TY - JOUR
T1 - Increased expression of aml1 during retinoic-acid-induced differentiation of U937 cells
AU - Tanaka, Kozo
AU - Tanaka, Tomoyuki
AU - Ogawa, Seishi
AU - Kurokawa, Mineo
AU - Mitani, Kinuko
AU - Yazaki, Yoshio
AU - Hirai, Hisamaru
PY - 1995/6/26
Y1 - 1995/6/26
N2 - The AML1 gene on chromosome 21 is disrupted in the (8;21)(q22;q22) and (3;21)(q26;q22) translocations associated with myelogenous leukemias and encodes a DNA binding protein. From the AML1 gene, three proteins, AML1a, AML1b and AML1c, are produced by alternative splicings. We previously showed that AML1 is potentially involved in myeloid cell differentiation. Here we analyzed the expression of AML1 in myeloid cell lines. It was revealed that AML1b and AML1c are the major AML1 proteins in these cell lines and that prior to morphological and functional differentiation, their expressions increase in U937 cells when treated with all-trans retinoic acid. These data suggest that the expression of AML1 is associated with myeloid cell differentiation.
AB - The AML1 gene on chromosome 21 is disrupted in the (8;21)(q22;q22) and (3;21)(q26;q22) translocations associated with myelogenous leukemias and encodes a DNA binding protein. From the AML1 gene, three proteins, AML1a, AML1b and AML1c, are produced by alternative splicings. We previously showed that AML1 is potentially involved in myeloid cell differentiation. Here we analyzed the expression of AML1 in myeloid cell lines. It was revealed that AML1b and AML1c are the major AML1 proteins in these cell lines and that prior to morphological and functional differentiation, their expressions increase in U937 cells when treated with all-trans retinoic acid. These data suggest that the expression of AML1 is associated with myeloid cell differentiation.
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U2 - 10.1006/bbrc.1995.1913
DO - 10.1006/bbrc.1995.1913
M3 - Article
C2 - 7598688
AN - SCOPUS:0029044689
SN - 0006-291X
VL - 211
SP - 1023
EP - 1030
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -