Journal
IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY
Volume 30, Issue 4, Pages 793-814Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/08923970802285164
Keywords
PTEN; Occupational Asthma; TDI; Signal Transduction
Categories
Funding
- Korea Science and Engineering Foundation (KOSEF)
- Ministry of Science and Technology [R0A-2005-000-10052-0]
- Korea Government (MOEHRD, Basic Research Promotion Fund) [KRF-2005-201-E00014]
- Korea Health 21 RD Project [0412-CR03-0704-0001]
Ask authors/readers for more resources
The tumor suppressor phosphatase and tensin homologue deleted on chromosome ten (PTEN) dephophorylates phosphatidylinositol 3,4,5-triphosphate (PIP3) and is a key negative regulator of phosphoinositide kinase-3 (PI3K) signaling pathway. PTEN also suppresses cellular motility through mechanisms that may be partially independent of phosphatase activity. PTEN is one of the most commonly lost tumor suppressors in human cancers, and its down-regulation is also implicated in several other diseases including airway inflammatory diseases. There is increasing evidence regarding the protective effects of PTEN on the bronchial asthma which is induced by complex signaling networks. Very recently, as for the occupational asthma (OA) with considerable controversy for its pathobiologic mechanisms, PTEN has been considered as a key molecule which is capable of protecting toluene diisocyanate (TDI)-induced asthma, suggesting that PTEN is located at switching point of various molecular signals in OA. Knowledge of the mechanisms of PTEN regulation/function could direct to the pharmacological manipulation of PTEN. This article reviews the latest knowledge and studies on the roles and mechanisms of PTEN in OA.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available