Fischer et al., United States. In Dev Neurobiol, Jan 2016
Inhibition of Wnt-signaling with XAV939 in damaged retinas suppressed the formation of MGPCs, increased expression of ascl1a and decreased hes5, but had no effect upon the differentiation of progeny produced by MGPCs.
Goldman et al., Ann Arbor, United States. In Cell Rep, 2014
Importantly, we find that ascl1a gene expression, which drives MG reprogramming in fish and mammals, is regulated in a Jak/Stat-dependent manner and requires consensus Stat-binding sites for injury-dependent activation.
Todd et al., Columbus, United States. In Glia, 2014
With the microglia ablated in damaged retinas, levels of Notch and related genes were unchanged or increased, whereas levels of ascl1a, TNFα, IL1β, complement component 3 (C3) and C3a receptor were significantly reduced.
Wallace et al., United States. In Adv Exp Med Biol, 2013
This review highlights studies that have already been performed using proteomic techniques and as well as our initial proteomic work comparing changes to the proteome between the ascl1a-/- and WT intestine.
Goldman et al., Ann Arbor, United States. In Nat Cell Biol, 2012
Insm1a was found to suppress ascl1a and its own expression, and link injury-dependent ascl1a induction with the suppression of the Wnt inhibitor dickkopf (dkk), which is necessary for MG dedifferentiation.
First, our genetic analyses reveal the requirement of the achaete-scute-like genes ascl1a and 1b in serotonergic and GABAergic neuron development, but they are dispensable for the specification of dopaminergic neurons, which is dependent on the atonal-like gene neurog1.