A group of researchers of the Virginia Commonwealth University while studying the hemoglobin genes, the mutations of which happen to play s significant role in genetic blood disorders like sickle cell anemia and beta-thalassemia have come out with the definite identification of two proteins which happen to be accountable to the regulation of the overlapping groups of genes during the development of red blood cells. There is also an expectation that the findings in due course will direct the researchers future gene therapies for patients with sickle cell anemia and beta-thalassemia.

In addition, the researchers also reported about the existence of a definite protein called KLF2 proficient in the coordination with a related and well-studied transcription factor, known as EKLF in the regulation of embryonic globin genes responsible for the development of mouse embryonic red blood cells. In respect of the developmental regulation of the adult beta-globin gene the EKLF   happens to play an essential role and is also vital for the maturation and stability of adult red blood cells. KLF2 is a protein crucial for making embryonic red blood cells.

While speaking on this identification Dr. Joyce A. Lloyd, Ph.D., Associate Professor of human genetics at the VCU Massey Cancer Center, and corresponding author for this study said, "If EKLF and KLF2 can turn on the embryonic globin genes in adult cells – we don't know if this is true yet - then these findings may provide a gene therapy approach for treating sickle cell anemia and beta-thalassemia. It is well-established that the expression of embryonic globin genes can help ameliorate these diseases." As a part of the study the Lloyd's team studied gene expression and red blood cell development in the mouse embryo in a meticulous note. They used mouse embryos missing both the KLF2 and EKLF genes for the demonstration of the severe reduction of the embryonic globin expression, and that the embryos as a result are anemic, compared to mice missing KLF2 or EKLF alone.

While asked to comment Dr. Lloyd said, "This likely means that EKLF and KLF2, which are related transcription factors, regulate overlapping groups of genes in developing red blood cells. In the absence of both factors, they cannot compensate for each other, causing more serious defects in red blood cell development."