|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Human intestinal acyl-CoA synthetase 5 is sensitive to the inhibitor triacsin C显示文摘AIM:To investigate whether human acyl-CoA synthetase 5(ACSL5) is sensitive to the ACSL inhibitor triacsin C.METHODS:The ACSL isoforms ACSL1 and ACSL5 from rat as well as human ACSL5 were cloned and recombinantly expressed as 6xHis-tagged enzymes.Ni 2+-affinity purified recombinant enzymes were assayed at pH 7.5 or pH 9.5 in the presence or absence of triacsin C.In addition,ACSL5 transfected CaCo2 cells and intestinal human mucosa were monitored.ACSL5 expression in cellular systems was verified using Western blot and immunofluorescence.The ACSL assay mix included TrisHCl(pH 7.4),ATP,CoA,EDTA,DTT,MgCl 2,[9,103 H] palmitic acid,and triton X-100.The 200 μL reaction was initiated with the addition of solubilized,purified recombinant proteins or cellular lysates.Reactions were terminated after 10,30 or 60 min of incubation with Doles medium.RESULTS:Expression of soluble recombinant ACSL proteins was found after incubation with isopropyl betaD-1-thiogalactopyranoside and after ultracentrifugation these were further purified to near homogeneity with Ni 2+-affinity chromatography.Triacsin C selectively and strongly inhibited recombinant human ACSL5 protein at pH 7.5 and pH 9.5,as well as recombinant rat ACSL1(sensitive control),but not recombinant rat ACSL5(insensitive control).The IC50 for human ACSL5 was about 10 μmol/L.The inhibitory triacsin C effect was similar for different incubation times(10,30 and 60 min) and was not modified by the N-or C-terminal location of the 6xHis-tag.In order to evaluate ACSL5 sensitivity to triacsin C in a cellular environment,stable human ACSL5 CaCo2 transfectants and mechanically dissected normal human intestinal mucosa with high physiological expression of ACSL5 were analyzed.In both models,ACSL5 peak activity was found at pH 7.5 and pH 9.5,corresponding to the properties of recombinant human ACSL5 protein.In the presence of triacsin C(25 μmol/L),total ACSL activity was dramatically diminished in human ACSL5 transfectants as well as in ACSL5-rich human intestinal mucosa.CONCLUSION:The data strongly indicate that human ACSL5 is sensitive to triacsin C and does not compensate for other triacsin C-sensitive ACSL isoforms. | Elke Kaemmerer Anne Peuscher Andrea Reinartz Christian Liedtke Ralf Weiskirchen Jürgen Kopitz Nikolaus Gassler | 2011 | World Journal of Gastroenterology2011，17，44： | 3 |
| 2 | Alexithymia and Emotional Distress in Patients With Central Serous Chorioretinopathy显示文摘 | Rupert Conrad Nina Friederike Weber Matthias Lehnert Frank Gerhard Holz Reinhard Liedtke Nicole Eter | 2011 | Psychosomatics2011，，6： | 2 |
| 3 | Lipid-induced up-regulation of human acyl-CoA synthetase 5 promotes hepatocellular apoptosis显示文摘 | Andrea Reinartz Josef Ehling Andrea Leue Christian Liedtke Ursula Schneider Jürgen Kopitz Thomas Weiss Claus Hellerbrand Ralf Weiskirchen Ruth Knüchel Nikolaus Gassler | 2010 | BBA - Molecular and Cell Biology of Lipids2010，，9： | 2 |
| 4 | Overexpression of c-myc in hepatocytes promotes activation of hepatic stellate cells and facilitates the onset of liver fibrosis显示文摘 | Yulia A. Nevzorova Wei Hu Francisco J. Cubero Ute Haas Julia Freimuth Frank Tacke Christian Trautwein Christian Liedtke | 2013 | BBA - Molecular Basis of Disease2013，，10： | 2 |
| 5 | Interferon - alpha enhances TRAIL - mediated apoptosis by up - regulating caspase - 8 transcription in human hepatoma cells 显示文摘 | Liedtke C Groger N Manns MP | 2006 | J Hepatol2006，44，2： | 1 |
| 6 | Response to neoadjuvant therapy and long-term survival in patients with triple-negative breast cancer显示文摘 | Liedtke C Mazouni C Hess KR | 2008 | J Clin Oncol2008，26，8： | 1 |
| 7 | 显示文摘 | Meyer R Liedtke R Waser R | 2005 | Appl Phys Lett2005，86，： | 1 |
| 8 | Computer simulation of an automatic classification procedure for digitally modulated communications signals with unknown parameters显示文摘 | LIEDTKE F | 1984 | Signal Processing1984，6，4： | 1 |
| 9 | Caspase 8 small interfering RNA prevents acute liver failure in mice显示文摘 | Zender L Hutker S Liedtke C | 2003 | Proc Natl Acad Sci USA2003，100，： | 1 |
| 10 | Response to neoadjuvant therapy and long-term survival in patients with triple-negative breast cancer 显示文摘 | Liedtke C Mazouni C Hess KR | 2008 | J Clin Oncol2008，26，8： | 1 |
| 11 | The Role of Coronary Artery Injury and Perfusion in the Development of Cardiac Contusion Secondary to Nonpenetrating Chest Trauma显示文摘 | ROBERT P. ALLEN A. JAMES LIEDTKE | 1979 | The Journal of Trauma: Injury Infection and Critical Care1979，，3： | 1 |
| 12 | Triple-negative breast cancer--current status and future directions 显示文摘 | Giuz 0 Liedtke C Gottschalk N | 2009 | Ann Oncol2009，20，12： | 1 |
| 13 | Toward real microkemels显示文摘 | LIEDTKE J | 1996 | Communications of the ACM1996，39，9： | 1 |
| 14 | The origin of vim-entin expression in invasive breast cancer:epithelial-mesenchymal transition,myoepithelial histogenesis or histogenesis from progenitor cells with bilinear differentiation potential显示文摘 | Korsching E Packeisen J Liedtke C | 2005 | J Pathol2005，206，4： | 1 |
| 15 | Regulation of electrolyte transport in rabbit tracheal epithelial cells by the I1-imidazoline agonist moxonidine显示文摘 | Liedtke CM Emsberger P | 1995 | Ann N Y Acad Sci1995，763，： | 1 |
| 16 | Improving IPC by Kernel Design显示文摘 | Liedtke J | 1993 | Operating System Review1993，27，5： | 1 |
| 17 | Response to neoadjuvant therapy and long-term survival in patients with triple-negative breast cancer显示文摘 | Liedtke C Mazouni C Hess K R | 2008 | J ClinOncol2008，26，12： | 1 |
| 18 | Effects of L-propionylcarnitine on mechanical recovery during reflow in intact hearts显示文摘 | Liedtke A J De Maison L Nellis SH | 1958 | American Journal of Physiology-Heart and Circulatory Physiology1958，255，1： | 1 |
| 19 | Postmenopausal sex hormones in relation to body fat distribution显示文摘 | Liedtke S Sehmidt ME Vrieling A | 2012 | Obe- sity2012，20，5： | 1 |
| 20 | Response to neoadjuvant therapy and long-term survival in patients with triple-negative breast Cancer显示文摘 | Liedtke C Mazouni C Hess KR | 2008 | J Clin Oncol2008，26，8： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员