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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: REGULATION OF TGF-BETA RECEPTOR-DEPENDENT VASCULAR DISEASE
MAINE MEDICAL CENTER
DUNS Number: 071732663
22 BRAMHALL STREET
PORTLAND, ME 04102-3134
Recipient Report: Grant or Loan
Prime Recipient

Reporting Information
Award Type Award Number Final Report
Grant 3R01HL083151-03S1 Recipient responsible for this data

Award Recipient Information
Recipient DUNS Number Recipient Account Number Recipient Congressional District
071732663 Recipient responsible for this data 1

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)  
$ 261,367 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
The long-term goal of this laboratory is to understand the processes by which endothelial cells (ECs) regulate vessel stability and homeostasis. Our focus is to understand the functional relationship between the TGF-beta receptor ALK1 and its co-receptor, endoglin. These molecules are important regulators of angiogenesis and wound healing, and are the target genes for the vascular disease hereditary hemorrhagic telangiectasia (HHT). We will test the hypothesis that endoglin transduces TGF-beta receptor signals in endothelial cells via a novel Smad-independent mechanism. Our studies demonstrate that endoglin is phosphorylated by ALK1, which we hypothesize regulates endoglin?s effects on focal adhesion re-organization, cytoskeletal architecture, and migration in ECs. To understand this novel endoglin signaling pathway and its relevance in the vasculature, the aims of this proposal are: Specific Aim 1: Examine the consequences of TGF-beta receptor-mediated phosphorylation of endoglin to determine how this pathway regulates EC function. Studies will focus on the role of putative protein-protein interactions mediated by endoglin?s cytosolic domain, emphasizing the regulation of EC focal adhesion assembly, tubulogenesis, TGF-beta receptor subcellular localization, and EC-specific intercellular signals. Specific Aim 2: Examine the consequences of EC-targeted expression of endoglin CD mutants in the yolk sac vasculature. This aim will emphasize cytosolic domain-dependent effects on EC tubulogenesis and angiogenic remodeling, and emphasize the endpoints used for Aim 1. The results obtained in these studies will elucidate the mechanism underlying endoglin?s regulation of intrinsic EC function as well as EC-initiated intercellular signals within the yolk sac vasculature in vivo. Specific Aim 3: Characterize the vascular abnormalities observed in the FVB:eng+/- mouse model. This aim builds on new preliminary data which suggests that the heterozygous eng+/- expressed on the FVB mouse genetic background constitutes a potentially novel and useful model of HHT vascular malformation. We will study the structural and biochemical properties of the FVB:eng+/- vasculature in order to understand the basis for its vascular malformations. This model will then be used to test whether EC-expressed transgenic endoglin is sufficient to rescue the vascular deficiencies. Our proposed mouse transgenic, genetic, and biochemical models of endoglin function will lead to a deeper understanding of novel mechanisms of TGF-beta receptor-dependent regulation of EC proliferation, adhesion, tubulogenesis, and angiogenic remodeling that culminate in the establishment and maintenance of vessel integrity. The proposed studies are highly relevant to normal vascular function, and will elucidate endoglin's role in adult-onset vascular diseases.

Project Information
Project Name or
Project/Program Title
Project Status Total Federal Amount ARRA Funds
Received/Invoiced
REGULATION OF TGF-BETA RECEPTOR-DEPENDENT VASCULAR DISEASE 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
22 BRAMHALL STREET Not Available Recipient responsible for this data
Infrastructure City Infrastructure State Infrastructure ZIP Code+4
PORTLAND ME 04102-3134
Infrastructure Purpose and Rationale
Recipient responsible for this data

Primary Place of Performance
Street Address 1 Street Address 2 City
Not Available Recipient responsible for this data PORTLAND
State Zip Code+4 Congressional District
ME 041023175 1
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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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.