A single point mutation is the cause of the Greek form of hereditary persistence of fetal haemoglobin

Article Abstract:

The -117 point mutation in the gamma-globulin promoter induces the hereditary persistence of fetal hemoglobin (HPFH) phenotype. Moreover, the suppression of the gamma-globulin gene in mice produces a parallel suppression of the linked human beta-globulin gene. These results, obtained by introducing the point mutation into the gamma-globulin gene through genetic engineering, are important because the abnormal presence of gamma-globulin in adults due to HPFH is known to lesson the severity of two diseases, beta-thalassemia and sickle cell anemia.

Physiological aspects, Genetic aspects, Mutation (Biology), Mutation, Fetal hemoglobin, Gamma globulins

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An intrinsic but cell-nonautonomous defect in GATA-1-overexpressing mouse erythroid cells

Article Abstract:

Research examining the tissue-specific transcription factor GATA-1, which is necessary for the production of red blood cells, is presented. Lethal anaemia results when there is overexpression of GATA-1 in erythroid cells.

Blood cells

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Positions, please

Article Abstract:

A gene gives rise to a phenotype through its ability to generate an RNA or protein product. Recent studies indicate that autonomy might be an optical feature for many genes.

United States, Science & research, RNA, DNA binding proteins, Genetic research

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