排序方式: 共有64条查询结果,搜索用时 187 毫秒
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Anuja Dubey Andrew Farmer Jessica Schlueter Steven B. Cannon Brian Abernathy Reetu Tuteja Jimmy Woodward Trushar Shah Benjamin Mulasmanovic Himabindu Kudapa Nikku L. Raju Ragini Gothalwal Suresh Pande Yongli Xiao Chris D. Town Nagendra K. Singh Gregory D. May Scott Jackson Rajeev K. Varshney 《DNA research》2011,18(3):153-164
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U Sharma SK Singh D Pal R Khajuria AK Mandal R Prasad 《Molecular and cellular biochemistry》2012,369(1-2):287-293
Previous study has documented reduced alkaline phosphatase (ALP) activity in brush border membrane (BBM) isolated from renal cell carcinoma (RCC). Diminished activity of ALP is associated with alteration in both increased K (m) as well as decreased V (max) of enzyme suggests that there may be a change in the conformation of enzyme as well as decreased number of ALP active molecules. The present study was conducted to find out any role of BBM lipid composition and its fluidity in diminished activity of alkaline phosphatase in renal cell carcinoma. Total phospholipids and glycolipids were significantly augmented in BBM from RCC as compared to control. Fractional analysis of total phospholipids revealed significantly increased phosphatidylethanolamine. Decreased fractions of sphingomyelin and phosphatidylinositol were observed. Cholesterol-to-total phospholipid molar ratios in tumor BBM was a significantly lower in tumor BBM. A significant reduction in polarization and microviscosity was found in BBM from RCC. Therefore, we conclude that alteration in membrane lipid composition and fluidity may play a substantial role in reduced activity of ALP in RCC. 相似文献
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Horowitz JC Rogers DS Sharma V Vittal R White ES Cui Z Thannickal VJ 《Cellular signalling》2007,19(4):761-771
Transforming growth factor-beta (TGF-beta) is a prototypical tumour-suppressor cytokine with cytostatic and pro-apoptotic effects on most target cells; however, mechanisms of its pro-survival/anti-apoptotic signalling in certain cell types and contexts remain unclear. In human lung fibroblasts, TGF-beta1 is known to induce myofibroblast differentiation in association with the delayed activation of focal adhesion kinase (FAK) and protein kinase B (PKB/AKT). Here, we demonstrate that FAK and AKT are independently regulated by early activation of SMAD3 and p38 MAPK, respectively. Pharmacologic or genetic approaches that disrupt SMAD3 signalling block TGF-beta1-induced activation of FAK, but not AKT; in contrast, disruption of early p38 MAPK signalling abrogates AKT activation, but does not alter FAK activation. TGF-beta1 is able to activate AKT in cells expressing mutant FAK or in cells treated with an RGD-containing peptide that interferes with integrin signalling, inhibits FAK activation and induces anoikis (apoptosis induced by loss of adhesion signalling). TGF-beta1 protects myofibroblasts from anoikis, in part, by activation of the PI3K-AKT pathway. Thus, TGF-beta1 co-ordinately and independently activates the FAK and AKT protein kinase pathways to confer an anoikis-resistant phenotype to myofibroblasts. Activation of these pro-survival/anti-anoikis pathways in myofibroblasts likely contributes to essential roles of TGF-beta1 in tissue fibrosis and tumour-promotion. 相似文献
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Singh Archana Singh Sujata Singh Ragini Kumar Sumit Singh Sanjay Kumar Singh Indrakant Kumar 《Functional & integrative genomics》2021,21(5-6):571-592
Functional & Integrative Genomics - Zea mays defense response is well-crafted according to the physical and chemical weapons utilized by their invaders during the coevolutionary period. Maize... 相似文献