How the erythropoietin receptor controls red blood cell recovery and excess red cell production
Erythropoietin receptor signaling in stress erythropoiesis and erythrocytosis
This research looks at how a key hormone receptor helps the body make extra red blood cells after anemia and why the same pathway can cause too many red cells in some blood cancers.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Ut Southwestern Medical Center NIH-funded |
| Lab location | 1 site (Dallas, United States) |
| Project ID | NIH-11322061 on NIH RePORTER |
What this research studies
If you follow this work, researchers are examining a recently discovered early red blood cell progenitor (called sCFU-E) that expands when the body needs to recover from anemia. They focus on how erythropoietin (Epo) binding to its receptor (EpoR) and the JAK2 signaling pathway drive survival, growth, and maturation of these cells. The team uses lab-grown human cells, genetic models, and samples tied to patients or disease-related mutations (like JAK2 V617F) to map the signaling steps. Their methods aim to find points in the pathway that could be targeted to help recovery from anemia or to block pathological overproduction of red blood cells.
Who could benefit from this research
Good fit: People who might be most relevant include adults recovering from anemia after surgery, chemotherapy or bone marrow transplant, and patients with erythrocytosis or JAK2-driven myeloproliferative disorders who could donate samples or be considered for future targeted therapies.
Not a fit: Patients with conditions unrelated to red blood cell production, pediatric patients, or anyone seeking immediate clinical treatment are unlikely to gain direct benefit from this basic-science project right away.
Why it matters
Potential benefit: If successful, this work could point to new drug targets or strategies to improve recovery from anemia and to treat conditions that cause excessive red blood cell production.
How similar studies have performed: Previous research has firmly established Epo/EpoR and JAK2 as central to red blood cell production and shown JAK2 mutations drive erythrocytosis, but work focused on the newly defined early progenitors (sCFU-E) and their unique signaling is a newer and less charted area.
Where this research is happening
Dallas, United States
- Ut Southwestern Medical Center — Dallas, United States (Active)
Researchers
- Principal investigator: Huang, Lily Junshen — Ut Southwestern Medical Center
- Study coordinator: Huang, Lily Junshen
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.