Reduction of KCTD13 protein in the hippocampus and striatum of heterozygous Kctd13 −/+ mice did not reach statistical significance, suggesting there may be compensatory changes at the transcriptional or post-transcriptional level to regulate KCTD13 levels (hippocampus 7% sd +/− 0.02, n = 3, p = 0.21; striatum 18% sd +/− 0.17, n = 3, p = 0.16).
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Regulation of purine metabolism connects KCTD13 to a metabolic disorder with autistic features.
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