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Mathias Seeliger


Short CV

  • Elelectrical engineer
  • Physician (ophthalmologist)
  • Heisenberg professor, Ocular Neurodegeneration

Documents

CV of Mathias Seeliger [pdf]

Scientifc Interest

  • Pathophysiology in hereditary retinal degenerations
  • (Preclinical) molecular therapy
  • Diagnostic in vivo technology (ERG, SLO, OCT)
  • Normal retinal physiology
  • Modelling of functional processes in the (outer) retina

Memberships

  • Association for Research in Vision and Ophthalmology (ARVO)
  • ISCEV
  • NWG
  • DOG
  • BVA
  • IEEE
  • VDE
  • DGBMT

Key Publications

  1. Knop G, Seeliger M, Thiel F, Mataruga A, Kaupp UB, Friedburg C, Tanimoto N, Müller F.
    Light responses in the mouse retina are prolonged upon targeted deletion of the HCN1 channel gene.
    Eur J Neurosci 2008; in press.
  2. Janssen A, Min SH, Molday LL, Tanimoto N, Seeliger MW, Hauswirth WW, Molday RS, Weber BH.
    Effect of late-stage therapy on disease progression in AAV-mediated rescue of photoreceptor cells in the retinoschisin-deficient mouse.
    Mol Ther 2008; 16:1010-1017
  3. Samardzija M, von Lintig J, Tanimoto N, Oberhauser V, Thiersch M, Remé CE, Seeliger M, Grimm C, Wenzel A.
    R91W mutation in Rpe65 leads to milder early-onset retinal dystrophy due to the generation of low levels of 11-cis-retinal.
    Hum Mol Genet 2008;17:281-292.
  4. Chen D, Opavsky R, Pacal M, Tanimoto N, Wenzel P, Seeliger MW, Leone G, Bremner R.
    Rb-mediated neuronal differentiation through cell cycle independent regulation of E2f3a.
    PLoS Biol 2007;5: E179.
  5. van de Pavert SA, Meuleman J, Malysheva A, Aartsen WM, Versteeg I, Tonagel F, Kam-phuis W, McCabe CJ, Seeliger MW, Wijnholds J.
    A single amino acid substitution (Cys249Trp) in Crb1 causes retinal degeneration and deregulates expression of Pituitary tumor transforming gene 1 (Pttg1).
    J Neurosci 2007; 27: 564-573.
  6. Bemelmans AP, Kostic C, Crippa SV, Hauswirth WW, Lem J, Seeliger MW, Wenzel A, Arsenijevic Y.
    Lentiviral-mediated transfer of the RPE65 cDNA rescues both survival and function of cone photoreceptors in a mouse model of Leber congenital amaurosis.
    PLoS Med 2006;3: 1892-1903.
  7. Tolmachova T, Anders R, Abrink M, Bugeon L, Dallman MJ, Futter CE, Ramalho JS, Tonagel F, Tanimoto N, Seeliger MW, Huxley C, Seabra MC.
    Cell-autonomous retinal degeneration in a conditional knock-out mouse model of choroideremia.
    J Clin Invest 2006; 116: 386-394.
  8. Grimm C, Wenzel A, Groszer M, Mayser H, Seeliger MW, Bauer C, Gassmann M, Reme CE.
    HIF-1–induced erythropoietin in the hypoxic retina protects against light–induced reti-nal degeneration.
    Nat Med 2002; 8: 718-24.
  9. Bolz H, von Brederlow B, Ramirez A, Bryda EC, Kutsche K, Nothwang HG, Seeliger M, C.-Salcedó Cabrera M, Caballeró Vila M, Pelaez Molina O, Gal A, Kubisch C.
    Mutations in cadherin-23 (otocadherin), a novel member of the cadherin gene family, cause Usher syndrome type 1D.
    Nat Genet 2001; 27: 108-112.
  10. Seeliger MW, Grimm C, Ståhlberg F, Friedburg C, Jaissle G, Zrenner E, Guo H, Remé ChE, Humphries P, Hofmann F, Biel M, Fariss RN, Redmond TM, Wenzel A.
    New views on RPE65 deficiency: the rod system is the source of vision in a mouse model of Leber congenital amaurosis.
    Nat Genet 2001; 29: 70-74.
Prof. Dr. med. Dipl.-Ing. Mathias Seeliger
Mathias Seeliger

Research Group

Division of Ocular Neurodegeneration

Contact

University of Tuebingen
Centre for Ophthalmology
Institute for Ophthalmic Research

Schleichstrasse 4/3
72076 Tuebingen
Germany

Phone: +49-7071-2980718
Fax: +49-7071-294789

Email:
see[at]ieee.org

Website:
www.uak.medizin.uni-tuebingen.de/neurodegen

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