Ghaith Habboub

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Although neurons are normally unable to regenerate their axons after injury to the CNS, this situation can be partially reversed by activating the innate immune system. In a widely studied instance of this phenomenon, proinflammatory agents have been shown to cause retinal ganglion cells, the projection neurons of the eye, to regenerate lengthy axons(More)
The optic nerve has been widely studied for insights into mechanisms that suppress or promote axon regeneration after central nervous system injury. Following optic nerve damage in adult mammals, retinal ganglion cells (RGCs) normally fail to regenerate their axons, resulting in blindness in patients who suffer from neurodegenerative diseases such as(More)
Somatic hypermutation (SHM) of antibody variable region genes is initiated in germinal center B cells during an immune response by activation-induced cytidine deaminase (AID), which converts cytosines to uracils. During accurate repair in nonmutating cells, uracil is excised by uracil DNA glycosylase (UNG), leaving abasic sites that are incised by AP(More)
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