Catálogo de publicaciones - libros

Disruption of the auto-inhibitory structure of ABL and ARG activates their kinase activity and oncogenic potential. The oncogenic forms of ABL family kinases, v-ABL, BCR-ABL, TEL-ABL, NUP214-ABL, EML1-ABL, and TEL-ARG, are implicated in a variety of hematological malignancies. The tyrosine kinase activity of all these oncoproteins is essential for the neoplastic transformation, yet additional activities, particularly those of the fusion partners of the ABL kinases, play important roles in determining the lineage and severity of the neoplastic transformation. A better understanding of the mechanism by which the oncogenic forms of ABL family kinases act in leukemogenesis will help to advance therapies for related human leukemias, as well as to understand the mechanism of leukemogenesis and he-matopoiesis in general.

Disruption of the auto-inhibitory structure of ABL and ARG activates their kinase activity and oncogenic potential. The oncogenic forms of ABL family kinases, v-ABL, BCR-ABL, TEL-ABL, NUP214-ABL, EML1-ABL, and TEL-ARG, are implicated in a variety of hematological malignancies. The tyrosine kinase activity of all these oncoproteins is essential for the neoplastic transformation, yet additional activities, particularly those of the fusion partners of the ABL kinases, play important roles in determining the lineage and severity of the neoplastic transformation. A better understanding of the mechanism by which the oncogenic forms of ABL family kinases act in leukemogenesis will help to advance therapies for related human leukemias, as well as to understand the mechanism of leukemogenesis and he-matopoiesis in general.

Disruption of the auto-inhibitory structure of ABL and ARG activates their kinase activity and oncogenic potential. The oncogenic forms of ABL family kinases, v-ABL, BCR-ABL, TEL-ABL, NUP214-ABL, EML1-ABL, and TEL-ARG, are implicated in a variety of hematological malignancies. The tyrosine kinase activity of all these oncoproteins is essential for the neoplastic transformation, yet additional activities, particularly those of the fusion partners of the ABL kinases, play important roles in determining the lineage and severity of the neoplastic transformation. A better understanding of the mechanism by which the oncogenic forms of ABL family kinases act in leukemogenesis will help to advance therapies for related human leukemias, as well as to understand the mechanism of leukemogenesis and he-matopoiesis in general.

Disruption of the auto-inhibitory structure of ABL and ARG activates their kinase activity and oncogenic potential. The oncogenic forms of ABL family kinases, v-ABL, BCR-ABL, TEL-ABL, NUP214-ABL, EML1-ABL, and TEL-ARG, are implicated in a variety of hematological malignancies. The tyrosine kinase activity of all these oncoproteins is essential for the neoplastic transformation, yet additional activities, particularly those of the fusion partners of the ABL kinases, play important roles in determining the lineage and severity of the neoplastic transformation. A better understanding of the mechanism by which the oncogenic forms of ABL family kinases act in leukemogenesis will help to advance therapies for related human leukemias, as well as to understand the mechanism of leukemogenesis and he-matopoiesis in general.

Disruption of the auto-inhibitory structure of ABL and ARG activates their kinase activity and oncogenic potential. The oncogenic forms of ABL family kinases, v-ABL, BCR-ABL, TEL-ABL, NUP214-ABL, EML1-ABL, and TEL-ARG, are implicated in a variety of hematological malignancies. The tyrosine kinase activity of all these oncoproteins is essential for the neoplastic transformation, yet additional activities, particularly those of the fusion partners of the ABL kinases, play important roles in determining the lineage and severity of the neoplastic transformation. A better understanding of the mechanism by which the oncogenic forms of ABL family kinases act in leukemogenesis will help to advance therapies for related human leukemias, as well as to understand the mechanism of leukemogenesis and he-matopoiesis in general.

Disruption of the auto-inhibitory structure of ABL and ARG activates their kinase activity and oncogenic potential. The oncogenic forms of ABL family kinases, v-ABL, BCR-ABL, TEL-ABL, NUP214-ABL, EML1-ABL, and TEL-ARG, are implicated in a variety of hematological malignancies. The tyrosine kinase activity of all these oncoproteins is essential for the neoplastic transformation, yet additional activities, particularly those of the fusion partners of the ABL kinases, play important roles in determining the lineage and severity of the neoplastic transformation. A better understanding of the mechanism by which the oncogenic forms of ABL family kinases act in leukemogenesis will help to advance therapies for related human leukemias, as well as to understand the mechanism of leukemogenesis and he-matopoiesis in general.

Disruption of the auto-inhibitory structure of ABL and ARG activates their kinase activity and oncogenic potential. The oncogenic forms of ABL family kinases, v-ABL, BCR-ABL, TEL-ABL, NUP214-ABL, EML1-ABL, and TEL-ARG, are implicated in a variety of hematological malignancies. The tyrosine kinase activity of all these oncoproteins is essential for the neoplastic transformation, yet additional activities, particularly those of the fusion partners of the ABL kinases, play important roles in determining the lineage and severity of the neoplastic transformation. A better understanding of the mechanism by which the oncogenic forms of ABL family kinases act in leukemogenesis will help to advance therapies for related human leukemias, as well as to understand the mechanism of leukemogenesis and he-matopoiesis in general.

Disruption of the auto-inhibitory structure of ABL and ARG activates their kinase activity and oncogenic potential. The oncogenic forms of ABL family kinases, v-ABL, BCR-ABL, TEL-ABL, NUP214-ABL, EML1-ABL, and TEL-ARG, are implicated in a variety of hematological malignancies. The tyrosine kinase activity of all these oncoproteins is essential for the neoplastic transformation, yet additional activities, particularly those of the fusion partners of the ABL kinases, play important roles in determining the lineage and severity of the neoplastic transformation. A better understanding of the mechanism by which the oncogenic forms of ABL family kinases act in leukemogenesis will help to advance therapies for related human leukemias, as well as to understand the mechanism of leukemogenesis and he-matopoiesis in general.

Disruption of the auto-inhibitory structure of ABL and ARG activates their kinase activity and oncogenic potential. The oncogenic forms of ABL family kinases, v-ABL, BCR-ABL, TEL-ABL, NUP214-ABL, EML1-ABL, and TEL-ARG, are implicated in a variety of hematological malignancies. The tyrosine kinase activity of all these oncoproteins is essential for the neoplastic transformation, yet additional activities, particularly those of the fusion partners of the ABL kinases, play important roles in determining the lineage and severity of the neoplastic transformation. A better understanding of the mechanism by which the oncogenic forms of ABL family kinases act in leukemogenesis will help to advance therapies for related human leukemias, as well as to understand the mechanism of leukemogenesis and he-matopoiesis in general.