Research Topics
Genomes and Genes
| Qing LuSummaryAffiliation: Brown University Country: USA Publications
| Collaborators
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Detail Information
Publications
Inhibition of ICMT induces endothelial cell apoptosis through GRP94Qing Lu
Providence VA Medical Center, Pulmonary Critical Care Medicine Section, 830 Chalkstone Avenue, Providence, RI 02908, USA
Am J Respir Cell Mol Biol 37:20-30. 2007..We speculate that changes in the pI, subcellular localization, and protein level of GRP94 cause endothelial cell apoptosis, possibly through UPR dysfunction. These studies suggest a novel link between RhoA GTPases and the UPR...- Pulmonary endothelial cell signaling and functionSharon Rounds
Vascular Research Laboratory, Department of Medicine, Warren Alpert Medical School of Brown University, Providence VA Medical Center, Providence, Rhode Island 02903, USA
Trans Am Clin Climatol Assoc 119:155-67; discussion 167-9. 2008..Our data suggest that increasing intracellular adenosine is a useful therapeutic strategy against diseases characterized by increased vascular permeability... 
Pyrimidine-based inhibitors of CaMKIIdeltaBabu Mavunkel
Scios, Inc, 6500 Paseo Padre Parkway, Fremont, CA 94555, USA
Bioorg Med Chem Lett 18:2404-8. 2008..The results of the computational studies led to the design of ATP competitive inhibitors with optimized hinge interactions. Inhibitors of this class possessed improved enzyme and cellular activity compared to early leads...- Sustained adenosine exposure causes lung endothelial apoptosis: a possible contributor to cigarette smoke-induced endothelial apoptosis and lung injuryQing Lu
Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA
Am J Physiol Lung Cell Mol Physiol 304:L361-70. 2013..Inhibition of adenosine uptake may become a new therapeutic target in treatment of CS-induced lung diseases... - Sustained adenosine exposure causes lung endothelial barrier dysfunction via nucleoside transporter-mediated signalingQing Lu
Alpert Medical School of Brown University, Providence VA Medical Center, Research Services, 830 Chalkstone Avenue, Providence, RI 02908, USA
Am J Respir Cell Mol Biol 47:604-13. 2012..Our data further suggest that sustained adenosine exposure may cause mitochondrial oxidative stress, leading to activation of p38, JNK, and RhoA in mitochondria and resulting in EC barrier dysfunction... 
Transforming growth factor-beta1-induced endothelial barrier dysfunction involves Smad2-dependent p38 activation and subsequent RhoA activationQing Lu
Vascular Research Laboratory, Providence VA Medical Center, Research Services, 151, 830 Chalkstone Ave, Providence, RI 02908, USA
J Appl Physiol 101:375-84. 2006..Our data indicate that TGF-beta1 induces endothelial barrier dysfunction involving Smad2-dependent p38 activation, resulting in RhoA activation by possible transcriptional regulation...- Transforming growth factor-beta1 protects against pulmonary artery endothelial cell apoptosis via ALK5Qing Lu
Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Providence, Rhode Island 02908, USA
Am J Physiol Lung Cell Mol Physiol 295:L123-33. 2008..Understanding the mechanism by which TGF-beta1 promotes endothelial cell survival may provide a better treatment for apoptosis-dependent vascular diseases, such as emphysema... - Transforming growth factor-beta1 causes pulmonary microvascular endothelial cell apoptosis via ALK5Qing Lu
Providence VA Medical Center, Research Services, Providence, RI 02908, USA
Am J Physiol Lung Cell Mol Physiol 296:L825-38. 2009..We speculate that imbalance of ALK1 and ALK5 may contribute to the development of pulmonary artery hypertension... - Cigarette smoke causes lung vascular barrier dysfunction via oxidative stress-mediated inhibition of RhoA and focal adhesion kinaseQing Lu
Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, RI, USA
Am J Physiol Lung Cell Mol Physiol 301:L847-57. 2011..Our data indicate that CS causes endothelial barrier dysfunction via oxidative stress-mediated inhibition of RhoA and FAK... - Adenosine protected against pulmonary edema through transporter- and receptor A2-mediated endothelial barrier enhancementQing Lu
Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, Rhode Island 02908, USA
Am J Physiol Lung Cell Mol Physiol 298:L755-67. 2010..The data suggest that adenosine deaminase inhibition may be useful in treatment of pulmonary edema in settings of ALI... - Isoprenylcysteine carboxyl methyltransferase modulates endothelial monolayer permeability: involvement of RhoA carboxyl methylationQing Lu
Pulmonary Vascular Biology Laboratory, Providence VA Medical Center, Providence, R 02908, USA
Circ Res 94:306-15. 2004..Therefore, carboxyl methylation of RhoA may modulate endothelial barrier function... - Alterations in molecular chaperones and eIF2alpha during lung endothelial cell apoptosisQing Lu
Department of Medicine, Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Alpert Medical School of Brown University, Providence, Rhode Island 02908, USA
Am J Physiol Lung Cell Mol Physiol 298:L501-8. 2010..We also speculate that increased eIF2alpha phosphorylation is a defensive response against endothelial cell apoptosis... - PKCdelta regulates endothelial basal barrier function through modulation of RhoA GTPase activityElizabeth O Harrington
Pulmonary Vascular Research Laboratory, Providence VA Medical Center, Department of Medicine, Brown Medical School, 151 Research Services, 830 Chalkstone Avenue, Providence, RI 02908, USA
Exp Cell Res 308:407-21. 2005..Thus, PKCdelta may regulate basal endothelial barrier function by stabilizing microfilaments and focal contacts by regulating RhoA GTPase activity through upstream modulators, p190RhoGAP and p120RasGAP... - Isoprenylcysteine carboxyl methyltransferase activity modulates endothelial cell apoptosisKristina Kramer
Pulmonary Vascular Biology Laboratory, Providence Veterans Affairs Medical Center, Brown Medical School, Rhode Island 02908, USA
Mol Biol Cell 14:848-57. 2003..These findings suggest that inhibition of ICMT causes endothelial cell apoptosis by attenuation of Ras GTPase methylation and activation and its downstream antiapoptotic signaling pathway... - Focal adhesion kinase and endothelial cell apoptosisQing Lu
Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA
Microvasc Res 83:56-63. 2012..This review summarizes the signaling pathways of FAK in prevention of apoptosis and the role of FAK in mediating adenosine and homocysteine-induced endothelial cell apoptosis and in cardiovascular diseases... - Steroid receptor coactivator 3 is a coactivator for myocardin, the regulator of smooth muscle transcription and differentiationHui Joyce Li
Molecular Cardiology Research Institute, Department of Medicine, and Division of Cardiology, New England Medical Center Hospitals, Tufts University School of Medicine, Boston, MA 02111, USA
Proc Natl Acad Sci U S A 104:4065-70. 2007..The SRC3-myocardin interaction identifies a site of convergence for nuclear hormone receptor-mediated and VSMC-specific gene regulation and suggests a possible mechanism for the vascular protective effects of estrogen on vascular injury... - Apoptosis and lung injuryQing Lu
Pulmonary Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine Brown Medical School, Providence, RI 02908, USA
Keio J Med 54:184-9. 2005..We also review the current understanding of the role of lung cell apoptosis in acute lung injury, pulmonary fibrosis and emphysema... - Striatin assembles a membrane signaling complex necessary for rapid, nongenomic activation of endothelial NO synthase by estrogen receptor alphaQing Lu
Molecular Cardiology Research Institute, Department of Medicine, Tufts New England Medical Center, Boston, MA 02111, USA
Proc Natl Acad Sci U S A 101:17126-31. 2004..Furthermore, by demonstrating independent regulation of nongenomic vs. genomic ER-dependent signaling, these findings provide conceptual support for the potential development of "pathway-specific" selective ER modulators... - Acetylation of cAMP-responsive element-binding protein (CREB) by CREB-binding protein enhances CREB-dependent transcriptionQing Lu
Department of Obstetrics and Gynecology, University of Michigan, 6428 Medical Science Building 1, 1301 S. Catherine Street, Ann Arbor, MI 48109, USA
J Biol Chem 278:15727-34. 2003..We propose that in addition to its functions as a bridging molecule and histone acetyltransferase, the ability of CBP to acetylate CREB may play a key role in modulating CREB-mediated gene expression... - Aryl-indolyl maleimides as inhibitors of CaMKIIdelta. Part 3: Importance of the indole orientationQing Lu
Scios, Inc, 6500 Paseo Padre Parkway, Fremont, CA 94555, USA
Bioorg Med Chem Lett 18:2399-403. 2008..Key interactions with the kinase ATP site and hinge region, predicted by homology modeling, were confirmed... - Aryl-indolyl maleimides as inhibitors of CaMKIIdelta. Part 2: SAR of the amine tetherDaniel E Levy
Scios, Inc, 6500 Paseo Padre Parkway, Fremont, CA 94555, USA
Bioorg Med Chem Lett 18:2395-8. 2008..Key interactions with the kinase ATP site and hinge region, predicted by homology modeling, were confirmed... - Aryl-indolyl maleimides as inhibitors of CaMKIIdelta. Part 1: SAR of the aryl regionDaniel E Levy
Scios, Inc, 6500 Paseo Padre Parkway, Fremont, CA 94555, USA
Bioorg Med Chem Lett 18:2390-4. 2008..Key interactions with the kinase ATP site and hinge region were found to be consistent with homology modeling predictions... - [Cloning of tight junction protein claudin-1 and construction of the mammalian expression vector]Lin Chen
Institute for Digestive Diseases, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China
Nan Fang Yi Ke Da Xue Xue Bao 27:349-51. 2007..To construct a recombinant plasmid containing the coding region of tight junction protein claudin-1 gene to understand the functional role of claudin-1 in human colorectal carcinoma... - Echocardiographic diagnosis of anomalous origin of the left coronary artery from the pulmonary arteryYa li Yang
Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People s Republic of China
Echocardiography 24:405-11. 2007..Based on the apprehension of ultrasonic features and the enhancement of diagnostic alertness, the echocardiography can evaluate ALCAPA accurately and give more information than angiography. It may be the first diagnostic choice... - Activation of protein kinase C induces mitogen-activated protein kinase dephosphorylation and pronucleus formation in rat oocytesQing Lu
State Key Laboratory of Reproductive Biology, Institute of Zoology, The Chinese Academy of Sciences, Beijing 100080, People's Republic of China
Biol Reprod 67:64-9. 2002..We also provide evidence supporting the involvement of such a process in fertilization... - Regulation of estrogen receptor alpha-mediated transcription by a direct interaction with protein phosphatase 2AQing Lu
Department of Medicine and Molecular Cardiology Research Institute, New England Medical Center Hospitals, Inc, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
J Biol Chem 278:4639-45. 2003.... - [p73 gene expression in apoptotic process of acute myeloid leukemia cell line U937 induced by methotrexate]Guang-Fen Xiao
Department of Hematology, The Second Affiliated Hospital of Nanhua University, Hengyang 421001, China
Zhongguo Shi Yan Xue Ye Xue Za Zhi 10:104-7. 2002..Sub-G(1) peak and S + G(2)/M arrest were also determined by FCM, but the quantity of p73 expression was generally constant. In conclusion, U937 cell apoptosis induced by MTX did not change p73 mRNA level... - High-density lipoprotein increases the abundance of eNOS protein in human vascular endothelial cells by increasing its half-lifeMaria E Rämet
Molecular Cardiology Research Institute and Department of Medicine, New England Medical Center Hospitals, Inc, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
J Am Coll Cardiol 41:2288-97. 2003.... - [Cytokine and inflammatory mediators in acute respiratory distress syndrome]Zhong-Ji Sun
Emergency Department, Affiliated Hospital of Chinese People's Armed Police Forces College, Tianjin 300162, China
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue 15:186-9. 2003 - Micro- and macrocirculatory effects of apheresis in patients with familial hyperlipidemiaQing Lu
Department of Medicine, Huddinge University Hospital, Karolinska Institutet, Stockholm, Sweden
Ther Apher Dial 7:115-8. 2003..We have found no previous report with parallel assessments at the microcirculatory and macrocirculatory levels... - The relationship between aromatase in primary breast tumors and response to treatment with aromatase inhibitors in advanced diseasePaul Chr de Jong
St. Antonius Hospital, P.O. Box 2500, 3430 EM Nieuwegein, The Netherlands
J Steroid Biochem Mol Biol 87:149-55. 2003.... - [Effect of percutaneous intervention on adrenomedullin and tumor necrosis factor in the coronary circulation]Hai chao Liu
Department of Cardiology, Zhujiang Hospital, First Military Medical University, Guangzhou 510282, China
Di Yi Jun Yi Da Xue Xue Bao 24:636-8, 645. 2004..To evaluate the effect of percutaneous intervention (PCI) on coronary circulation levels of adrenomedullin (ADM) and tumor necrosis factor alpha (TNF-alpha) in patients with coronary heart disease (CHD)... - Modulator recognition factor 1, an AT-rich interaction domain family member, is a novel corepressor for estrogen receptor alphaSerban P Georgescu
Molecular Cardiology Research Institute, New England Medical Center and Department of Medicine, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
Mol Endocrinol 19:2491-501. 2005..These data identify MRF1 as a repressor of ERalpha-mediated transcriptional activation and support a role for MRF1 in regulating ER-dependent gene expression in cardiovascular and other cells... - 4-Aryl-1,2,3-triazole: a novel template for a reversible methionine aminopeptidase 2 inhibitor, optimized to inhibit angiogenesis in vivoLara S Kallander
GlaxoSmithKline Pharmaceuticals, King of Prussia, Pennsylvania 19406, USA
J Med Chem 48:5644-7. 2005..Compound 24, a potent inhibitor of cobalt-activated hMetAP2, also inhibits human and mouse endothelial cell growth. Using a mouse matrigel model, this reversible hMetAP2 inhibitor was also shown to inhibit angiogenesis in vivo... - [Effects of D-limonene on leukemia cells HL-60 and K562 in vitro]Xiao-Ming Guo
Department of Pediatrics, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, China
Zhongguo Shi Yan Xue Ye Xue Za Zhi 14:692-5. 2006..It is concluded that D-L can inhibit proliferation and induce apoptosis of HL-60 and K562 cells. The bcl-2, mutant type of p53 and bax may be involved in the gene regulation of D-L-induced apoptosis... - MAP kinase mediates growth factor-induced nuclear translocation of estrogen receptor alphaQing Lu
Molecular Cardiology Research Institute, Department of Medicine, and Division of Cardiology, New England Medical Center Hospitals, Tufts University School of Medicine, 750 Washington Street, P O Box 80, 02111, Boston, MA, USA
FEBS Lett 516:1-8. 2002....