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UID:DSC-15460
DTSTART;TZID=Europe/Berlin:20190125T110000
SEQUENCE:1548374999
TRANSP:OPAQUE
DTEND;TZID=Europe/Berlin:20190125T120000
URL:https://www.dresden-science-calendar.de/calendar/de/detail/15460
LOCATION:TUD CRTD\, Fetscherstraße 10501307 Dresden
SUMMARY:Rodriguez-Muela: Resistance versus vulnerability: unraveling the fa
 te of neuronal subtypes in neuropathologies
CLASS:PUBLIC
DESCRIPTION:Speaker: Dr. Natalia Rodriguez-Muela\nInstitute of Speaker: Har
 vard University\, Dept. Stem Cell and Regenerative Biology & Biological Re
 search Center-Spanish National Research Council - Dept. Cellular and Molec
 ular Biology\nTopics:\nBiologie\, Medizin\n Location:\n  Name: TUD CRTD (C
 RTD\, auditorium left)\n  Street: Fetscherstraße 105\n  City: 01307 Dresd
 en\n  Phone: +49 (0)351 458 82052\n  Fax: +49 (0)351 458 82059 \nDescripti
 on: AbstractWhy a given neuropathology does not impact all neurons of the 
 same type to a similar level? This is a fascinating question in neurodegen
 eration research that remains unanswered.In most neurodegenerative disease
 s certain neuronal subgroups degenerate fast while others\, carrying the s
 ame mutations -if any-\, subjected to theoretically analogous stress and d
 isplaying comparable functional properties remain unaffected\, even at the
  latest stages of the disease. Motor neuron diseases are a group of disord
 ers in which motor neurons (MNs) of the spinal cord and/or the motor corte
 x are the primary cell type affected where this perplexing feature can als
 o be observed.Using a variety of approaches ranging from cellular biology 
 techniques and live imaging to genome editing and single cell genomics\, a
 nd utilizing hiPSC together with transgenic animal models\, we investigate
  the molecular mechanisms underlying such selective MN death. We devote a 
 special focus at exploring the molecular basis of proteostasis failure -ma
 jor causative event in neurodegeneration-\, and at examining the contribut
 ion of cell autonomous and non-cell autonomous factors to the selective MN
  loss. Our ultimate goal is to understand the molecular cause of this dist
 inctive neuronal vulnerability to design effective therapeutics targeting 
 specific neuronal subtypes or phases of the disease.  5 most recent papers
 1. Rodriguez-Muela N*\, Parkhitko A\, Grass T\, Gibbs R\, Norabuena E\, Pe
 rrimon N\, Singh R\, Rubin LL*. Blocking p62/SQSTM1- dependent SMN degrada
 tion ameliorates the Spinal Muscular Atrophy disease phenotype. (*Correspo
 nding authors\; J Clin Invest. 2018 Jul 2\;128(7):3008-3023\; highlighted 
 in  JCI This Month  for July2018 Issue\, reference 95231).  2. Rodriguez-M
 uela N1*\, Litterman NK1\, Norabuena EM\, Mull JL\, Galazo MJ\, Sun C\, Ng
  SY\, Makhortova NR\, White A\, Lynes MM\, Chung WK\, Davidow LS\, Macklis
  JD\, Rubin LL*. Single-Cell Analysis of SMN Reveals Its Broader Role in N
 euromuscular Disease. Cell Reports. 2017 Feb 7\;18(6):1484-1498 (*Correspo
 nding authors\, 1equal contribution). 3. Ng SY1\, Soh BS1\, Rodriguez-Muel
 a N\, Hendrickson DG\, Price F\, Rinn JL\, Rubin LL. Genome-wide RNA-Seq o
 f Human Motor Neurons Implicates Selective ER Stress Activation in Spinal 
 Muscular Atrophy. Cell Stem Cell. 2015 Nov 5\;17(5):569-84 (1equal contrib
 ution).  4. Rodríguez-Muela N\, Koga H\, et al.. Balance between autophag
 ic pathways preserves retinal homeostasis. Aging Cell. 2013 Jun\;12(3):478
 -88. (Featured on Aging Cell cover\, June 2013 vol 12). 5. Rodríguez-Muel
 a N\, Germain F\, et al.. Autophagy promotes survival of retinal ganglion 
 cells after optic nerve axotomy in mice. Cell Death Differ. 2012 Jan\;19(1
 ):162-9. (Awarded  Article of the month  by SEBBM\, July 2011)
DTSTAMP:20260403T221133Z
CREATED:20181215T000858Z
LAST-MODIFIED:20190125T000959Z
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