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Anna La Torre

Researcher at University of California, Davis

Publications -  33
Citations -  1310

Anna La Torre is an academic researcher from University of California, Davis. The author has contributed to research in topics: Retina & Medicine. The author has an hindex of 14, co-authored 26 publications receiving 980 citations. Previous affiliations of Anna La Torre include University of Washington & University of Barcelona.

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Conserved microRNA pathway regulates developmental timing of retinal neurogenesis

TL;DR: Three microRNAs, let-7, micro RNA-125, and microRNA-9, serve as key regulators of the early to late developmental transition in retinal progenitors and demonstrate how progenitor temporal identity is controlled, a finding that will impact efforts to generate specific neural types from pluripotent stem cells.
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Molecular Anatomy of the Developing Human Retina

TL;DR: Three key epochs are defined in the transcriptome dynamics of human retina from fetal day (D) 52 to 136 to confirm the cellular basis of transcriptional changes and highlight the dramatic acceleration of development in the fovea compared with peripheral retina.
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MAP1B is required for Netrin 1 signaling in neuronal migration and axonal guidance.

TL;DR: It is shown that Netrin 1 regulates, both in vivo and in vitro, mode I MAP1B phosphorylation, which controlsMAP1B activity, in a signaling pathway that depends essentially on the kinases GSK3 and CDK5 and that map1B-deficient neurons from the lower rhombic lip and other brain regions have reduced chemoattractive responses to Netrin 2 in vitro.
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A role of MAP1B in Reelin-dependent Neuronal Migration

TL;DR: It is shown that Reelin can induce mode I MAP1B phosphorylation, both in vivo and in vitro, through gsk3 and cdk5 activation, and proposed that this could correlate with its function in neuronal migration.
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Lack of GPR88 enhances medium spiny neuron activity and alters motor- and cue-dependent behaviors.

TL;DR: Targeted viral expression of GPR88 in MSNs rescued the molecular and electrophysiological properties and normalized behavior, suggesting that aberrant MSN activation in the absence of G PR88 underlies behavioral deficits and its dysfunction may contribute to behaviors observed in neuropsychiatric disease.