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Stress Pathways in Alcohol Induced Organ Injury and Protection (R01)
Purpose.
This Funding Opportunity Announcement (FOA) issued by the National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, encourages Research Project Grant (R01) applications that propose studying the role of cellular stress responses, the cytoplasmic classical stress
response or heat shock response (HSR) and the endoplasmic reticulum (ER) stress, in alcohol-induced tissue injury and tissue protection.
While excessive alcohol use causes organ damage, moderate alcohol consumption may be beneficial.
The underlying molecular mechanisms for this apparent dichotomy of alcohols harmful and salutary effects are currently not fully understood.
Alcohol induces cellular stress pathways in the cytoplasm and in the endoplasmic reticulum that may significantly be involved in alcohol-induced tissue injury or mediate tissue protection depending on the quantity, frequency, duration, and temporal pattern of drinking.
Hence, studies of the effects of alcohol on cellular stress pathways are critical to understand the mechanisms of alcohol-induced injuries or protection to develop new strategies for prevention, diagnosis and treatment.
The purpose of this FOA is to:
(1) acquire insight into how acute or chronic alcohol consumption affects cellular stress pathways and in turn, how these changes contribute to alcohol-induced injury/protection; (2) investigate how alcohol induced stress responses mediate cell survival and death signaling pathways at macromolecular, organelle, cellular and organism level contributing to alcohol-induced tissue injury/protection; (3) develop potential stress related biomarkers for prognosis, diagnosis of tissue injury/protection, furthermore identify new targets for their therapeutic interventions.
Utilizing innovative experimental design and emerging technologies, such as deep sequencing, genomics, proteomics, metabolomics, bioinformatics, and novel imaging techniques these investigations are expected to provide a more comprehensive understanding of how alcohol affects the evolutionally conserved stress pathways and elucidate their roles in tissue injuries and repair.
Mechanism of Support.
This FOA will utilize the NIH Research Project Grant (R01)grant mechanism and runs in parallel with a FOA of identical scientific scope, PA-10-094, that encourages applications under the under the R21 mechanism.
Funds Available and Anticipated Number of Awards.
Awards issued under this FOA are contingent upon the availability of funds and the submission of a sufficient number of meritorious applications.
Because the nature and scope of the proposed research will vary from application to application, it is anticipated that the size and duration of each award will also vary.
The total amount awarded and the number of awards will depend upon the mechanism numbers, quality, duration, and costs of the applications received.
This Funding Opportunity Announcement (FOA) issued by the National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, encourages Research Project Grant (R01) applications that propose studying the role of cellular stress responses, the cytoplasmic classical stress
response or heat shock response (HSR) and the endoplasmic reticulum (ER) stress, in alcohol-induced tissue injury and tissue protection.
While excessive alcohol use causes organ damage, moderate alcohol consumption may be beneficial.
The underlying molecular mechanisms for this apparent dichotomy of alcohols harmful and salutary effects are currently not fully understood.
Alcohol induces cellular stress pathways in the cytoplasm and in the endoplasmic reticulum that may significantly be involved in alcohol-induced tissue injury or mediate tissue protection depending on the quantity, frequency, duration, and temporal pattern of drinking.
Hence, studies of the effects of alcohol on cellular stress pathways are critical to understand the mechanisms of alcohol-induced injuries or protection to develop new strategies for prevention, diagnosis and treatment.
The purpose of this FOA is to:
(1) acquire insight into how acute or chronic alcohol consumption affects cellular stress pathways and in turn, how these changes contribute to alcohol-induced injury/protection; (2) investigate how alcohol induced stress responses mediate cell survival and death signaling pathways at macromolecular, organelle, cellular and organism level contributing to alcohol-induced tissue injury/protection; (3) develop potential stress related biomarkers for prognosis, diagnosis of tissue injury/protection, furthermore identify new targets for their therapeutic interventions.
Utilizing innovative experimental design and emerging technologies, such as deep sequencing, genomics, proteomics, metabolomics, bioinformatics, and novel imaging techniques these investigations are expected to provide a more comprehensive understanding of how alcohol affects the evolutionally conserved stress pathways and elucidate their roles in tissue injuries and repair.
Mechanism of Support.
This FOA will utilize the NIH Research Project Grant (R01)grant mechanism and runs in parallel with a FOA of identical scientific scope, PA-10-094, that encourages applications under the under the R21 mechanism.
Funds Available and Anticipated Number of Awards.
Awards issued under this FOA are contingent upon the availability of funds and the submission of a sufficient number of meritorious applications.
Because the nature and scope of the proposed research will vary from application to application, it is anticipated that the size and duration of each award will also vary.
The total amount awarded and the number of awards will depend upon the mechanism numbers, quality, duration, and costs of the applications received.
Agency: Department of Health and Human Services
Office: National Institutes of Health
Estimated Funding: Not Available
Office: National Institutes of Health
Estimated Funding: Not Available
Who's Eligible
Obtain Full Opportunity Text:
http://grants.nih.gov/grants/guide/pa-files/PA-10-093.html
Additional Information of Eligibility:
Other Eligible Applicants include the following: Alaska Native and Native Hawaiian Serving Institutions; Eligible Agencies of the Federal Government; Faith-based or Community-based Organizations; Hispanic-serving Institutions; Historically Black Colleges and Universities (HBCUs); Indian/Native American Tribal Governments (Other than Federally Recognized); Non-domestic (non-U.S.) Entities (Foreign Organizations); Regional Organizations; Tribally Controlled Colleges and Universities (TCCUs) ; U. S. Territory or Possession.
Full Opportunity Web Address:
http://grants.nih.gov/grants/guide/pa-files/PA-10-093.html
Contact:
NIH OER WebmasterFBOWebmaster@OD.NIH.GOV
Agency Email Description:
If you have any problems linking to this funding announcement, please contact the NIH OER Webmaster
Agency Email:
FBOWebmaster@OD.NIH.GOV
Date Posted:
2010-03-17
Application Due Date:
2013-05-07
Archive Date:
2013-06-07
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