Learn More
Tumour cells can use strategies that make them resistant to nutrient deprivation to outcompete their neighbours. A key integrator of the cell's responses to starvation and other stresses is amino-acid-dependent mechanistic target of rapamycin complex 1 (mTORC1). Activation of mTORC1 on late endosomes and lysosomes is facilitated by amino-acid transporters(More)
How do the pioneer networks in the axial core of the vertebrate nervous system first develop? Fundamental to understanding any full-scale neuronal network is knowledge of the constituent neurons, their properties, synaptic interconnections, and normal activity. Our novel strategy uses basic developmental rules to generate model networks that retain(More)
In this paper we develop a computational model of the anatomy of a spinal cord. We address a long-standing ambition of neuroscience to understand the structure-function problem by modeling the complete spinal cord connectome map in the 2-day old hatchling Xenopus tadpole. Our approach to modeling neuronal connectivity is based on developmental processes of(More)
Tottering mouse is an ataxic mutant that carries a mutation in a gene encoding for the apha1A subunit of P/Q-type Ca2+ channel (Cav2.1). This study revisited to examine whether a Purkinje cell loss occurred in the cerebellum of tottering mice. In tottering mice, Calbindin D-28k negative gaps were apparent in the vermis but not in the hemisphere. Calbindin(More)
Relating structure and function of neuronal circuits is a challenging problem. It requires demonstrating how dynamical patterns of spiking activity lead to functions like cognitive behaviour and identifying the neurons and connections that lead to appropriate activity of a circuit. We apply a "developmental approach" to define the connectome of a simple(More)
BCL-2 family proteins BAK and BAX orchestrate outer mitochondrial membrane permeabilization (MOMP) during apoptosis by forming pores in the membrane to release apoptogenic factors that commits a cell to death. BAK and BAX therefore function as a ‘point of no return’ in the apoptotic cascade. BAK activation is a multi-step process involving conformational(More)
The BCL-2 family protein BAK is a key regulator of mitochondrial apoptosis. BAK activation first involves N-terminal conformational changes that lead to the transient exposure of the BAK BH3 domain that then inserts into a hydrophobic groove on another BAK molecule to form symmetric dimers. We showed recently that post-translational modifications are(More)
Lanthanide cuprates of formula Ln₂CuO₄ exist in two principal forms, T and T' which are renowned for their exhibition at low temperatures of hole and electronic types of superconductivity, respectively. These structures differ primarily in the arrangement of oxygen between the perovskite layers and also in nature of the copper oxygen planes. The Cu-O(More)
The Bcl-2 protein BAK is a key player in mitochondrial apoptosis and responds to a myriad of different death signals. Activation of BAK is a multistep process that involves a number of conformational changes mediated by BH3-only proteins or p53 which leads to BAK multimerization and pore formation in the mitochondrial outer membrane. We previously reported(More)