@article {152956,
	title = {The Lkb1 metabolic sensor maintains haematopoietic stem cell survival.},
	journal = {Nature},
	volume = {468},
	number = {7324},
	year = {2010},
	month = {2010 Dec 2},
	pages = {659-63},
	abstract = {
	Haematopoietic stem cells (HSCs) can convert between growth states that have marked differences in bioenergetic needs. Although often quiescent in adults, these cells become proliferative upon physiological demand. Balancing HSC energetics in response to nutrient availability and growth state is poorly understood, yet essential for the dynamism of the haematopoietic system. Here we show that the Lkb1 tumour suppressor is critical for the maintenance of energy homeostasis in haematopoietic cells. Lkb1 inactivation in adult mice causes loss of HSC quiescence followed by rapid depletion of all haematopoietic subpopulations. Lkb1-deficient bone marrow cells exhibit mitochondrial defects, alterations in lipid and nucleotide metabolism, and depletion of cellular ATP. The haematopoietic effects are largely independent of Lkb1 regulation of AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) signalling. Instead, these data define a central role for Lkb1 in restricting HSC entry into cell cycle and in broadly maintaining energy homeostasis in haematopoietic cells through a novel metabolic checkpoint.

},
	keywords = {Adenosine Triphosphate, AMP-Activated Protein Kinases, Animals, Apoptosis, Autophagy, Bone Marrow, Cell Cycle, Cell Proliferation, Cell Survival, Energy Metabolism, Enzyme Activation, Female, Hematopoiesis, Hematopoietic Stem Cells, Homeostasis, Lipid Metabolism, Male, Membrane Potential, Mitochondrial, Mice, Mice, Inbred C57BL, Mitochondria, Multiprotein Complexes, Protein-Serine-Threonine Kinases, Proteins, TOR Serine-Threonine Kinases, Tumor Suppressor Proteins},
	issn = {1476-4687},
	doi = {10.1038/nature09572},
	author = {Gurumurthy, Sushma and Xie, Stephanie Z and Alagesan, Brinda and Kim, Judith and Yusuf, Rushdia Z and Saez, Borja and Tzatsos, Alexandros and Ozsolak, Fatih and Milos, Patrice and <b>Ferrari, Francesco</b> and <b>Park, Peter J</b> and Shirihai, Orian S and Scadden, David T and Bardeesy, Nabeel}
}
