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HHS Recovery Act Recipient Reporting Readiness Tool

Step 4. Review and Copy the Grant Awards Data

TAGGS provides some – but not all – of the data needed for the Recipient Report. Recipients are responsible for directly collecting and reporting all required data to FederalReporting.gov. Data that HHS does not currently collect are highlighted in yellow. Do not copy this highlighted information. Please enter the appropriate data for your organization in these required fields. For assistance with entering these data please contact FederalReporting.gov.

You may capture the data HHS does provide by copying data from this screen and pasting it into the reporting format of your choice, such as the Excel spreadsheet template, the XML template, or by logging into the online form. For assistance with copying and pasting these data please e-mail our help desk at Readiness Help.

 

Award Detail for: ROLE OF ADIPOSE AUTOPHAGY IN METABOLISM
UNIVERSITY OF MINNESOTA, OFFICE OF STUDENT FINANCE AID
DUNS Number: 555917996
106 PLEASANT SE, 210 FRASER HL
MINNEAPOLIS, MN 55455
Recipient Report: Grant or Loan
Prime Recipient

Reporting Information
Award Type Award Number Final Report
Grant 1R56DK083474-01A1 Recipient responsible for this data

Award Recipient Information
Recipient DUNS Number Recipient Account Number Recipient Congressional District
555917996 Recipient responsible for this data 5

Award Information
Funding Agency Code Awarding Agency Code Award Date
7529 7529 01-25-2010
Amount of Award Sub Account Number for Program Source (TAS)  
$ 220,002 Recipient responsible for this data
Program Source (TAS)* CFDA Number 
750883 93.701
Total Number of Sub Awards to Individuals Total Amount of Sub Awards to Individuals
Recipient responsible for this data Recipient responsible for this data
Total Number of Payments to Vendors less than $25,000/award Total Amount of Payments to Vendors less than $25,000/award
Recipient responsible for this data Recipient responsible for this data
Total Number of Sub Awards less than $25,000/award Total Amount of Sub Awards less than $25,000/award
Recipient responsible for this data Recipient responsible for this data
Award Description
Our long-term goal is to increase knowledge on autophagy-mediated mechanisms pertaining to metabolic diseases such as diabetes, obesity, and insulin resistance. Autophagy is an evolutionarily-conserved cellular process through which eukaryotic cells digest macromolecules, organelles or faulty cellular components under starvation or stress, and it has a significant growing number of links to a variety of human disease and physiology including cancer, aging, neurodegeneration, and microbial infection. The common theme emerging in a variety of studies on autophagy is induction in cells in response to mitochondrial dysfunction or endoplasmic reticulum (ER) stress as a mechanism for homeostatic control. Despite such wide spread appreciation for autophagy and its link to metabolic diseases, the molecular linkage between autophagy, obesity and type 2 diabetes has not been widely examined and the role(s) of autophagy in adipose metabolism has not been explored at all. Our proposed study is intended to define crucial molecular steps of autophagy induction and the autophagy roles in the regulation of adipose energy metabolism and insulin resistance. The central hypothesis is that mTOR-regulated protein complex, which consists of ULK1 (Unc51-like protein 1) and Atg13 (mammalian homolog of yeast AuToPhagy gene 13), plays a crucial role in the regulation of the induction of autophagy, insulin resistance, and energy metabolism in adipose tissue. A crucial step for autophagy induction involves inhibition of mammalian target of rapamycin (mTOR), a master controller of cell growth and a nutrient-regulated protein kinase. The mechanism through which mTOR regulates autophagy induction has remained elusive. Aim #1 will address this question by determining the roles of Atg13 and mTOR-mediated phosphorylation of Atg13 and ULK1 in the regulation of ULK1 kinase activity. Given the mechanical knowledge obtained from aim #1, the studies in Aim #2 will be oriented toward defining how autophagy is regulated in adipose cells and tissue in response to nutrients or stress and how Atg13 and ULK1 are involved in the regulation. Aim #3 will be focused to understand the roles of adipose autophagy in the regulation of metabolism and insulin sensitivity by determining several metabolic parameters in adipose cells and tissue where autophagy is disturbed. This project will be made possible through the close, synergistic collaboration between two investigators, Dr. Kim having expertise in the mTOR field and Dr. Bernlohr having expertise in adipose biology. Both laboratories have joined forces to study adipose autophagy by determining crucial molecular steps in the regulation of fat cell energy metabolism and the relationship of autophagy to obesity and insulin resistance.

Project Information
Project Name or
Project/Program Title
Project Status Total Federal Amount ARRA Funds
Received/Invoiced
ROLE OF ADIPOSE AUTOPHAGY IN METABOLISM Recipient responsible for this data Recipient responsible for this data
Number of Jobs Description of Jobs Created
Recipient responsible for this data Recipient responsible for this data
Quarterly Activities/Project Description
Recipient responsible for this data
 
Activity Code (NAICS or NTEE-NPC)
1Recipient responsible for this data2Recipient responsible for this data
3Recipient responsible for this data4Recipient responsible for this data
5Recipient responsible for this data6Recipient responsible for this data
7Recipient responsible for this data8Recipient responsible for this data
9Recipient responsible for this data10Recipient responsible for this data
Total Federal Amount of ARRA
Expenditure
Total Federal ARRA
Infrastructure Expenditure
Infrastructure Contact Name
Recipient responsible for this data Recipient responsible for this data Recipient responsible for this data
Infrastructure Contact Email Infrastructure Contact Phone Infrastructure Contact Phone Ext.
Recipient responsible for this data Recipient responsible for this data Recipient responsible for this data
Infrastructure Contact Street Address 1 Infrastructure Contact Street Address 2 Infrastructure Contact Street Address 3
106 PLEASANT SE, 210 FRASER HL Not Available Recipient responsible for this data
Infrastructure City Infrastructure State Infrastructure ZIP Code+4
MINNEAPOLIS MN 55455
Infrastructure Purpose and Rationale
Recipient responsible for this data

Primary Place of Performance
Street Address 1 Street Address 2 City
321 CHURCH STREET Recipient responsible for this data MINNEAPOLIS
State Zip Code+4 Congressional District
MN 554551214 Not Available
Country  
US

Recipient Highly Compensated Officers
Prime Recipient Indication of Reporting Applicability # Officer Name Officer Compensation
Recipient responsible for this data 1 Recipient responsible for this data Recipient responsible for this data
2 Recipient responsible for this data Recipient responsible for this data
3 Recipient responsible for this data Recipient responsible for this data
4 Recipient responsible for this data Recipient responsible for this data
5 Recipient responsible for this data Recipient responsible for this data

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USE IN THE RECIPIENT REPORT

The information provided by this tool is baseline data that the Recipient should include in the Recipient Report that must be submitted to FederalReporting.gov beginning October 1, 2009. The data from this tool can be cut and pasted directly into the Recipient Report.