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. 2007 Sep 4;274(1627):2801–2810. doi: 10.1098/rspb.2007.0876

Table 2.

Significant maximum-likelihood results on the human lineage for genes associated with schizophrenia.

gene model ω (proportion) λ −2Δλ p
NRG1a (neuregulin 1) MA 999 (0.050) −2010.46
MAofix −2012.50 4.07 <0.05
PLP1 (proteolipid protein 1) MA 482.65 (0.004) −1630.56
MAofix −1636.11 11.08 <0.01
TNXB (tenascin XB) MA 999 (0.006) −38 734.00
MAofix −38 745.00 21.90 <0.01
TP53 (tumour protein p53) MA 25.38 (0.007) −5115.85
MAofix −5118.93 3.78 <0.05
a

Association with schizophrenia is especially strong and well replicated. The PAML analyses also yielded a category of sites with an ω>1, providing evidence that positive selection may have acted on those sites along the specific lineage analysed, for a set of genes that did not show significance under the likelihood ratio tests. These genes, and the putatively selected lineages, include AHI1 (human–chimpanzee), AKT1 (human), CAPON (human–chimpanzee), CCK-AR (human), CHRM5 (human–chimpanzee), CNP (human–chimpanzee), CNTF (human), DRD4 (human–chimpanzee), DRP-2 (human), GABRP (human–chimpanzee), GAD1 (primate), HOPA (human), GPR50 (human), GRIN2A (human and human–chimpanzee), GRIN2B (primate), GSTM1 (human), MLC1 (human–chimpanzee), MTHFR (primate), NOTCH4 (human–chimpanzee), NT3N (human), PCM1 (human), PDLIM5 (human), PTGS2 (human), RGS4 (human–chimpanzee), SLC6A4 (primate), SNAP29 (human) and STOP (human–chimpanzee and primate). Table 3 shows the human–chimpanzee and primate branch results.