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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.

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Award Detail for: ERK SIGNALING AND A HYBRID SURGICAL/MOLECULAR APPROACH FOR CHRONIC HEART FAILURE
NORTHERN CALIFORNIA INSTITUTE FOR RESEARCH & EDUCATION
DUNS Number: 613338789
4150 CLEMENT STREET
SAN FRANCISCO, CA 94121-1545
Recipient Report: Grant or Loan
Prime Recipient

Reporting Information
Award Type Award Number Final Report
Grant 3R01HL083118-03S1 Recipient responsible for this data

Award Recipient Information
Recipient DUNS Number Recipient Account Number Recipient Congressional District
613338789 Recipient responsible for this data 8

Award Information
Funding Agency Code Awarding Agency Code Award Date
7529 7529 07-15-2009
Amount of Award Sub Account Number for Program Source (TAS)  
$ 289,157 Recipient responsible for this data
Program Source (TAS)* CFDA Number 
750871 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
DESCRIPTION (provided by applicant): The leading cause of congestive heart failure (CHF) is post-myocardial infarction (MI) cardiomyopathy, which results from pathologic remodeling of viable heart muscle after loss of infarcted tissue. Some pharmacologic interventions slow declines in cardiac function, but there remain no means to halt the progression of post-MI remodeling to end-stage failure. Molecular and cellular interventions in cardiac function are therefore viewed as an important new horizon. Cardiac hypertrophy can be physiologic, a stable and reversible process observed in exercise and pregnancy, or pathologic, an irreversible response to stresses such as hypertension and MI that degenerates to dilated cardiomyopathy. Many molecular pathways are known to be active during pathologic and, to a lesser degree, physiologic hypertrophy, but it is not clear how these distinct responses are regulated, nor how differing stresses are translated into different outcomes. During the course of the current R01, we discovered that loss of alpha adrenergic receptors, an important source of physiologic hypertrophic signaling, leads to an increase, rather than a decrease, in post-MI hypertrophy. This increase, however, was characterized by pathologic hypertrophy, suggesting a dynamic balance between physiologic and pathologic hypertrophy, even in response to pathologic stresses. If a loss of the former can increase the latter, therapeutic instigation of a heightened level of physiologic hypertrophy may lessen the induction of pathologic hypertrophy. In the proposed studies, we will test this translational hypothesis utilizing a new and unique genetic model of regulatable MEK1-ERK1/2 signaling. Our first Specific Aim will involve induction of physiologic hypertrophic MEK1-ERK1/2 signaling at critical time points after MI to assess a resulting shift away from pathologic hypertrophy during post-MI remodeling. The second Aim will focus on a careful dissection of the downstream molecular effectors of this change, and elucidate specific pathways by which the myocardium is shifted toward physiologic or pathologic hypertrophy. In the third Specific Aim, we will evaluate whether these observations are specific to post-MI pathophysiology or whether they represent a generalizable, novel understanding of cardiac hypertrophy by applying the most successful strategy and analyses from Aims 1 and 2 to an alternative form of pathologic hypertrophy observed after experimental aortic constriction. Finally, our new model of regulatable MEK1-ERK1/2 upregulation will allow us to combine the induction of physiologic hypertrophy with surgical ventricular reconstruction, a necessary adjunct to any molecular therapy applied to severely misshapen hearts in the later stages of cardiomyopathy.

Project Information
Project Name or
Project/Program Title
Project Status Total Federal Amount ARRA Funds
Received/Invoiced
ERK SIGNALING AND A HYBRID SURGICAL/MOLECULAR APPROACH FOR CHRONIC HEART FAILURE 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
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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
4150 CLEMENT STREET Not Available Recipient responsible for this data
Infrastructure City Infrastructure State Infrastructure ZIP Code+4
SAN FRANCISCO CA 94121-1545
Infrastructure Purpose and Rationale
Recipient responsible for this data

Primary Place of Performance
Street Address 1 Street Address 2 City
BOX 1724 Recipient responsible for this data SAN FRANCISCO
State Zip Code+4 Congressional District
CA 941431724 12
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
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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.