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Abstract
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.
ACKNOWLEDGMENT
We thank Professor Mie-Jae Im for critical readings of the manuscript. This work was supported by a grant of the Korea Science and Engineering Foundation (KOSEF) through the National Research Lab. Program funded by the Ministry of Science and Technology (R0A-2005-000-10052-0 (2008)), by a Korea Research Foundation Grant funded by Korea Government (MOEHRD, Basic Research Promotion Fund) (KRF-2005-201-E00014), and also by a grant from the Korea Health 21 R&D Project (0412-CR03-0704-0001).