Caleb binds via its acidic stretch to the fibrinogen-like domain of tenascin-c or tenascin-r and its expression is dynamically regulated after optic nerve lesion*

HIGHLIGHTS

• who: Stefan Schumacher from the mRNAAfter ONL, the number of RGCs synthesizing rCALEB/ NGC mRNA declines until , dac. During this period, most of the RGCs survive indicating that after loss of target innervation rCALEB/NGC synthesizing RGCs down-regulate their rCALEB/NGC-encoding mRNA. However, days after ONL, when the quantity of RGCs begin to decline due to cell death, the number of RGCs producing rCALEB/NGC mRNA did not decline further suggesting that at , dac most of the surviving RGCs continue to synthesize rCALEB/NGC mRNA. One possible interpretation for this temporal pattern of rCALEB/ NGC . . .
  

   

  

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