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  • S. Karger AG  (2)
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  • S. Karger AG  (2)
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  • 1
    In: Neuropsychobiology, S. Karger AG, Vol. 78, No. 3 ( 2019), p. 113-117
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Schizophrenia (SCZ) is a complex, heritable, and devastating psychiatric disorder. Mutations in the members of ABC transporters have been associated with psychiatric illnesses. 〈 b 〉 〈 i 〉 Aims: 〈 /i 〉 〈 /b 〉 In this study, we investigated whether 9 SNPs in 〈 i 〉 ABCB1 〈 /i 〉 (rs6946119, rs28401781, rs4148739, and rs3747802), 〈 i 〉 ABCB6 〈 /i 〉 (rs1109866, rs1109867, rs3731885, and rs3755047), and 〈 i 〉 ABCG1 〈 /i 〉 (rs182694) contribute to the risk of SCZ in a Han Chinese population. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 We conducted a case-control study in a Han Chinese population, involving 1,034 SCZ patients and 1,034 unrelated healthy controls to genotype 9 SNPs. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 The analysis demonstrated that rs182694 of 〈 i 〉 ABCG1 〈 /i 〉 was significantly different between SCZ patients and controls as to allele (rs182694: 〈 i 〉 p 〈 /i 〉 = 0.0070, χ 〈 sup 〉 2 〈 /sup 〉 = 7.27) and genotype frequencies (rs182694: 〈 i 〉 p 〈 /i 〉 = 0.0013, χ 〈 sup 〉 2 〈 /sup 〉 = 13.35). 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Our findings support an association between 〈 i 〉 ABCG1 〈 /i 〉 polymorphism and SCZ in a Han Chinese population.
    Type of Medium: Online Resource
    ISSN: 0302-282X , 1423-0224
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2019
    detail.hit.zdb_id: 1483094-2
    SSG: 5,2
    SSG: 15,3
    Location Call Number Limitation Availability
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  • 2
    Online Resource
    Online Resource
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 51, No. 5 ( 2018), p. 2185-2197
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 51, No. 5 ( 2018), p. 2185-2197
    Abstract: Background/Aims: VCP-interacting membrane selenoprotein (VIMP), an ER resident selenoprotein, is highly expressed in β-cells, however, the role of VIMP in β-cells has not been characterized. In this study, we studied the relationship between VIMP deficiency and β-cell survival in MIN6 insulinoma cells. Methods: To determine the role of VIMP in β-cells, lentiviral VIMP shRNAs were used to knock down (KD) expression of VIMP in MIN6 cells. Cell death was quantified by propidium iodide (PI) staining followed by flow cytometric analyses using a FACS Caliber and FlowJo software. Cell apoptosis and proliferation were determined by TUNEL assay and Ki67 staining, respectively. Cell cycle was analyzed after PI staining. Results: The results show that 1) VIMP suppression induces β-cell apoptosis, which is associated with a decrease in Bcl-xL, and the β-cell apoptosis induced by VIMP suppression can be inhibited by overexpression of Bcl-xL; 2) VIMP knockdown (KD) decreases cell proliferation and G1 cell cycle arrest by accumulating p27 and decreasing E2F1; 3) VIMP KD suppresses unfolded protein response (UPR) activation by regulating the IRE1α and PERK pathways; 4) VIMP KD increases insulin secretion. Conclusion: These results suggest that VIMP may function as a novel regulator to modulate β-cell survival, proliferation, cell cycle, UPR and insulin secretion in MIN6 cells.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
    Location Call Number Limitation Availability
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