Diana Zala

TL;DR: It is demonstrated that glycolysis provides ATP for the FAT of vesicles and that vesicular GAPDH is necessary and sufficient to provide on-board energy for fast vesicle transport.

TL;DR: It is demonstrated that phosphorylation of wild‐type huntingtin at S421 is crucial to control the direction of vesicles in neurons and promoted anterograde transport, suggesting an essential role for huntingtin in the control of vESicular directionality in neurons.

TL;DR: It is demonstrated here that huntingtin is essential to control mitosis, and Drosophila huntingtin restores spindle misorientation in mammalian cells, revealing an unexpected role for huntingtin in dividing cells, with potential important implications in health and disease.

TL;DR: The present results strongly suggest that complex II defects in HD may be instrumental in striatal cell death and that the overexpression of either Ip or Fp subunit restored complex II levels and blocked mitochondrial dysfunction and striatalcell death induced by Htt171-82Q instriatal neurons.

TL;DR: In this paper, a review of the cellular functions in which huntingtin is involved and how a better understanding of pathogenic pathways can lead to new therapeutic approaches is presented. But the exact molecular mechanisms by which mutant huntingtin induces cell death are not completely understood but may involve the gain of new toxic functions and the loss of the beneficial properties of huntingtin.