TFII-I/Gtf2i and Erythro-Megakaryopoiesis
| Autor: | Zhijian Qian, Rukiye Nar, John Strouboulis, Jörg Bungert, Marjorie Brand, Kimberly Paulsen, Qiong Wu, Alexis Trumbull, Aishwarya Gurumurthy, Ryan C Fishman |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Physiology Repressor Macrocytosis Gtf2i Biology lcsh:Physiology 03 medical and health sciences 0302 clinical medicine Physiology (medical) Gene expression medicine Gene Transcription factor transcription factor Megakaryopoiesis lcsh:QP1-981 globin Brief Research Report medicine.disease 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Cancer research Erythropoiesis Bone marrow TFII-I megakaryopoiesis erythropoiesis |
| Zdroj: | Frontiers in Physiology, Vol 11 (2020) Frontiers in Physiology |
| ISSN: | 1664-042X |
| Popis: | TFII-I is a ubiquitously expressed transcription factor that positively or negatively regulates gene expression. TFII-I has been implicated in neuronal and immunologic diseases as well as in thymic epithelial cancer. Williams–Beuren Syndrome (WBS) is caused by a large hemizygous deletion on chromosome 7q11.23 which encompasses 26–28 genes, including GTF2I, the human gene encoding TFII-I. A subset of WBS patients has recently been shown to present with macrocytosis, a mild anemia characterized by enlarged erythrocytes. We conditionally deleted the TFII-I/Gtf2i gene in adult mice by tamoxifen induced Cre-recombination. Bone marrow cells revealed defects in erythro-megakaryopoiesis and an increase in expression of the adult β-globin gene. The data show that TFII-I acts as a repressor of β–globin gene transcription and that it is implicated in the differentiation of erythro-megakaryocytic cells. |
| Databáze: | OpenAIRE |
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