The src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia-like disease in mice but not for lymphoid leukemogenesis or activation of phosphatidylinositol 3-kinase.
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A direct binding site for Grb2 contributes to transformation and leukemogenesis by the Tel-Abl (ETV6-Abl) tyrosine kinaseThe Philadelphia chromosome in leukemogenesisTargeting the SH2-Kinase Interface in Bcr-Abl Inhibits LeukemogenesisA BCR-ABL mutant lacking direct binding sites for the GRB2, CBL and CRKL adapter proteins fails to induce leukemia in miceModeling Philadelphia chromosome positive leukemias.Dissecting the molecular mechanism of chronic myelogenous leukemia using murine models.The molecular mechanism of chronic myelogenous leukemia and its therapeutic implications: studies in a murine model.Studying the pathogenesis of BCR-ABL+ leukemia in mice.Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib.Targeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia in mice.Chronic myelogenous leukemia as a paradigm of early cancer and possible curative strategies.Loss of Ikaros DNA-binding function confers integrin-dependent survival on pre-B cells and progression to acute lymphoblastic leukemiaPD166326, a novel tyrosine kinase inhibitor, has greater antileukemic activity than imatinib mesylate in a murine model of chronic myeloid leukemia.Essential role for Stat5a/b in myeloproliferative neoplasms induced by BCR-ABL1 and JAK2(V617F) in mice.Inhibition of heat shock protein 90 prolongs survival of mice with BCR-ABL-T315I-induced leukemia and suppresses leukemic stem cells.Diverging fates of cells of origin in acute and chronic leukaemia.Src kinases as targets for B cell acute lymphoblastic leukaemia therapy.Structure, regulation, signaling, and targeting of abl kinases in cancer.Loss of beta-catenin impairs the renewal of normal and CML stem cells in vivoDistinct GAB2 signaling pathways are essential for myeloid and lymphoid transformation and leukemogenesis by BCR-ABL1.Absence of SKP2 expression attenuates BCR-ABL-induced myeloproliferative diseaseSuppression of E-protein activity interferes with the development of BCR-ABL-mediated myeloproliferative diseaseIRF-4 functions as a tumor suppressor in early B-cell development.Inhibitory effects of omacetaxine on leukemic stem cells and BCR-ABL-induced chronic myeloid leukemia and acute lymphoblastic leukemia in miceSuperenhancer reprogramming drives a B-cell-epithelial transition and high-risk leukemia.BCR/ABL can promote CD19+ cell growth but not render them long-term stemness.IKK-dependent activation of NF-κB contributes to myeloid and lymphoid leukemogenesis by BCR-ABL1.ABL1 fusion genes in hematological malignancies: a review.Tyrosine kinase gene fusions in cancer: translating mechanisms into targeted therapies.Mechanisms of pre-B-cell receptor checkpoint control and its oncogenic subversion in acute lymphoblastic leukemia.Curcumin inhibits proliferation and induces apoptosis of leukemic cells expressing wild-type or T315I-BCR-ABL and prolongs survival of mice with acute lymphoblastic leukemia.Requirement for CD44 in homing and engraftment of BCR-ABL-expressing leukemic stem cells.Identification of transcriptional targets associated with the expression of p210 Bcr-Abl.A novel dasatinib-sensitive RCSD1-ABL1 fusion transcript in chemotherapy-refractory adult pre-B lymphoblastic leukemia with t(1;9)(q24;q34).Murine retroviral bone marrow transplantation models for the study of human myeloproliferative disorders.Growth autonomy and lineage switching in BCR-ABL-transduced human cord blood cells depend on different functional domains of BCR-ABL.Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia.BCR-ABL regulates phosphatidylinositol 3-kinase-p110gamma transcription and activation and is required for proliferation and drug resistance.The calcineurin protein phosphatase is dispensable for BCR-ABL-induced B-ALL maintenance, propagation and response to dasatinib.G-protein coupled receptor 34 activates Erk and phosphatidylinositol 3-kinase/Akt pathways and functions as alternative pathway to mediate p185Bcr-Abl-induced transformation and leukemogenesis.
P2860
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P2860
The src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia-like disease in mice but not for lymphoid leukemogenesis or activation of phosphatidylinositol 3-kinase.
description
2001 nî lūn-bûn
@nan
2001年の論文
@ja
2001年学术文章
@wuu
2001年学术文章
@zh-cn
2001年学术文章
@zh-hans
2001年学术文章
@zh-my
2001年学术文章
@zh-sg
2001年學術文章
@yue
2001年學術文章
@zh
2001年學術文章
@zh-hant
name
The src homology 2 domain of B ...... phosphatidylinositol 3-kinase.
@en
type
label
The src homology 2 domain of B ...... phosphatidylinositol 3-kinase.
@en
prefLabel
The src homology 2 domain of B ...... phosphatidylinositol 3-kinase.
@en
P2093
P356
P1433
P1476
The src homology 2 domain of B ...... phosphatidylinositol 3-kinase.
@en
P2093
Roumiantsev S
Van Etten RA
Varticovski L
P356
10.1182/BLOOD.V97.1.4
P407
P577
2001-01-01T00:00:00Z