AbstractAML1-ETO fusion protein is observed in approximately 12% of acute myeloid leukemia. In the present research, we found that AML1-ETO is able to inhibit Sp1 transactivity. We also found that this inhibition of Sp1 transactivity by AML1-ETO is achieved by interaction between Sp1 and RUNT domain of AML1. AML1b is able to abrogate the inhibition of AML1-ETO. Since Sp1 is involved in hematopoietic cell differentiation, we proposed that AML1-ETO promotes leukemogenesis by blocking cell differentiation through inhibition of Sp1 transactivity.Structured summaryMINT-6549474: AML1-ETO (genbank_protein_gi:AAB34820) physically interacts (MI:0218) with Sp1 (uniprotkb:P08047) by anti bait coimmunoprecipitation (MI:0006)MINT-6549439: Sp1 (uniprotkb...
The AML1/ETO fusion protein found in acute myeloid leukemias functions as a transcriptional regulato...
Acute myeloid leukemia (AML) is the most prevalent form of adult leukemia. The most common chromosom...
The mechanisms by which AML1/ETO (A/E) fusion protein induces leukemogenesis in acute myeloid leukem...
AbstractAML1-ETO fusion protein is observed in approximately 12% of acute myeloid leukemia. In the p...
The AML1/ETO fusion protein is essential to the development of t(8;21) acute myeloid leukemia (AML) ...
AML1/ETO is the fusion protein resulting from the t(8;21) found in acute myeloid leukemia (AML) of t...
The AML1 and ETS families of transcription factors play critical roles in hematopoiesis; AML1, and i...
RUNX1/AML1 is required for definitive hematopoiesis and is frequently targeted by chromosomal transl...
The t(8;21) acute myeloid leukemia (AML)-associated oncoprotein AML1-ETO disrupts normal hematopoiet...
The translocation (8;21), generating the AML1-ETO fusion protein, is one of the most frequent chromo...
A reciprocal translocation involving chromosomes 8 and 21 generates the AML1/ETO oncogenic transcrip...
SummaryThe t(8;21) acute myeloid leukemia (AML)-associated oncoprotein AML1-ETO disrupts normal hema...
Leukemic disease can be linked to aberrant gene expression. This often is the result of molecular al...
Recently, SIRT1 was found to play an important role in a variety of solid and hematologic malignanci...
Somatic rearrangements of transcription factors are common abnormalities in the acute leukemias. Wit...
The AML1/ETO fusion protein found in acute myeloid leukemias functions as a transcriptional regulato...
Acute myeloid leukemia (AML) is the most prevalent form of adult leukemia. The most common chromosom...
The mechanisms by which AML1/ETO (A/E) fusion protein induces leukemogenesis in acute myeloid leukem...
AbstractAML1-ETO fusion protein is observed in approximately 12% of acute myeloid leukemia. In the p...
The AML1/ETO fusion protein is essential to the development of t(8;21) acute myeloid leukemia (AML) ...
AML1/ETO is the fusion protein resulting from the t(8;21) found in acute myeloid leukemia (AML) of t...
The AML1 and ETS families of transcription factors play critical roles in hematopoiesis; AML1, and i...
RUNX1/AML1 is required for definitive hematopoiesis and is frequently targeted by chromosomal transl...
The t(8;21) acute myeloid leukemia (AML)-associated oncoprotein AML1-ETO disrupts normal hematopoiet...
The translocation (8;21), generating the AML1-ETO fusion protein, is one of the most frequent chromo...
A reciprocal translocation involving chromosomes 8 and 21 generates the AML1/ETO oncogenic transcrip...
SummaryThe t(8;21) acute myeloid leukemia (AML)-associated oncoprotein AML1-ETO disrupts normal hema...
Leukemic disease can be linked to aberrant gene expression. This often is the result of molecular al...
Recently, SIRT1 was found to play an important role in a variety of solid and hematologic malignanci...
Somatic rearrangements of transcription factors are common abnormalities in the acute leukemias. Wit...
The AML1/ETO fusion protein found in acute myeloid leukemias functions as a transcriptional regulato...
Acute myeloid leukemia (AML) is the most prevalent form of adult leukemia. The most common chromosom...
The mechanisms by which AML1/ETO (A/E) fusion protein induces leukemogenesis in acute myeloid leukem...