Abstract: TGF-β Activated kinase 1, a serine threonine kinase, was first discovered as a member of the MAPK kinase kinase (MAP3K) family, named as MAP3K7, and is activated by TGF-β1. TAK1 is an extensively expressed kinase which, as the name implies, was originally spotted as a TGFβ-activated enzyme. In addition to TGF-β1, TAK1 can be activated by various other stimuli encompassing lipopolysaccharides, pro-inflammatory cytokines like interleukin (IL)-1, Tumor Necrosis Factor (TNF)-α and environmental stress. TAK-1 is an intracellular hub molecule that regulates a wide array of cellular processes encompassing apoptosis, embryonic development, cellular differentiation and cell survival. Apart from these processes TAK-1 plays a very important role in regulating the mTOR pathway, which is a central pathway in the regulation of cellular proliferation and autophagy. Activation of TAK-1 requires its binding with certain binding partners, called as the TAK-1 binding proteins. The binding of these proteins to TAK-1 is stimuli dependent. We successfully generated various truncation mutants of TAK1 in mammalian expression system and assessed their activity in presence and absence of TAB1 (TAK 1 binding partner) using MKK7 as a substrate. We report that TAB1 is indispensable for the activity of TAK1.
Keywords: apoptosis, autophagy, kinase, lipopolysaccharides, pro-inflammatory.
Title: Deletion Mutagenesis of TAK-1: Role of TAB1 as an Activator
Author: Sabreena Aashaq, Asiya Batool, Khurshid I. Andrabi
International Journal of Life Sciences Research
ISSN 2348-313X (Print), ISSN 2348-3148 (online)
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