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Job talk practice - Dr. Michael Telias

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Li Ka Shing Center

room 315

Berkeley, CA 94720

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Event description
Come join us for Michael's job talk practice, and give him some feedback before his interview.

About this Event

Li Ka Shing 315 at 3pm. We will meet in the lobby at 3pm sharp.

The Speaker:

Michael Telias is a bio-medical researcher in the fields of neurobiology and neurological disorders. As a Med School undergrad in the Hebrew University, he had his first research experience in biochemistry and proteomics. For his MSc degree, he moved to the field of biophysics and electrophysiology, becoming an expert in patch-clamp. In his PhD at Tel Aviv University, he combined his patch-clamp skills with advanced molecular, cellular and developmental biology to develop a novel model for the research of Fragile X Syndrome and Autism, using neurons differentiated from human embryonic stem cells in-vitro. In his postdoc, he is working on the biology of the retina and photoswitching. He developed a strategy to improve residual vision in model organisms undergoing retinal degeneration, with the hope of one day translating this discovery into a clinical treatment.

Abstract of talk:

Retinoic acid is the trigger for neural hyperactivity in retinal degeneration and blocking its receptor unmasks light responses and augments vision.

Light responses are initiated in photoreceptors, processed by interneurons, and synaptically transmitted to retinal ganglion cells (RGCs), which send information to the brain. Retinitis pigmentosa (RP) is a blinding disease caused by photoreceptor degeneration, depriving downstream neurons of light-sensitive input. In addition, photoreceptor degeneration triggers hyperactive firing of RGCs that obscures light responses initiated by surviving photoreceptors. Here we show that retinoic acid (RA), signaling through its receptor (RAR), is the trigger for hyperactivity. A genetically encoded fluorescent reporter shows elevated RAR signaling in degenerated retinas from murine models of RP. Enhancing RAR signaling in healthy retinas mimics the pathophysiology of degenerating retinas. Drug inhibition of RAR reduces hyperactivity in degenerating retinas and unmasks light responses in RGCs. Gene therapy inhibition of RAR increases innate and learned light-elicited behaviors in vision-impaired mice. Identification of RAR as the trigger for hyperactivity presents a degeneration-dependent therapeutic target for enhancing low-level vision in RP and other blinding disorders.

הפעילות ממומנת ע”י משרד העלייה והקליטה – המרכז לקליטה במדע ואגף יזמות עסקית.

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Li Ka Shing Center

room 315

Berkeley, CA 94720

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