The objective of the Administrative Core (Core A) is to provide the administrative support for the efficient functioning of the program project. The PI, Dr. Asrar Malik, will be responsible for evaluating the progress of the program project as a whole and of the individual research projects. The Administrative Core will coordinate the inter-project collaborators and develop new arrangements as deemed necessary for the scientific progress of the program. The Administrative Core will also provide the projects and cores with a monthly review of all expenditures and will deal with University Accounting and Grants offices concerning grant budgets. The Administrative Core will also be responsible for the completion of all annual Progress Reports for the program project sent to the NIH. Additionally, the administrative support provided by the Administrative Core will reconcile all budgets of the projects and cores.. The Administrative Core will also be responsible for organizing various weekly research meetings and seminars as well as meetings of the members of the Internal and External Advisory Committees invited to visit the program (outiined in the Introduction of the grant). The Administrative Core will be used equally by the four projects.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL060678-14
Application #
8620694
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
Project End
Budget Start
2014-03-01
Budget End
2015-02-28
Support Year
14
Fiscal Year
2014
Total Cost
$108,592
Indirect Cost
$39,425
Name
University of Illinois at Chicago
Department
Type
DUNS #
098987217
City
Chicago
State
IL
Country
United States
Zip Code
60612
Chen, Zhenlong; D S Oliveira, Suellen; Zimnicka, Adriana M et al. (2018) Reciprocal regulation of eNOS and caveolin-1 functions in endothelial cells. Mol Biol Cell 29:1190-1202
Le Master, Elizabeth; Huang, Ru-Ting; Zhang, Chongxu et al. (2018) Proatherogenic Flow Increases Endothelial Stiffness via Enhanced CD36-Mediated Uptake of Oxidized Low-Density Lipoproteins. Arterioscler Thromb Vasc Biol 38:64-75
Marsboom, Glenn; Rehman, Jalees (2018) Hypoxia Signaling in Vascular Homeostasis. Physiology (Bethesda) 33:328-337
Lv, Yang; Kim, Kyungho; Sheng, Yue et al. (2018) YAP Controls Endothelial Activation and Vascular Inflammation Through TRAF6. Circ Res 123:43-56
Christoforidis, Theodore; Driver, Tom G; Rehman, Jalees et al. (2018) Generation of controllable gaseous H2S concentrations using microfluidics. RSC Adv 8:4078-4083
Di, Anke; Xiong, Shiqin; Ye, Zhiming et al. (2018) The TWIK2 Potassium Efflux Channel in Macrophages Mediates NLRP3 Inflammasome-Induced Inflammation. Immunity 49:56-65.e4
Komarova, Yulia; Kruse, Kevin J; Mehta, Dolly et al. (2017) Response by Komarova et al to Letter Regarding Article, ""Protein Interactions at Endothelial Junctions and Signaling Mechanisms Regulating Endothelial Permeability"". Circ Res 120:e28
Mittal, Manish; Nepal, Saroj; Tsukasaki, Yoshikazu et al. (2017) Response by Mittal et al to Letter Regarding Article, ""Neutrophil Activation of Endothelial Cell-Expressed TRPM2 Mediates Transendothelial Neutrophil Migration and Vascular Injury"". Circ Res 121:e87
Soni, Dheeraj; Regmi, Sushil C; Wang, Dong-Mei et al. (2017) Pyk2 phosphorylation of VE-PTP downstream of STIM1-induced Ca2+ entry regulates disassembly of adherens junctions. Am J Physiol Lung Cell Mol Physiol 312:L1003-L1017
Oliveira, Suellen D S; Castellon, Maricela; Chen, Jiwang et al. (2017) Inflammation-induced caveolin-1 and BMPRII depletion promotes endothelial dysfunction and TGF-?-driven pulmonary vascular remodeling. Am J Physiol Lung Cell Mol Physiol 312:L760-L771

Showing the most recent 10 out of 200 publications