancy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0898-6568
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
381-95
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:11882383-Animals, pubmed-meshheading:11882383-Apoptosis, pubmed-meshheading:11882383-Cell Cycle, pubmed-meshheading:11882383-Cell Survival, pubmed-meshheading:11882383-Gene Amplification, pubmed-meshheading:11882383-Humans, pubmed-meshheading:11882383-Mice, pubmed-meshheading:11882383-Models, Biological, pubmed-meshheading:11882383-Neoplasms, pubmed-meshheading:11882383-Neovascularization, Pathologic, pubmed-meshheading:11882383-Organisms, Genetically Modified, pubmed-meshheading:11882383-Phosphatidylinositol 3-Kinases, pubmed-meshheading:11882383-Protein Structure, Tertiary, pubmed-meshheading:11882383-Protein-Serine-Threonine Kinases, pubmed-meshheading:11882383-Proto-Oncogene Proteins, pubmed-meshheading:11882383-Proto-Oncogene Proteins c-akt, pubmed-meshheading:11882383-Signal Transduction
pubmed:year
2002
pubmed:articleTitle
The protein kinase B/Akt signalling pathway in human malignancy.
pubmed:affiliation
Division of Cancer Studies, School of Medicine, University of Manchester, G.38, Stopford Building, Oxford Road, M13 9PT, Manchester, UK.
pubmed:publicationType
Journal Article, Review