Fructose-6-phosphate 2-kinase and fructose 2,6-bisphosphatase have been partially purified from maize leaves by PEG fractionadon and by chromatography on TSK-DEAE ion exchanger and Blue-Sepharose 4B. Fructose-6-phosph...Fructose-6-phosphate 2-kinase and fructose 2,6-bisphosphatase have been partially purified from maize leaves by PEG fractionadon and by chromatography on TSK-DEAE ion exchanger and Blue-Sepharose 4B. Fructose-6-phosphate 2-kinase was activated by phosphate and inhibited by 3-pnosphoglycerate. Furctose 2,6-bisphosphatase was inhibited by inorganic phosphate and fructose-6-phosphate.The observed pattern of reguladon suggests that systhesis and degradation of Fru-2,6-P<sub>2</sub> respond to changes in the concentration of effectors. An increase in the level of glycerate-3-phosphate or dihydroxyacetonephosphate will result in a decrease in the level of Fru-2,6-P<sub>2</sub>. Conversely a rise in Fru-6-P concentration will lead to an increase in the Fru-2, 6-P<sub>2</sub> concentration.展开更多
目的:研究活血化瘀治法(the medicine group of promoting blood circulation and removing stasis,PBCRS)对7,12-二甲基苯蒽[7,12-dimethylbenz(a) anthracene,DMBA]诱发性大鼠乳腺癌的抑制作用,及运用转录组测序技术(RNA sequencing,R...目的:研究活血化瘀治法(the medicine group of promoting blood circulation and removing stasis,PBCRS)对7,12-二甲基苯蒽[7,12-dimethylbenz(a) anthracene,DMBA]诱发性大鼠乳腺癌的抑制作用,及运用转录组测序技术(RNA sequencing,RNA-seq)和信号网络分析(ingenuity pathway analysis,IPA)软件筛选关键基因和验证。方法:将96只SD大鼠随机分为空白组,DMBA模型组,枸橼酸他莫昔芬(Tamoxifen,TAM)组(1.9 mg·kg^(-1)·d-1),PBCRS高、中、低剂量组(12.96,6.48,3.24 g·kg^(-1)·d-1)。药物干预1周后,除空白组外,采用DMBA诱导大鼠乳腺癌模型(灌服2次,间隔1周,剂量100 mg·kg^(-1))。给药10周后,观察大鼠荷瘤重、荷瘤体积变化,用总RNA提取试剂盒提取总RNA,从DMBA模型组和PBCRS中剂量组各取3个RNA样品进行基因检测,筛选出关键差异基因,用实时荧光定量PCR(Real-time PCR)验证关键基因。结果:与DMBA模型组比较,PBCRS中剂量组荷瘤重和荷瘤体积均明显降低(P<0.05),PBCRS高、低剂量组荷瘤重和荷瘤体积虽有降低,但与DMBA模型组比较差异均无统计学意义;基于RNA-seq技术及IPA分析软件筛选出果糖1,6二磷酸酶1 (fructose-1,6-bisphosphatase1,FBP1),浦肯野细胞蛋白4(purkinje cell protein 4,PCP4),肌红蛋白(myoglobin,MB) 3个关键基因;与DMBA模型组比较,PBCRS高、中剂量组FBP1 mRNA表达均明显升高(P<0.05),PBCRS低剂量组FBP1 mRNA表达升高,但差异无统计学意义,PBCRS高、中、低剂量组PCP4 mRNA的表达增高,但无统计学差异,PBCRS低剂量组MB mRNA的表达虽降低,差异无统计学意义。结论:PBCRS可能通过干预乳腺癌组织中FBP1的表达,抑制乳腺癌的发生。展开更多
文摘Fructose-6-phosphate 2-kinase and fructose 2,6-bisphosphatase have been partially purified from maize leaves by PEG fractionadon and by chromatography on TSK-DEAE ion exchanger and Blue-Sepharose 4B. Fructose-6-phosphate 2-kinase was activated by phosphate and inhibited by 3-pnosphoglycerate. Furctose 2,6-bisphosphatase was inhibited by inorganic phosphate and fructose-6-phosphate.The observed pattern of reguladon suggests that systhesis and degradation of Fru-2,6-P<sub>2</sub> respond to changes in the concentration of effectors. An increase in the level of glycerate-3-phosphate or dihydroxyacetonephosphate will result in a decrease in the level of Fru-2,6-P<sub>2</sub>. Conversely a rise in Fru-6-P concentration will lead to an increase in the Fru-2, 6-P<sub>2</sub> concentration.