Molecular mechanisms of <Emphasis Type="Italic">Bombyx batryticatus</Emphasis> ethanol extract inducing gastric cancer SGC-7901 cells apoptosis

Bombyx batryticatus is a traditional Chinese medicine. To understand apoptotic effect of B. batryticatus ethanol extract (BBE), we investigated the role of BBE in inducing apoptosis of human gastric cancer cells SGC-7901. Cells treated with BBE and apoptosis was assessed by methyl thiazolyl tetrazolium (MTT) assay, morphological changes, DNA fragmentation and flow cytometry assays. The expression of Bcl-2, Bax and P21 were evaluated by western blot analysis and real time polymerase chain reaction. MTT assay showed that the cytotoxicity of BBE extract on SGC-7901 cells was correlated with treatment time and concentration. After treatment with 6 mg/mL of BBE the microscopy showed that, the majority of SGC-7901 cells were obviously reduced, distorted and grew slowly. Annexin-V/propidium iodide double-staining assay emerge the early apoptosis and the late apoptosis after treatment with different times by laser confocal fluorescence microscopy and flow cytometer. Cell cycle analysis of SGC 79 cells showed that BBE induced cell cycle arrest in the G1 and G2 phases. DNA fragmentation indicated the trend of BBE inducing apoptosis on SGC-7901 cells. The qRT-PCR and western blot analysis indicated that the mRNA and protein expressions of Bax and P21 were significantly up-regulated whereas that of Bc1-2 was down-regulated after treatment with BBE for 24 h. Our results revealed a correlation between gene regulation and BBE-induced apoptosis, which might indicate the potential of BBE in cancer therapy.     

Role of Drosophila gene dunc-115 in nervous system

Axonal guidance signals are transduced through growth cone surface receptors to the interior leading to changes of actin dynamics and actin binding proteins, which are critical in determining the outcome of actin cytoskeleton reorganization. We report here the characterization of the Drosophila actin binding protein abLIM/Unc-115 homolog Dunc-115 and its role in the nervous system. Three Dunc-115 isoforms are identified as Dunc-115L, M and S, respectively. While Dunc-115L is a canonical homolog of Unc-115 with four LIM domains and one villin headpiece domain, Dunc-115M and S are novel isoforms without counterparts in other species. Our molecular modeling shows Dunc-115L is likely to bind to actin. Mutant analysis reveals that Dunc-115 is involved in axonal projection in both the visual and central nervous system.     

Biochemical and photochemical changes in response to triacontanol in rice (Oryza sativa L.)

Triacontanol (TRIA) increased the contents of total chlorophyll (Chl), Chl a and Chl b by 25.1%, 26.1% and 22.4% respectively 4 h after treatment in rice seedlings. The minimal fluorescence (F₀), the maximal fluorescence (Fm) and Fv/Fm were also higher in TRIA-treated plants. In actinic light, other Chl fluorescence parameters were measured at different photon flux densities (PFD) to construct light response curves of the quantum yield of PSII electron transport (_PSII), light response curves of photochemical quenching (qp), and light response curves of non-photochemical quenching (qN), respectively. The _PSII and qp declined with the increasing PFD with a higher level present in TRIA-treated plants. The qN increased with the increasing PFD with a lower level present in TRIA-treated plants. Two-dimensional gel electrophoresis indicated a protein expression difference between TRIA-treated materials and the controls at the total-soluble-protein level. Rubisco was 30% higher in TRIA-treated plants than in controls. The quantity of other proteins was unchanged in response to TRIA. These data provide biochemical and photochemical evidence for the effects of TRIA on photosynthesis.     

水温对虹鳟血清中血糖含量的影响

度下的动态变化对虹鳟南移温水驯化养殖具有参考价值.     

The putative propeptide of MycP1 in mycobacterial type VII secretion system does not inhibit protease activity but improves protein stability

Mycosin-1 protease (MycP1) is a serine protease anchored to the inner membrane of Mycobacterium tuberculosis, and is essential in virulence factor secretion through the ESX-1 type VII secretion system (T7SS). Bacterial physiology studies demonstrated that MycP1 plays a dual role in the regulation of ESX-1 secretion and virulence, primarily through cleavage of its secretion substrate EspB. MycP1 contains a putative N-terminal inhibitory propeptide and a catalytic triad of Asp-His-Ser, classic hallmarks of a subtilase family serine protease. The MycP1 propeptide was previously reported to be initially inactive and activated after prolonged incubation. In this study, we have determined crystal structures of MycP1 with (MycP1^24-422) and without (MycP1^63-422) the propeptide, and conducted EspB cleavage assays using the two proteins. Very high structural similarity was observed in the two crystal structures. Interestingly, protease assays demonstrated positive EspB cleavage for both proteins, indicating that the putative propeptide does not inhibit protease activity. Molecular dynamic simulations showed higher rigidity in regions guarding the entrance to the catalytic site in MycP1^24-422 than in MycP1^63-422, suggesting that the putative propeptide might contribute to the conformational stability of the active site cleft and surrounding regions.     

RBM10 inhibits cell proliferation of lung adenocarcinoma via RAP1/AKT/CREB signalling pathway

Initial functional studies have demonstrated that RNA‐binding motif protein 10 (RBM10) can promote apoptosis and suppress cell proliferation; however, the results of several studies suggest a tumour‐promoting role for RBM10. Herein, we assessed the involvement of RBM10 in lung adenocarcinoma cell proliferation and explored the potential molecular mechanism. We found that, both in vitro and in vivo, RBM10 overexpression suppresses lung adenocarcinoma cell proliferation, while its knockdown enhances cell proliferation. Using complementary DNA microarray analysis, we previously found that RBM10 overexpression induces significant down‐regulation of RAP1A expression. In this study, we have confirmed that RBM10 decreases the activation of RAP1 and found that EPAC stimulation and inhibition can abolish the effects of RBM10 knockdown and overexpression, respectively, and regulate cell growth. This effect of RBM10 on proliferation was independent of the MAPK/ERK and P38/MAPK signalling pathways. We found that RBM10 reduces the phosphorylation of CREB via the AKT signalling pathway, suggesting that RBM10 exhibits its effect on lung adenocarcinoma cell proliferation via the RAP1/AKT/CREB signalling pathway.