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Prepublished online as a Blood First Edition Paper on December 5, 2002; DOI 10.1182/blood-2002-09-2838.
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Blood, 1 April 2003, Vol. 101, No. 7, pp. 2870-2876
TRANSFUSION MEDICINE
A novel I-branching
 -1,6-N-acetylglucosaminyltransferase involved in human
blood group I antigen expression
Niro Inaba,
Toru Hiruma,
Akira Togayachi,
Hiroko Iwasaki,
Xiao-Hui Wang,
Yusuke Furukawa,
Ryoichi Sumi,
Takashi Kudo,
Katsuya Fujimura,
Toshie Iwai,
Masanori Gotoh,
Mitsuru Nakamura, and
Hisashi Narimatsu
From the National Institute of Advanced Industrial
Science and Technology (AIST), Glycogene Function Team and Cell
Regulation Analysis Team, Research Center for Glycoscience (RCG),
Tsukuba, Ibaraki; JGS Japan Genome Solutions, Inc, Hachioji, Tokyo;
Fujirebio Inc, Frontier Research Division, Hachioji, Tokyo; Jichi
Medical School, Division of Stem Cell Regulation, Minamikawachi,
Tochigi; Amersham Biosciences KK, Tokyo; and Gifu Prefecture Blood
Center, Japan.
The human blood group i and I antigens are determined by linear and
branched poly-N-acetyllactosamine structures, respectively. In erythrocytes, the fetal i antigen is converted to the adult I
antigen by I-branching
 -1,6-N-acetylglucosaminyltransferase (IGnT) during
development. Dysfunction of the I-branching enzyme may result in the
adult i phenotype in erythrocytes. However, the I gene
responsible for blood group I antigen has not been fully confirmed. We
report here a novel human I-branching enzyme, designated
IGnT3. The genes for IGnT1 (reported in 1993),
IGnT2 (also presented in this study), and IGnT3
consist of 3 exons and share the second and third exons. Bone marrow
cells preferentially expressed IGnT3 transcript. During
erythroid differentiation using CD34+ cells,
IGnT3 was markedly up-regulated with concomitant decrease in IGnT1/2. Moreover, reticulocytes expressed the
IGnT3 transcript, but IGnT1/2 was
below detectable levels. By molecular genetic analyses of an adult i
pedigree, individuals with the adult i phenotype were revealed to have
heterozygous alleles with mutations in exon 2 (1006G>A; Gly336Arg) and
exon 3 (1049G>A; Gly350Glu), respectively, of the IGnT3
gene. Chinese hamster ovary (CHO) cells transfected with each mutated
IGnT3 cDNA failed to express I antigen. These findings
indicate that the expression of the blood group I antigen in
erythrocytes is determined by a novel IGnT3, not by
IGnT1 or IGnT2.
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