Linked Life Data

19189642

Source:http://linkedlifedata.com/resource/pubmed/id/19189642

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6A
pubmed:dateCreated
2009-2-4
pubmed:abstractText
The PTEN (phosphatase and tensin homolog deleted on chromosome ten) tumor suppressor gene is mutated in a wide range of malignancies and recent studies have demonstrated that PTEN prevents tumorigenesis through multiple mechanisms. PTEN functions as a plasma-membrane lipid phosphatase that antagonizes the PI3K (phosphoinositide 3 kinase)-AKT pathway. PTEN physically and genetically interacts with the central genome guardian p53. PTEN also associates with the centromeric protein CENP-C to maintain centromere integrity and suppresses chromosomal instability from DNA double-strand breaks (DSBs) through transcriptional regulation of Rad51 (radiosensitive yeast mutant 51). Moreover PTEN controls the growth and proliferation of haematopoietic stem cells (HSC) and restrains cells from leukemia in an mTOR (mammalian target of rapamycin) dependent manner. Thus, restoring PTEN functions in cancer cells directly or indirectly holds great promise for cancer therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0250-7005
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3613-9
pubmed:dateRevised
2009-5-27
pubmed:meshHeading
pubmed:articleTitle
PTEN mutation: many birds with one stone in tumorigenesis.
pubmed:affiliation
Department of Life Sciences, Huaihua University, Huaihua, Peoples Republic of China.
pubmed:publicationType
Journal Article, Review