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| http://dx.doi.org/10.1155/2013/436481 | DOI Listing |
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Human genomic studies have identified protein-truncating variants in associated with both bipolar disorder and schizophrenia, implicating a shared disease mechanism driven by loss-of-function. AKAP11, a protein kinase A (PKA) adaptor, plays a key role in degrading the PKA-RI complex through selective autophagy. However, the neuronal functions of AKAP11 and the impact of its loss-of-function remains largely uncharacterized.
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