NUAK1 links genomic instability and senescence
Author(s) -
David Bernard,
Arnaud Augert
Publication year - 2010
Publication title -
aging
Language(s) - English
Resource type - Journals
ISSN - 1945-4589
DOI - 10.18632/aging.100153
Subject(s) - genome instability , senescence , instability , biology , computational biology , genetics , dna damage , dna , physics , mechanics
The AMP-activated protein kinase-related kinase (ARK) family comprises 13 proteins, amongst them NUAK1, that can be classified into five subfamilies: AMP-activated protein kinase (AMPK), salt-induced kinase (SIK), microtubule-affinity-regulating kinase (MARK), brain specific kinase (BRSK), and SNF1-like kinase 1 (NUAK). These proteins regulate biological responses such as metabolism, polarity, cell proliferation or cell death, presumably in a sub-family specific manner [1]. Although the different proteins regulate different responses, their activities are thought to be controlled by the same kinase, LKB1 [2], which phosphorylates a threonine residue in the conserved Tloop of ARK proteins. AMPK proteins are phosphorylated and activated by LKB1 when ATP levels decrease, whereas ARK proteins are phosphorylated and activated independently of intracellular ATP levels [1].
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom