Ramesh C Nayak
University of Cincinnati, Cincinnati Children's Hospital Medical Center, Jawaharlal Nehru University, Utkal University, UT health science center at Tyler
0000-0002-3206-8152
About
I have a broad research background in vascular biology, normal and malignant HSC/Ps biology, hematopoietic disease modeling in a dish using patient derived and gene-edited isogenic iPSCs. The central focus of my research program is to decipher the epigenetic landscape and transcriptomic program controlling hematopoietic stem cells functions and transformation to hematologic malignancies. In addition, my laboratory studies optimization of hematopoietic cell regeneration using induced pluripotent stem cells (iPSC), and modeling of hematopoietic disorder using patient-derived and gene-edited isogenic iPSCs.
Employment
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University of Cincinnati Assistant Professor2022 - Present
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University of Cincinnati Research Scientist2019 - 2022
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Cincinnati Children's Hospital Medical Center Research associate2011 - 2019
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UT health science center at Tyler Post doctoral fellow2007 - 2011
Education
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Jawaharlal Nehru University PhD2002 - 2008
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Utkal University M. Sc.1998 - 2000
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Utkal University B.Sc.1995 - 1998
Projects & Funding
Projects & funding information is unavailable.
Publications (28)
- Genetic and epigenetic regulation of Treg cell fitness by autism-related chromatin remodeler CHD8. Save
- Modeling Immune Lineage Co-Development in Human Pluripotent Stem Cell-derived Liver Organoids. Save
- G-CSF resistance of ELANE-mutant neutropenia depends on SERF1-containing truncated-neutrophil elastase aggregates. Save
- Retinoid X receptor promotes hematopoietic stem cell fitness and quiescence and preserves hematopoietic homeostasis. Save
- Nuclear Vav3 is required for polycomb repression complex-1 activity in B-cell lymphoblastic leukemogenesis. Save
- FOXO activity adaptation safeguards the hematopoietic stem cell compartment in hyperglycemia Save
- Yap1-Scribble polarization is required for hematopoietic stem cell division and fate Save
- The signaling axis atypical protein kinase C λ/ι-Satb2 mediates leukemic transformation of B-cell progenitors Save
- Ubiquitination is not omnipresent in myeloid leukemia Save
- Neutrophils Derived from Genetically Modified Human Induced Pluripotent Stem Cells Circulate and Phagocytose Bacteria In Vivo Save