The Experts below are selected from a list of 6 Experts worldwide ranked by ideXlab platform
Kim Schaefer-rego - One of the best experts on this subject based on the ideXlab platform.
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ABL oncogene expression during erythroleukemia cell differentiation.
Leukemia Research, 2004Co-Authors: David Leibowitz, Daniel Popenoe, J. Gregory Mears, Arthur Bank, Kim Schaefer-regoAbstract:Abstract The translocation between Chromosome 9 and Chromosome 22 which creates the Philadelphia 1 Chromosome moves the ABL oncogene from its normal location on Chromosome 9 and fuses it with a portion of the BCR gene on Chromosome 22. This new BCR/ABL fusion gene generates a unique 8.7 kilobase (kb) RNA which codes for a new 210 kilodalton (kd, p210) protein which has a protein tyrosine kinase activity that is greatly increased in comparison to the normal ABL protein. The human K562 cell line was derived from a patient with CML, and serves as one model for the regulation of expression of the ABL and BCR/ABL genes. This study examines the expression of the BCR/ABL fusion gene and the normal ABL gene in relation to differentiation and changes in proliferative state. The expression of both the normal ABL transcripts and the BCR ABL fusion transcript decrease approximately ten-fold when the cells are induced to differentiate with hemin. In contrast, expression of the MYC oncogene is unaffected by hemin-induced differentiation. The results suggest that both ABL and BCR/ABL expression vary in proportion to the differentiation of the cells, but minimally if at all as a function of the cells' proliferative state.
David Leibowitz - One of the best experts on this subject based on the ideXlab platform.
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ABL oncogene expression during erythroleukemia cell differentiation.
Leukemia Research, 2004Co-Authors: David Leibowitz, Daniel Popenoe, J. Gregory Mears, Arthur Bank, Kim Schaefer-regoAbstract:Abstract The translocation between Chromosome 9 and Chromosome 22 which creates the Philadelphia 1 Chromosome moves the ABL oncogene from its normal location on Chromosome 9 and fuses it with a portion of the BCR gene on Chromosome 22. This new BCR/ABL fusion gene generates a unique 8.7 kilobase (kb) RNA which codes for a new 210 kilodalton (kd, p210) protein which has a protein tyrosine kinase activity that is greatly increased in comparison to the normal ABL protein. The human K562 cell line was derived from a patient with CML, and serves as one model for the regulation of expression of the ABL and BCR/ABL genes. This study examines the expression of the BCR/ABL fusion gene and the normal ABL gene in relation to differentiation and changes in proliferative state. The expression of both the normal ABL transcripts and the BCR ABL fusion transcript decrease approximately ten-fold when the cells are induced to differentiate with hemin. In contrast, expression of the MYC oncogene is unaffected by hemin-induced differentiation. The results suggest that both ABL and BCR/ABL expression vary in proportion to the differentiation of the cells, but minimally if at all as a function of the cells' proliferative state.
Daniel Popenoe - One of the best experts on this subject based on the ideXlab platform.
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ABL oncogene expression during erythroleukemia cell differentiation.
Leukemia Research, 2004Co-Authors: David Leibowitz, Daniel Popenoe, J. Gregory Mears, Arthur Bank, Kim Schaefer-regoAbstract:Abstract The translocation between Chromosome 9 and Chromosome 22 which creates the Philadelphia 1 Chromosome moves the ABL oncogene from its normal location on Chromosome 9 and fuses it with a portion of the BCR gene on Chromosome 22. This new BCR/ABL fusion gene generates a unique 8.7 kilobase (kb) RNA which codes for a new 210 kilodalton (kd, p210) protein which has a protein tyrosine kinase activity that is greatly increased in comparison to the normal ABL protein. The human K562 cell line was derived from a patient with CML, and serves as one model for the regulation of expression of the ABL and BCR/ABL genes. This study examines the expression of the BCR/ABL fusion gene and the normal ABL gene in relation to differentiation and changes in proliferative state. The expression of both the normal ABL transcripts and the BCR ABL fusion transcript decrease approximately ten-fold when the cells are induced to differentiate with hemin. In contrast, expression of the MYC oncogene is unaffected by hemin-induced differentiation. The results suggest that both ABL and BCR/ABL expression vary in proportion to the differentiation of the cells, but minimally if at all as a function of the cells' proliferative state.
J. Gregory Mears - One of the best experts on this subject based on the ideXlab platform.
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ABL oncogene expression during erythroleukemia cell differentiation.
Leukemia Research, 2004Co-Authors: David Leibowitz, Daniel Popenoe, J. Gregory Mears, Arthur Bank, Kim Schaefer-regoAbstract:Abstract The translocation between Chromosome 9 and Chromosome 22 which creates the Philadelphia 1 Chromosome moves the ABL oncogene from its normal location on Chromosome 9 and fuses it with a portion of the BCR gene on Chromosome 22. This new BCR/ABL fusion gene generates a unique 8.7 kilobase (kb) RNA which codes for a new 210 kilodalton (kd, p210) protein which has a protein tyrosine kinase activity that is greatly increased in comparison to the normal ABL protein. The human K562 cell line was derived from a patient with CML, and serves as one model for the regulation of expression of the ABL and BCR/ABL genes. This study examines the expression of the BCR/ABL fusion gene and the normal ABL gene in relation to differentiation and changes in proliferative state. The expression of both the normal ABL transcripts and the BCR ABL fusion transcript decrease approximately ten-fold when the cells are induced to differentiate with hemin. In contrast, expression of the MYC oncogene is unaffected by hemin-induced differentiation. The results suggest that both ABL and BCR/ABL expression vary in proportion to the differentiation of the cells, but minimally if at all as a function of the cells' proliferative state.
Arthur Bank - One of the best experts on this subject based on the ideXlab platform.
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ABL oncogene expression during erythroleukemia cell differentiation.
Leukemia Research, 2004Co-Authors: David Leibowitz, Daniel Popenoe, J. Gregory Mears, Arthur Bank, Kim Schaefer-regoAbstract:Abstract The translocation between Chromosome 9 and Chromosome 22 which creates the Philadelphia 1 Chromosome moves the ABL oncogene from its normal location on Chromosome 9 and fuses it with a portion of the BCR gene on Chromosome 22. This new BCR/ABL fusion gene generates a unique 8.7 kilobase (kb) RNA which codes for a new 210 kilodalton (kd, p210) protein which has a protein tyrosine kinase activity that is greatly increased in comparison to the normal ABL protein. The human K562 cell line was derived from a patient with CML, and serves as one model for the regulation of expression of the ABL and BCR/ABL genes. This study examines the expression of the BCR/ABL fusion gene and the normal ABL gene in relation to differentiation and changes in proliferative state. The expression of both the normal ABL transcripts and the BCR ABL fusion transcript decrease approximately ten-fold when the cells are induced to differentiate with hemin. In contrast, expression of the MYC oncogene is unaffected by hemin-induced differentiation. The results suggest that both ABL and BCR/ABL expression vary in proportion to the differentiation of the cells, but minimally if at all as a function of the cells' proliferative state.