Some of the important genetic variants associated with MDD that could be affected by shiftwork are APOE, SLC6A4, ACE, GNB3, HS6ST3, HTR1A, LHFPL2, PDE11A
, DISC1, MAOA, SLC6A3 (DAT1), SLC25A21, VGLL4 BDNF, P2RX7, TPH2, PDE9A, and GRIK3 [95, 100].
In the NCL green group, the EPHB2, KIT, ANTXR2, ESCO2, MSR1, EXT1, TSC1, BUB1B, EPCAM, FANCD2, NF1, DIS3L2, and RET genes were significantly expressed at higher levels, while 6 genes, DKC1, ERCC5, GPC3, MSH6, PDE11A, and TP53, showed significantly lower expression.
In the DMCL blue group, RUNX1, FANCD2, BMPR1A, BUB1B, EPHB2, EHBP1, PDE11A, RET, and KDR were significantly upregulated, while NF1, KIT, GALNT12, TMC6, ERCC5, DKC1, and TP53 were significantly downregulated.
In addition, in the DMCL blue group, the 9 genes shown in Table 3 (RUNX1, FANCD2, BMPR1A, BUB1B, EPHB2, EHBP1, PDE11A, RET, and KDR) were highly activated and all of them can significantly affect embryonic hemopoiesis, transferase activities, and protein phosphorylation.
In contrast, 6 genes (DKC1, ERCC5, GPC3, MSH6, PDE11A, and TP53) were detected with significantly lower expression (Table 3).
Disease or Function p-Value Molecules # Mole Annotation cules Mood disorders 3.73E--04 ADRA2B, ALOX12, AQP4, CA9, 22 CACNB2, CCKBR, CHRNA1, CHR NB4, CHRNG, DDC, ESR1, GRIA3, GRIK2, GRIN1, KCNK2, MTNR 1A, MYOM1, NCAM1, NDUFS7, PDE11A
, SCN11A, SCN2B Depressive disorder 7.90E--04 ADRA2B, AQP4, CACNB2, 14 CCKBR, CHRNA1, CHRNB4, CHRNG, ESR1, GRIA3, GRIN1, KCNK2, MYOM1, NCAM1, PDE11A
Table 3 Effect of Rhodiola on genes involved in depression ([section]).
Researchers at the National Institutes of Health found that the genetic variations impair the enzyme phosphodiesterase 11A (PDE11A), which helps regulate cell's responses to hormones and other signals.
Previous studies by NIH researchers have linked genetic variations that inactivate PDE11A with increased susceptibility to testicular cancer and adrenal tumours.
The researchers found that a group of men with prostate cancer were nearly four times more likely to have variations affecting the activity of PDE11A than did men who did not have prostate cancer.
The researchers found that seven different mutations in the gene in question, PDE11A, created abnormal versions of the PDE11A enzyme that slowed down the enzyme's destruction of cyclic AMP.
Stratakis and his colleagues analyzed the portion of the DNA from 95 familial testicular cancer patients that contains the PDE11A gene.
Stratakis said that learning how disruptions in the PDE11A enzyme lead to an increased risk of tumor formation may help researchers identify other proteins that also play a role.