Xu Luo, Ph.D. Selected Publications

Luo, X.*, Budiharjo, I.*, Zou, H., Slaughter, C., and Wang, X. (1998).  Bid, a Bcl-2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors.  Cell 94, 481-490. (* Equal contribution)

 

Lutter, M., Fang, M., Luo, X., Nishijima, M., Xie, X., Wang, X. (2000).  Cardiolipin provides specificity for targeting of tBid to mitochondria.  Nat. Cell Biol. 10, 754-761.

 

Li, L., Luo, X., and Wang, X. (2001). Endonuclease G is an apoptotic DNase when released from mitochondria.  Nature 412, 95-99.

 

Huang, Y., Erdmann, N., Peng, H., Herek, S., Davis, J., Luo, X., Ikezu, T., and Zheng, J. (2006).  TRAIL-Mediated Apoptosis in HIV-1-Infected Macrophages Is Dependent on the Inhibition of Akt-1 Phosphorylation.  J. Immunol. 177, 2304-2313.

 

George, N. M., Evans, J.D., and Luo, X. (2007).  A Three Helix Homo-oligomerization Domain Containing BH3 and BH1 is Responsible for the Apoptotic Activity of Bax.  Genes & Dev. 21, 1937-1948.

 

George, N. M., Targy, N.M., Evans, J.D., Zhang, L., and Luo, X. (2010).  Bax Contains Two Functional Mitochondrial Targeting Sequences and Translocates to Mitochondria in a Conformational Change- and Homo-oligomerization-driven Process.  J. Biol. Chem. 285, 1385-1392.

 

Lopez, H.*, Zhang, L.*, George, N.M., Liu, X., Pang, X., Evans, J.D., Targy, N.M., and Luo, X. (2010).  Perturbation of the Bcl-2 Network and an Induced Noxa/Bcl-xL Interaction Trigger Mitochondrial Dysfunction Following DNA Damage.  J. Biol. Chem. 285, 15016-15026. (* Equal contribution)

 

Zhang, L.*, Lopez, H.*, George, N.M., Liu, X., Pang, X., and Luo, X. (2011).  Selective Involvement of BH3-only Proteins and Differential Targets of Noxa in Diverse Apoptotic Pathways.  Cell Death & Differ. 18, 864-873. (* Equal contribution)

 

Pang, X., Moussa, S.H., Targy, N.M., Bose, J.L., George, N.M., Gries, C., Lopez, H., Zhang, L., Bayles, K., Young, R., and Luo, X. (2011).  Active Bax and Bak are Functional Holins.  Genes & Dev., 25, 2278-2290.

 

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