HOXB6 gene is only expressed inerythroid progenitor cells, which are the precursor tored blood cells used for transport of oxygen and carbon dioxide throughout the body. During development, the formation of the HOX gene factor happens in the first stages offetal development, namely soon after the establishment of themesoderm, which is the “middle layer” of the future embryo. However, HOXB6 is only expressed once the undifferentiatedstem cells of the embryo distinguish themselves into the erythpoietic phase. The research has shown that HOXB6 is not expressed inhematopoietic stem cells located in thered bone marrow, which are the precursor cells to all types of blood cells, orprimordial germ cells (PGCs), the precursor to cells passed on in each generation.[8] Since it is a transcriptional factor, HOXB6 regulateserythropoiesis (red blood cell formation) using mRNA as the basis for certain protein productions. The specific gene factor for erythrogenesis has relatively been unobserved in the scientific community, and no known diseases have been associated with a defect HOXB6 gene. However, it has been shown in correlation with major skeletal deformations.[9]
HOXB6 is a structural protein that has been shown to influence the growth and differentiation of the different blood lineages. This gene has also been shown to encourage the growth ofgranulocytes andmonocytes, but at the cost of other blood cells. HOXB6 has the ability to cause the indefinite proliferation of murine marrow cells, as well as expand hematopoietic stem cells. When expressed abnormally, HOXB6 displays many characteristics of a potentoncoprotein. An oncoprotein can cause the transformation of a normal cell into a tumor cell. Overexpression of HOXB6, along with the addition ofMEIS1 protein, has been implicated in the development of acute myeloid leukemia (AML). Acute myeloid leukemia is a cancer of the blood cells, specifically theleukocytes. The chromosomal irregularity most frequently seen in HOXB6 AML is a reappearinginterstitial deletion of chromosome 2. Fundamental HOXB6 expression stops myeloid differentiation and debilitates erythropoiesis,megakaryopoiesis, andlymphopoiesis.[10]
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Apiou F, Flagiello D, Cillo C, Malfoy B, Poupon MF, Dutrillaux B (1996). "Fine mapping of human HOX gene clusters".Cytogenetics and Cell Genetics.73 (1–2):114–5.doi:10.1159/000134320.PMID8646877.
Sawcer S, Jones HB, Feakes R, Gray J, Smaldon N, Chataway J, Robertson N, Clayton D, Goodfellow PN, Compston A (Aug 1996). "A genome screen in multiple sclerosis reveals susceptibility loci on chromosome 6p21 and 17q22".Nature Genetics.13 (4):464–8.doi:10.1038/ng0896-464.PMID8696343.S2CID20543659.
Vider BZ, Zimber A, Hirsch D, Estlein D, Chastre E, Prevot S, Gespach C, Yaniv A, Gazit A (Mar 1997). "Human colorectal carcinogenesis is associated with deregulation of homeobox gene expression".Biochemical and Biophysical Research Communications.232 (3):742–8.Bibcode:1997BBRC..232..742V.doi:10.1006/bbrc.1997.6364.PMID9126347.
Ohnishi K, Tobita T, Sinjo K, Takeshita A, Ohno R (Nov 1998). "Modulation of homeobox B6 and B9 genes expression in human leukemia cell lines during myelomonocytic differentiation".Leukemia & Lymphoma.31 (5–6):599–608.doi:10.3109/10428199809057620.PMID9922051.
Vider BZ, Zimber A, Chastre E, Gespach C, Halperin M, Mashiah P, Yaniv A, Gazit A (Jun 2000). "Deregulated expression of homeobox-containing genes, HOXB6, B8, C8, C9, and Cdx-1, in human colon cancer cell lines".Biochemical and Biophysical Research Communications.272 (2):513–8.Bibcode:2000BBRC..272..513V.doi:10.1006/bbrc.2000.2804.PMID10833444.
1ahd: DETERMINATION OF THE NMR SOLUTION STRUCTURE OF AN ANTENNAPEDIA HOMEODOMAIN-DNA COMPLEX
1hom: DETERMINATION OF THE THREE-DIMENSIONAL STRUCTURE OF THE ANTENNAPEDIA HOMEODOMAIN FROM DROSOPHILA IN SOLUTION BY 1H NUCLEAR MAGNETIC RESONANCE SPECTROSCOPY
1san: THE DES(1-6)ANTENNAPEDIA HOMEODOMAIN: COMPARISON OF THE NMR SOLUTION STRUCTURE AND THE DNA BINDING AFFINITY WITH THE INTACT ANTENNAPEDIA HOMEODOMAIN
2hoa: STRUCTURE DETERMINATION OF THE ANTP(C39->S) HOMEODOMAIN FROM NUCLEAR MAGNETIC RESONANCE DATA IN SOLUTION USING A NOVEL STRATEGY FOR THE STRUCTURE CALCULATION WITH THE PROGRAMS DIANA, CALIBA, HABAS AND GLOMSA
