Update: The following update relating to this announcement has been issued:
- July 16, 2012 - See Notice NOT-DK-12-007. Notice to Announce Additional Research Objectives and Funding.
Release Date: November 14, 2011
NOT-DK-11-004: Notice to Announce Additional Research Objectives and Funding for PAS-10-046: Stimulating Hematology Investigation: New Endeavors (SHINE) (R01)
National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK)
NIDDK is pleased to announce additional funding and research objectives for PAS-10-046: Stimulating Hematology Investigation: New Endeavors (SHINE) (R01).
This Notice provides three updates to PAS-10-046:
1) An additional $750,000 has been set-aside in fiscal year 2012 to make approximately 1 - 2 awards issued under this FOA in addition to those funded within NIDDK regular funding policies;
2) The research objective stated in PAS-10-046 entitled, "Non-erythroid Expression and Function of Erythropoietin Receptors" will no longer be eligible for the SHINE program; and
3) A new research objective for the SHINE program is, "Stress Erythropoiesis". In addition to the other research objectives listed in PAS-10-046 and in NOT-DK-11-004, R01 applications requesting support for research on "Stress Erythropoiesis" will now be accepted under PAS-10-046.
This additional research area has been added in response to an NIDDK-sponsored workshop (in collaboration with NHLBI) on this topic on October 17, 2011 (for more information on topics and a summary of the workshop, see: http://conferences.thehillgroup.com/NIDDK/StressErythropoeisis/). Research questions to be addressed by projects on Stress Erythropoiesis eligible for submission under PAS-10-046 include, but are not limited to:
- What are the micro-environment parameters in acute and chronic conditions needed to invoke stress erythropoiesis?
- In humans, where (in what organ or tissue) is the capacity to respond to stress erythropoiesis?
- Are there differences in the "quality" of resulting erythroid cells depending on the source (e.g., bone marrow, spleen, cord blood fetal liver) from where they were generated in response to stress erythropoiesis or in the timing of when they are produced?
- What are the molecular mechanisms controlling cell survival during stress erythropoiesis?
- What are the molecules that work during late (protein stabilization) stages vs. early progenitor stages (cytokine response pathways)?
- Are there any evolutionarily conserved features of stress erythropoiesis?
- Are there new pathways involved in stress erythropoiesis? Or are normal (homeostatic) pathways modulated to respond to stress? And if so, how are they modulated?
- How is iron metabolism modulated during stress erythropoiesis? How does erythropoiesis regulate hepcidin, ferroportin, etc.?
- Erythropoietin alone is not sufficient to recover from stress. What other components are needed to achieve stress erythropoiesis (e.g., iron availability, inflammatory environment, macrophages, or genetic background)?
- What are the signals that dictate the exodus of bone marrow erythroid progenitors? And, in the mouse, what are the signals that dictate entry into the spleen?
- What are the transcriptional regulatory factors, epigenetic modifiers, noncoding RNA players (including long noncoding RNAs and miRNAs), cell signaling pathways and translational regulators involved with stress erythropoiesis?
All other policies and aspects of this FOA remain in effect.
Please direct all inquiries to:
Terry Rogers Bishop, Ph.D.
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
6707 Democracy Boulevard, Room 619
Bethesda, MD 20892-5458
TEL: 301-594-7726
FAX: 301-480-3510
EMAIL: [email protected]
Daniel Wright, M.D.
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
6707 Democracy Boulevard, Room 621
Bethesda, MD 20892-5458
TEL: 301-594-7714
FAX: 301-480-3510
EMAIL: [email protected]
and Human Services (HHS)
