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          <att_value att_id="a451" value="o94882" value_object_name="Presenilin-1" />
          <att_value att_id="a354" value="o82369" value_object_name="Reduces" />
          <att_value att_id="a355" value="o243" serial_no="0" value_object_name="I L high threshold" />
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          <att_value att_id="a365" value="o74597" serial_no="0" value_object_name="16148264" />
          <att_value att_id="a366" value="Presenilins 1 and 2 (PS1 and PS2, respectively) play a critical role in mediating gamma-secretase cleavage of the amyloid precursor protein (APP). Numerous mutations in the presenilins are known to cause early-onset familial Alzheimer's disease (FAD). In addition, it is well established that PS1 deficiency leads to altered intracellular Ca(2+) homeostasis involving endoplasmic reticulum Ca(2+) stores. However, there has been little evidence suggesting Ca(2+) signals from extracellular sources are influenced by PS1. Here we report that the Ca(2+) currents carried by voltage-dependent Ca(2+) channels are increased in PS1-deficient cortical neurons. This increase is mediated by a significant increase in the contributions of L- and P-type Ca(2+) channels to the total voltage-mediated Ca(2+) conductance in PS1 (-/-) neurons. (Cook et al. 2005)" />
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