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Nutrients and starvation
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Tubular network formation protects mitochondria from autophagosomal degradation during nutrient starvation
Angelika S. Rambold, Brenda Kostelecky, Natalie Elia, and Jennifer Lippincott-Schwartz
http://www.pnas.org/content/108/25/10190.abstract?etoc
Mitochondria regulate autophagy by conserved signalling pathways
Martin Graef and Jodi Nunnari
http://www.nature.com/emboj/journal/v30/n11/full/emboj2011104a.html
AMPK Is a Direct Adenylate Charge-Regulated Protein Kinase
J. S. Oakhill et al.
The cellular energy sensor adenosine monophosphate–activated protein kinase also binds and is regulated by adenosine diphosphate.
http://www.sciencemag.org/cgi/content/abstract/332/6036/1433
Phospholipase D mediates nutrient input to mTORC1
Limei Xu, Darin Salloum, Phil S. Medlin, Mahesh Saqcena, Paige Yellen, Benjamin Perrella, and David A Foster
http://www.jbc.org/cgi/content/abstract/M111.249631v2
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Cancer metabolism
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Acetylation Targets the M2 Isoform of Pyruvate Kinase for Degradation through Chaperone-Mediated Autophagy and Promotes Tumor Growth
L. Lv, D. Li, D. Zhao, R. Lin, Y. Chu, H. Zhang, Z. Zha, Y. Liu, Z. Li, Y. Xu, G. Wang, Y. Huang, Y. Xiong, K.-L. Guan, and Q.-Y. Lei
http://www.cell.com/molecular-cell/abstract/S1097-2765%2811%2900371-6
Mitochondrial Dysfunction in Cancer Cells Due to Aberrant Mitochondrial Replication
Yuriy Shapovalov, David Hoffman, Daniel Zuch, Karen L. de Mesy Bentley, and Roman A. Eliseev
http://www.jbc.org/content/286/25/22331.abstract?sid=1372cbd0-db93-4f43-b9a7-6ed7962bb639
Glycolytic Phenotype and AMP Kinase Modify the Pathologic Response of Tumor Xenografts to VEGF Neutralization
Giorgia Nardo, Elena Favaro, Matteo Curtarello, Lidia Moserle, Elisabetta Zulato, Luca Persano, Elisabetta Rossi, Giovanni Esposito, Marika Crescenzi, Oriol Casanovas, Ulrike Sattler, Wolfgang Mueller-Klieser, Barbara Biesalski, Oliver Thews, Rossella Canese, Egidio Iorio, Paola Zanovello, Alberto Amadori, and Stefano Indraccolo
http://cancerres.aacrjournals.org/cgi/content/abstract/71/12/4214
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Hypoxia
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A HIF-1 Target, ATIA, Protects Cells from Apoptosis by Modulating the Mitochondrial Thioredoxin, TRX2
S. Choksi, Y. Lin, Y. Pobezinskaya, L. Chen, C. Park, M. Morgan, T. Li, S. Jitkaew, X. Cao, Y.-S. Kim, H.-S. Kim, P. Levitt, G. Shih, M. Birre, C.-X. Deng, and Z.-g. Liu
http://www.cell.com/molecular-cell/abstract/S1097-2765%2811%2900335-2
HIF-1α Mediates Tumor Hypoxia to Confer a Perpetual Mesenchymal Phenotype for Malignant Progression
Young-Gun Yoo, Jared Christensen, Jie Gu, L. Eric Huang
Hypoxia-induced genetic alterations induce epithelial-mesenchymal transition and tumor progression.
http://stke.sciencemag.org/cgi/content/abstract/sigtrans;4/178/pt4?etoc
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Ischemia
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Iduna protects the brain from glutamate excitotoxicity and stroke by interfering with poly(ADP-ribose) polymer-induced cell death
Shaida A Andrabi, Ho Chul Kang, Jean-Francois Haince, Yun-Il Lee, Jian Zhang, Zhikai Chi, Andrew B West, Raymond C Koehler, Guy G Poirier, Ted M Dawson and Valina L Dawson
http://www.nature.com/nm/journal/v17/n6/full/nm.2387.html
Preconditioning Involves Selective Mitophagy Mediated by Parkin and p62/SQSTM1
Chengqun Huang, Allen M. Andres, Eric P. Ratliff, Genaro Hernandez, Pamela Lee, Roberta A. Gottlieb
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0020975
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Autophagy
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TFEB Links Autophagy to Lysosomal Biogenesis
C. Settembre et al.
Starvation activates a transcriptional program controlling autophagosome formation, lysosome fusion, and substrate degradation.
http://www.sciencemag.org/cgi/content/abstract/332/6036/1429
Relieving Autophagy and 4EBP1 from Rapamycin Resistance
Beat Nyfeler, Philip Bergman, Ellen Triantafellow, Christopher J. Wilson, Yanyi Zhu, Branko Radetich, Peter M. Finan, Daniel J. Klionsky, and Leon O. Murphy
http://mcb.asm.org/cgi/content/abstract/31/14/2867
Concurrent detection of autolysosome formation and lysosomal degradation by flow cytometry in a high-content screen for inducers of autophagy
Phillip Hundeshagen, Anne Hamacher-Brady, Roland Eils, Nathan R Brady
http://www.biomedcentral.com/1741-7007/9/38
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Reviews
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Biochimica et Biophysica Acta (BBA) – Molecular Cell Research
Volume 1813, Issue 7, Pages 1261-1394 (July 2011)
Mitochondria and Cardioprotection
Edited by F. Di Lisa, E. Murphy and R. Schulz
http://www.sciencedirect.com/science/journal/01674889
Including:
- Hypoxia-inducible factor 1: Regulator of mitochondrial metabolism and mediator of ischemic preconditioning
Gregg L. Semenza
http://www.sciencedirect.com/science/article/pii/S0167488910002223
- Targeting fatty acid and carbohydrate oxidation – A novel therapeutic intervention in the ischemic and failing heart
Jagdip S. Jaswal, Wendy Keung, Wei Wang, John R. Ussher, Gary D. Lopaschuk
http://www.sciencedirect.com/science/article/pii/S0167488911000231
Mitochondrial oxidant stress triggers cell death in simulated ischemia-reperfusion
Gabriel Loor, Jyothisri Kondapalli, Hirotaro Iwase, Navdeep S. Chandel, Gregory B. Waypa, Robert D. Guzy, Terry L. Vanden Hoek, Paul T. Schumacker
http://www.sciencedirect.com/science/article/pii/S0167488910003186
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News and views
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The autophagy initiating kinase ULK1 is regulated via opposing phosphorylation by AMPK and mTOR
Dan Egan, Joungmok Kim, Reuben J. Shaw and Kun-Liang Guan
http://www.landesbioscience.com/journals/autophagy/article/15123/
Mitochondria breathe for autophagy
Koji Okamoto
http://www.nature.com/emboj/journal/v30/n11/full/emboj2011149a.html
Mitochondrial Dynamics: A Strategy for Avoiding Autophagy
L. Galluzzi, O. Kepp, and G. Kroemer
http://www.sciencedirect.com/science/article/pii/S096098221100529X
ATIA: A Link between Inflammation and Hypoxia
A. Lin
http://www.cell.com/molecular-cell/abstract/S1097-2765%2811%2900390-X
Shifting the Metabolic Program
Elizabeth M. Adler
Pyruvate kinase M2 interacts directly with hypoxia-inducible factor 1 to promote glycolytic metabolism.
http://stke.sciencemag.org/cgi/content/abstract/sigtrans;4/176/ec157?etoc
Cancer metabolism: Feed it forward
Semenza and colleagues identify a positive feedback loop between the pyruvate kinase PKM2 and HIF1 that may explain how PKM2 can promote metabolic reprogramming of cancer cells.
http://www.nature.com/nrc/journal/v11/n7/full/nrc3094.html?WT.ec_id=NRC-201108
Ramping Up AMPK
L. Bryan Ray
The cellular energy sensor adenosine monophosphate–activated protein kinase also binds and is regulated by adenosine diphosphate.
http://stke.sciencemag.org/cgi/content/abstract/sigtrans;4/178/ec174?etoc
ADaPting to Energetic Stress
M. L. Bland and M. J. Birnbaum
What is the true activator of a key enzyme that controls cell energetics?
http://www.sciencemag.org/cgi/content/summary/332/6036/1387
Coordinating Autophagy and Lysosome Regulation
Stella M. Hurtley
Starvation activates a transcriptional program controlling autophagosome formation, lysosome fusion, and substrate degradation.
http://stke.sciencemag.org/cgi/content/abstract/sigtrans;4/178/ec175?etoc
Autophagy’s Top Chef
Ana Maria Cuervo
The transcription factor EB both controls lysosome formation and increases autophagy in cells experiencing starvation.
http://www.sciencemag.org/cgi/content/summary/332/6036/1392
Acetylation for Autophagy
Wei Wong
Acetylation of pyruvate kinase M2 inhibits its activity and triggers its autophagic degradation, leading to increased tumor cell proliferation.
http://stke.sciencemag.org/cgi/content/abstract/sigtrans;4/179/ec182?etoc
PKM2 and the Tricky Balance of Growth and Energy in Cancer
A.N. Macintyre and J.C. Rathmell
http://www.cell.com/molecular-cell/abstract/S1097-2765%2811%2900416-3
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I found this website is very usefull since now I have great interest in metabolim and cancer.I think it would be a good choice to make it the study area in my post doctor career.In my opinion,the main difficulty with cancer study is the inhomogeneity of cancer cells.They have different genetic background(mutations),time,location,even cell type.But in metabolic level all cancer cells in a cancer microenviroment should share some basic metabolic characteristic (glucose untilization,FFA synthesis,mitochondrial activity,etl…) which may be targeted for cancer therapy.So I appreciate your study very much and I’m looking forward to communicate with you.Thanks a lot!
Xiangbo Ruan
Room 110,Institute for Nutritional Science,SIBS,CAS
294 TaiYuan Rd.Shanghai 200031.China
Tel:86-21-54920940