Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 4

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
Purple-fleshed sweet potato (Ipomoea batatas (L.) Lam) accumulates a large amount of anthocyanins in its tubers. Activation of anthocyanin gene expression requires transcription factors such as MYB domain, basic helix-loop-helix domain, or WD40-repeat domain-containing proteins. However, the mechanisms controlling pigmentation in underground organs remain unresolved. We used a principal component analysis to identify the most important gene in anthocyanin biosynthesis in pigmented sweet potato tubers, because this gene was the most likely to be regulated by IbMYB1. Anthocyanidin synthase was identified as the most important gene. Functional analysis of its promoter identified four MYB DNA-binding sites. In gel mobility shift experiments with recombinant IbMYB1, the IbMYB1 protein bound specifically to TAACCG box and TATCC box motifs in vitro. We conducted transient expression experiments in which various promoter fragments were used to drive expression of the LUC reporter gene. The reporter gene was strongly expressed under the control of the full-length promoter, but weakly expressed under the control of promoter fragments that lacked the MYB DNA-binding domains. This provided direct evidence that IbMYB1 activates the expression of this structural anthocyanin gene. Together, these results show that IbMYB1 is important in controlling the expression of genes in the anthocyanin biosynthetic pathway in cells.
The objective of this study was to investigate the effect of exogenous selenium (Se) supply (0, 2, 4, 8, 16 μM) on the growth, lipid peroxidation and antioxidative enzyme activity of 100 mM NaCl-stressed melon (Cucumis melo L.) seedlings. Salt stress significantly reduced the growth attributes including stem length, stem diameter, dry weight and increased antioxidative enzyme activity [superoxide dismutase (SOD), peroxidase (POD), catalase (CAT)]. Moreover, the plant exhibited a significant increase in electrolyte leakage and malondialdehyde (MDA) content under NaCl stress. Se supplementation not only improved the growth parameters but also successfully ameliorated the adverse effect caused by salt stress in melon seedlings. However, the mitigation of NaCl-stressed seedlings was different depending on the Se concentration. At lower concentrations (2–8 μM), Se improved growth and acted as antioxidant by inhibiting lipid peroxidation and increasing in SOD and POD enzymes activity under salt stress. At higher concentrations (16 μM), Se exerted diminished beneficial effects on growth. Whereas CAT activity was enhanced. The result indicated that Se supplementation had a positive physiological effect on the growth and development of salt-stressed melon seedlings.
The role of Survivin in the pathogenesis of leukemia was explored in order to discover the effective avenues for gene therapy. Most primary leukemia cells isolated from patients as well as three leukemia cell lines (HL-60, K562, and U937) all expressed Survivin gene. To investigate the relationship between Survivin and chemotherapeutic resistance, HL-60 cells were treated with daunorubicin (DNR), mitoxantrone (MIT) or arsenious oxide (As2O3), and it was found that after 24h the level of Survivin mRNA was decreased by 9.7%, 41.0% and 27.5%, respectively. At 72 h, the level of Survivin mRNA was increased by 21.2% and 65.2% in HL-60 cells treated with DNR or MIT, but decreased by 33.2% in those treated with As2O3 as compared with that in the cells treated for 24 h. These results showed that DNR and MIT could initally decrease the expression of Survivin and then increase it, but As2O3 could decrease the Survivin expression continually. Furthermore, shRNA plasmids targeting the Survivin gene (pEGFP-Survivin), which can silence the expression of Survivin with a high specificity, were constructed. pEGFP-Survivin and pEGFP-H1 were transfected into HL-60 cells via electroporation and selected by G418, and HL-60/Survivin and HL-60/EGFP cells were obtained. After treatment with DNR, the cell survival rate and IC50 of DNR in HL-60/Survivin cells were decreased substantially as compared with those of HL-60/EGFP and HL-60 cells (IC50of DNR:18.3±2.45 vs40.8±6.37 and 39.2±5.91 ng/ml, respectively), and the apoptosis rate was elevated ((84.3±19.7)% vs(45.8±13.8)% and (50.9±12.4)%, respectively). These results suggest that shRNA can down-regulate the expression of Survivin in HL-60 cells substantially and improve their sensitivity to DNR. They also further explain the pathogenesis of leukemia drug resistance and provide new theory in the design of clinical therapies.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.