Blood group B gene is barely expressed in in vitro erythroid culture of Bm‐derived CD34+ cells without an erythroid cell‐specific regulatory element. Issue 3 (18th December 2014)
- Record Type:
- Journal Article
- Title:
- Blood group B gene is barely expressed in in vitro erythroid culture of Bm‐derived CD34+ cells without an erythroid cell‐specific regulatory element. Issue 3 (18th December 2014)
- Main Title:
- Blood group B gene is barely expressed in in vitro erythroid culture of Bm‐derived CD34+ cells without an erythroid cell‐specific regulatory element
- Authors:
- Sano, R.
Nogawa, M.
Nakajima, T.
Takahashi, Y.
Takahashi, K.
Kubo, R.
Kominato, Y.
Yokohama, A.
Tsukada, J.
Yamao, H.
Kishida, T.
Ogasawara, K.
Uchikawa, M. - Abstract:
- <abstract abstract-type="main" id="vox12220-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="vox12220-sec-0001" sec-type="section"> <title>Background and Objectives</title> <p>Previously, a weak phenotype A<sub>m</sub> or B<sub>m</sub> was assumed to be caused by a reduction of A or B gene expression in bone marrow cells, but not in mucus‐secreting cells. However, <italic>ABO</italic> expression has not been examined in erythroid progenitor cells of A<sub>m</sub> or B<sub>m</sub> individuals.</p> </sec> <sec id="vox12220-sec-0002" sec-type="section"> <title>Materials and Methods</title> <p>We carried out <italic>in vitro</italic> erythroid differentiation of CD34<sup>+</sup> cells from peripheral blood of a B<sub>m</sub> individual harbouring a 3·0‐kb deletion including an erythroid cell‐specific regulatory element, named the +5·8‐kb site, in intron 1 of the human <italic>ABO</italic> blood group gene.</p> </sec> <sec id="vox12220-sec-0003" sec-type="section"> <title>Results</title> <p>During the <italic>in vitro</italic> differentiation of CD34<sup>+</sup> cells from this B<sub>m</sub> individual into erythroid cells, B‐antigens were not detectable on the cultured cells by flow cytometric analysis, and allele‐specific RT‐PCR consistently detected the transcripts from the <italic>O</italic> allele, but not from the <italic>B</italic> allele. Moreover, chromatin immunoprecipitation assay demonstrated that both RUNX1 and GATA‐2 or GATA‐1 were bound to<abstract abstract-type="main" id="vox12220-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="vox12220-sec-0001" sec-type="section"> <title>Background and Objectives</title> <p>Previously, a weak phenotype A<sub>m</sub> or B<sub>m</sub> was assumed to be caused by a reduction of A or B gene expression in bone marrow cells, but not in mucus‐secreting cells. However, <italic>ABO</italic> expression has not been examined in erythroid progenitor cells of A<sub>m</sub> or B<sub>m</sub> individuals.</p> </sec> <sec id="vox12220-sec-0002" sec-type="section"> <title>Materials and Methods</title> <p>We carried out <italic>in vitro</italic> erythroid differentiation of CD34<sup>+</sup> cells from peripheral blood of a B<sub>m</sub> individual harbouring a 3·0‐kb deletion including an erythroid cell‐specific regulatory element, named the +5·8‐kb site, in intron 1 of the human <italic>ABO</italic> blood group gene.</p> </sec> <sec id="vox12220-sec-0003" sec-type="section"> <title>Results</title> <p>During the <italic>in vitro</italic> differentiation of CD34<sup>+</sup> cells from this B<sub>m</sub> individual into erythroid cells, B‐antigens were not detectable on the cultured cells by flow cytometric analysis, and allele‐specific RT‐PCR consistently detected the transcripts from the <italic>O</italic> allele, but not from the <italic>B</italic> allele. Moreover, chromatin immunoprecipitation assay demonstrated that both RUNX1 and GATA‐2 or GATA‐1 were bound to the +5·8‐kb site in cultured erythroid cells expressing <italic>ABO</italic>.</p> </sec> <sec id="vox12220-sec-0004" sec-type="section"> <title>Conclusion</title> <p>It is likely that the +5·8‐kb site enhances transcription from the <italic>ABO</italic> promoter in erythroid cells through binding of RUNX1 and GATA‐2 or GATA‐1.</p> </sec> </abstract> … (more)
- Is Part Of:
- Vox sanguinis. Volume 108:Issue 3(2015)
- Journal:
- Vox sanguinis
- Issue:
- Volume 108:Issue 3(2015)
- Issue Display:
- Volume 108, Issue 3 (2015)
- Year:
- 2015
- Volume:
- 108
- Issue:
- 3
- Issue Sort Value:
- 2015-0108-0003-0000
- Page Start:
- 302
- Page End:
- 309
- Publication Date:
- 2014-12-18
- Subjects:
- Blood -- Periodicals
Blood -- Transfusion -- Periodicals
Immunohematology -- Periodicals
Immunopathology -- Periodicals
615.39 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1423-0410 ↗
http://www.blackwell-synergy.com/member/institutions/issuelist.asp?journal=vox ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1111/vox.12220 ↗
- Languages:
- English
- ISSNs:
- 0042-9007
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 9258.700000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 3938.xml