The RHD variants in Chinese population

The Rhesus (Rh) blood group system is the most important blood group system in hemolytic disease of the fetus and newborn (HDFN). In clinical transfusions, the D antigen in the Rh blood group system comes third, behind antigens A and B which from ABO blood group system. Over the past decade, molecular technologies have been used to investigate the RHD allele in different ethnic groups. This review first introduces the basic structure of RhD protein and coding genes, then focuses on D-negative, weak D, partial D, DEL, RhD_null variants reported in the Chinese population. To date, more than 460 RHD variants have been reported around the world, but less than 70 RHD variants have been reported in the Chinese population. Further research is needed to identify more RHD polymorphism and establish criteria for blood detection and transfusion guidelines for RHD variants. Only in this way can we better guarantee the safety of blood transfusion and prevent the occurrence of HDFN. With the accumulation of research and clinical data, we should be clearer which RHD variants are to be regarded as RhD negative and which need to be regarded as RhD positive.     

Human glycolipid transfer protein (GLTP) expression modulates cell shape

Glycolipid transfer protein (GLTP) accelerates glycosphingolipid (GSL) intermembrane transfer via a unique lipid transfer/binding fold (GLTP-fold) that defines the GLTP superfamily and is the prototype for GLTP-like domains in larger proteins, i.e. phosphoinositol 4-phosphate adaptor protein-2 (FAPP2). Although GLTP-folds are known to play roles in the nonvesicular intracellular trafficking of glycolipids, their ability to alter cell phenotype remains unexplored. In the present study, overexpression of human glycolipid transfer protein (GLTP) was found to dramatically alter cell phenotype, with cells becoming round between 24 and 48 h after transfection. By 48 h post transfection, ～70% conversion to the markedly round shape was evident in HeLa and HEK-293 cells, but not in A549 cells. In contrast, overexpression of W96A-GLTP, a liganding-site point mutant with abrogated ability to transfer glycolipid, did not alter cell shape. The round adherent cells exhibited diminished motility in wound healing assays and an inability to endocytose cholera toxin but remained viable and showed little increase in apoptosis as assessed by poly(ADP-ribose) polymerase cleavage. A round cell phenotype also was induced by overexpression of FAPP2, which binds/transfers glycolipid via its C-terminal GLTP-like fold, but not by a plant GLTP ortholog (ACD11), which is incapable of glycolipid binding/transfer. Screening for human protein partners of GLTP by yeast two hybrid screening and by immuno-pulldown analyses revealed regulation of the GLTP-induced cell rounding response by interaction with δ-catenin. Remarkably, while δ-catenin overexpression alone induced dendritic outgrowths, coexpression of GLTP along with δ-catenin accelerated transition to the rounded phenotype. The findings represent the first known phenotypic changes triggered by GLTP overexpression and regulated by direct interaction with a p120-catenin protein family member.     

干旱对小麦幼苗诱导蛋白表达与某些生理特性的初步探讨

试验以－１．２ＭＰａＰＥＧ６０００处理动小麦种子（ＴｒｉｔｉｃｕｍａｅｓｔｌｉｖｕｍＬ．）．ＳＤＳ－ＰＡＧＥ图谱分析表明,水分胁迫诱导幼芽及整株均产生４８．４ｋＤ、４１．５ｋＤ二个蛋白质亚基。在幼根中未出现以上二个蛋白亚基。胁迫４８ｈ后,根干重／芽干重比呈上升趋势,幼芽细胞膜楔对透性增大和相对含水量降幅度均大于幼根。     

Discovery of benzimidazole derivatives as novel multi-target EGFR, VEGFR-2 and PDGFR kinase inhibitors

Multi-target EGFR, VEGFR-2 and PDGFR inhibitors are highly useful anticancer agents with improved therapeutic efficacies. In this work, we used two virtual screening methods, support vector machines (SVM) and molecular docking, to identify a novel series of benzimidazole derivatives, 2-aryl benzimidazole compounds, as multi-target EGFR, VEGFR-2 and PDGFR inhibitors. 2-Aryl benzimidazole compounds were synthesized and their biological activities against a tumor cell line HepG-2 and specific kinases were evaluated. Among these compounds, compounds 5a and 5e exhibited high cytotoxicity against HepG-2 cells with IC?? values at ～2 μM. Further kinase assay study showed that compound 5a have good EGFR inhibitory activity and moderate VEGFR-2 and PDGFR inhibitory activities, while 5e have moderate EGFR inhibitory activity and slightly weaker VEGFR-2 and PDGFR inhibitory activities. Molecular docking analysis suggested that compound 5a more tightly interacts with EGFR and PDGFR than compound 5e. Our study discovered a novel series of benzimidazole derivatives as multi-target EGFR, VEGFR-2 and PDGFR kinases inhibitors.     

Circular RNA circ‐RCCD promotes cardiomyocyte differentiation in mouse embryo development via recruiting YY1 to the promoter of MyD88

Congenital heart disease (CHD) is the most common birth defect, affecting approximately 1% of live births. Genetic and environmental factors are leading factors to CHD, but the mechanism of CHD pathogenesis remains unclear. Circular RNAs (circRNAs) are kinds of endogenous non‐coding RNAs (ncRNAs) involved in a variety of physiological and pathological processes, especially in heart diseases. In this study, three significant differently expressed circRNA between maternal embryonic day (E) E13 and E17 was found by microarray assay. Among them, the content of circ‐RCCD increases with the development of heart and was enriched in primary cardiomyocytes of different species, which arouses our attention. Functional experiments revealed that inhibition of circ‐RCCD dramatically suppressed the formation of beating cell clusters, the fluorescence intensity of cardiac differentiation marker MF20, and the expression of the myocardial‐specific markers CTnT, Mef2c, and GATA4. Next, we found that circ‐RCCD was involved in cardiomyocyte differentiation through negative regulation of MyD88 expression. Further experiments proved that circ‐RCCD inhibited MyD88 levels by recruiting YY1 to the promoter of MyD88; circ‐RCCD inhibited nuclear translocation of YY1. These results reported that circ‐RCCD promoted cardiomyocyte differentiation by recruiting YY1 to the promoter of MyD88. And, this study provided a potential role and molecular mechanism of circ‐RCCD as a target for the treatment of CHD.     

Visualization Analysis of CRISPR Gene-editing Knowledge Map based on Citespace

Biology Bulletin - CRISPR is an adaptive immune defense system found in bacteria and archaea that is resistant to heterologous invasive genetic material. Later studies showed that the CRISPR system...