@article{NitschkeWangSchmiederetal.2013,
  author    = {Nitschke, Felix and Wang, Peixiang and Schmieder, Peter and Girard, Jean-Marie and Awrey, Donald E. and Wang, Tony and Israelian, Johan and Zhao, XiaoChu and Turnbull, Julie and Heydenreich, Matthias and Kleinpeter, Erich and Steup, Martin and Minassian, Berge A.},
  title     = {Hyperphosphorylation of glucosyl C6 carbons and altered structure of glycogen in the neurodegenerative epilepsy lafora disease},
  series = {Cell metabolism},
  volume    = {17},
  journal   = {Cell metabolism},
  number    = {5},
  publisher = {Cell Press},
  address   = {Cambridge},
  issn      = {1550-4131},
  doi       = {10.1016/j.cmet.2013.04.006},
  pages     = {756 -- 767},
  year      = {2013},
  abstract  = {Laforin or malin deficiency causes Lafora disease, characterized by altered glycogen metabolism and teenage-onset neurodegeneration with intractable and invariably fatal epilepsy. Plant starches possess small amounts of metabolically essential monophosphate esters. Glycogen contains similar phosphate amounts, which are thought to originate from a glycogen synthase error side reaction and therefore lack any specific function. Glycogen is also believed to lack monophosphates at glucosyl carbon C6, an essential phosphorylation site in plant starch metabolism. We now show that glycogen phosphorylation is not due to a glycogen synthase side reaction, that C6 is a major glycogen phosphorylation site, and that C6 monophosphates predominate near centers of glycogen molecules and positively correlate with glycogen chain lengths. Laforin or malin deficiency causes C6 hyperphosphorylation, which results in malformed long-chained glycogen that accumulates in many tissues, causing neurodegeneration in brain. Our work advances the understanding of Lafora disease pathogenesis and suggests that glycogen phosphorylation has important metabolic function.},
  language  = {en}
}
@article{YangZhuWolfetal.2018,
  author    = {Yang, Jie and Zhu, Xiaolei and Wolf, Thomas J. A. and Li, Zheng and Nunes, Jo{\~a}o Pedro Figueira and Coffee, Ryan and Cryan, James P. and G{\"u}hr, Markus and Hegazy, Kareem and Heinz, Tony F. and Jobe, Keith and Li, Renkai and Shen, Xiaozhe and Veccione, Theodore and Weathersby, Stephen and Wilkin, Kyle J. and Yoneda, Charles and Zheng, Qiang and Martinez, Todd J. and Centurion, Martin and Wang, Xijie},
  title     = {Imaging CF3I conical intersection and photodissociation dynamics with ultrafast electron diffraction},
  series = {Science},
  volume    = {361},
  journal   = {Science},
  number    = {6397},
  publisher = {American Assoc. for the Advancement of Science},
  address   = {Washington},
  issn      = {0036-8075},
  doi       = {10.1126/science.aat0049},
  pages     = {64 -- 67},
  year      = {2018},
  abstract  = {Conical intersections play a critical role in excited-state dynamics of polyatomic molecules because they govern the reaction pathways of many nonadiabatic processes. However, ultrafast probes have lacked sufficient spatial resolution to image wave-packet trajectories through these intersections directly. Here, we present the simultaneous experimental characterization of one-photon and two-photon excitation channels in isolated CF3I molecules using ultrafast gas-phase electron diffraction. In the two-photon channel, we have mapped out the real-space trajectories of a coherent nuclear wave packet, which bifurcates onto two potential energy surfaces when passing through a conical intersection. In the one-photon channel, we have resolved excitation of both the umbrella and the breathing vibrational modes in the CF3 fragment in multiple nuclear dimensions. These findings benchmark and validate ab initio nonadiabatic dynamics calculations.},
  language  = {en}
}