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Dr Christine Hall
1 Wakefield Street
London
WC1N 1PJ
Appointment
  • Honorary Senior Lecturer
  • Department of Neuromuscular Diseases
  • UCL Queen Square Institute of Neurology
  • Faculty of Brain Sciences
Research Themes
Research Summary
Neuronal remodelling: regulation by Rho molecular switches Functional neuronal networks are formed during brain development as neurones migrate, differentiate and encounter positional guidance signals. Attractive and repulsive guidance signals activate intracellular signalling pathways controlling the actin and tubulin cytoskeleton, where Rho GTPases act as molecular switches. When GTP-bound, RhoGTPases engage with an array of effector proteins. Rac and Cdc42 together with kinases and actin regulators promote lamellipodial and filopodial formation and neurite outgrowth. Conversely RhoA, through Rho kinase, increases contractility and growth cone retraction. Directional sensing by growth cones, and the remodelling of synapses, involve the transient activation of RhoGTPases, through a cycle that is regulated by GEFs (guanine exchange factors) and GAPs (GTPase activating proteins). GEFs enable GTP loading of Rho GTPases, the â??onâ?? state, whilst GAPs are down-regulators that enhance intrinsic GTPase activity, turning the signal off. #945;-Chimaerin is a major Rac down-regulator that is involved in axonal guidance signalling (1,2). Early work characterized chimaerin as a prototypic multidomain RhoGAP (3,4). #945;1 and #945;2-Chimaerin are alternate gene transcripts which are differentially expressed in brain development (5,6,7). An N-terminal SH2 domain, involved in phosphotyrosine-regulated interactions, is present only in #945;2-chimaerin. Both isoforms contain a regulatory C1 domain that binds diacylglycerol (or phorbol ester), and a C-terminal RhoGAP domain. The closely related #946;-chimaerin gene is also expressed as 2 isoforms, with an SH2 domain only in #946;2-chimaerin (8). Two binding partners of #945;2-chimaerin are collapsin response mediator protein (CRMP-2) involved in axonal outgrowth, and Cdk5/p35, a serine/threonine kinase (1). Both are important components of sema3A repulsive guidance signaling.
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