Role of BCL-XL in Photoreceptor Survival

  • Yun-Zheng Le
  • Lixin Zheng
  • Yuwei Le
  • Edmund B. RuckerIII
  • Robert E. Anderson
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 613)

Photoreceptors are post-mitotic neurons and understanding their survival mechanisms holds a key to the treatment of retinal degeneration. Many studies have demonstrated that phosphoinositide 3-kinase (PI3K) and its product phosphatidylinositol-3,4,5-trisphosphate (PIP3) are involved in the survival of neurons through growth factor receptor-mediated activation of the serine-threonine kinase, AKT (Barber et al., 2000; D’Mello et al., 1997; Yao and Cooper, 1995). Activation of AKT further activates a number of down-stream targets, including the anti-apoptotic protein BCL-XL, which can serve as a survival factor in a number of alternative pathways(Bui et al., 2001; Kim et al., 2005; Zha et al., 1996). For the past few years, we have investigated the roles of PI3K, insulin receptor, AKT, and BCL-XL in photoreceptor survival.


Retinal Degeneration Outer Nuclear Layer Cone Photoreceptor Light Damage Photoreceptor Survival 
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Copyright information

© Springer Science+Business Media, LLC 2008

Authors and Affiliations

  • Yun-Zheng Le
    • 1
  • Lixin Zheng
    • 2
  • Yuwei Le
    • 2
  • Edmund B. RuckerIII
    • 3
  • Robert E. Anderson
    • 4
  1. 1.Departments of Medicine;Cell BiologyDean A. McGee Eye InstituteOklahoma CityUSA
  2. 2.Dean A. McGee Eye Institute, OphthalmologyUniversity of Oklahoma Health Sciences CenterOklahoma City
  3. 3.Department of Veterinary Physiology and PharmacologyTexas A&M University, College Station
  4. 4.Cell Biology; Dean A. McGee Eye InstituteOphthalmology, University of Oklahoma Health Sciences CenterOklahoma City

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