Associations of TAP1 genetic polymorphisms with atopic diseases: asthma, rhinitis and dermatitis.

Controversial findings have been reported regarding to the effect of the transporter associated with antigen processing 1 (TAP1) polymorphisms exerted on the atopic diseases susceptibility. To gain a better understanding of the effects of TAP1 polymorphisms on the risk of atopic diseases, a retrospective study was carried out to evaluate the association of the most common TAP1 polymorphisms, rs1057141 and rs1135216, with the risk of atopic diseases. From studies published in PubMed, Embase, and Web of Science up to July 2017, ten eligible studies were selected for meta-analysis. The pooled results from rs1135216 polymorphism showed increased risk of atopic diseases in homozygote and recessive comparison. From the subgroup analysis by ethnicity, it was found that rs1135216 polymorphism contributed to atopic diseases susceptibility among Africans in all the five genetic models. Subgroup analysis by atopic types indicated significant association of TAP1 polymorphism rs1135216 with asthma in the allele, dominant and recessive models and with allergic rhinitis in the recessive model. As to rs1057141, increased risk of atopic disease in the allelic, dominant and heterozygous model was found in African population. Overall, this meta-analysis study demonstrated that rs1135216 polymorphism may contribute to atopic diseases susceptibility in Asians and Africans as assessed in this study. However, well designed large-scale case-control studies are needed to confirm such preliminary findings.

Correlation of proliferation, TGF-ß3 promoter methylation, and Smad signaling in MEPM cells during the development of ATRA-induced cleft palate.

Mesenchymal cell proliferation is one of the processes in shelf outgrowth. Both all-trans retinoic acid (atRA) and transforming growth factor-ß3 (TGF-ß3) play an important role in mouse embryonic palate mesenchymal (MEPM) cell proliferation. The cellular effects of TGF-ß are mediated by Smad-dependent or Smad-independent pathways. In the present study, we demonstrate that atRA promotes TGF-ß3 promoter demethylation and protein expression, but can cause depression of mesenchymal cell proliferation, especially at embryonic day 14 (E14). Moreover, the inhibition of MEPM cell proliferation by atRA results in the downregulation of Smad signaling mediated by transforming growth interacting factor (TGIF). We speculate that the effects of atRA on MEPM cell proliferation may be mediated by Smad pathways, which are regulated by TGIF but are not related to TGF-ß3 expression. Finally, the cellular effects of TGF-ß3 on MEPM cell proliferation may be mediated by Smad-independent pathways.

Dunaliella salina as a novel host for the production of recombinant proteins.

Although several expression systems are currently available for the production of recombinant proteins, they still have some inherent disadvantages, thereby resulting in the desire to explore a novel expression system for producing recombinant proteins. Dunaliella salina (D. salina) has been exploited as a novel expression system for the field of genetic engineering because of its distinct advantages, including low production cost, fast growth, easy culture, ease of transgenic manipulation, and modified abilities of transcription and translation. Thus far, studies on D. salina host have made great development and significant progress. This paper presents a comprehensive summary of the achievements of D. salina host from the following aspects: the advantages of D. salina cells, transformation methods, cloning of D. salina genes, and expression of exogenous genes into D. salina. Furthermore, the authors identified the current main obstacles and future application prospects for the recombinant proteins produced by D. salina, which could be used as a basis for the future maturation of D. salina expression system.