Subcellular localization of Bcr, Abl, and Bcr-Abl proteins in normal and leukemic cells and correlation of expression with myeloid differentiation.
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MUC1 oncoprotein blocks nuclear targeting of c-Abl in the apoptotic response to DNA damageThe BCR-ABL oncoprotein potentially interacts with the xeroderma pigmentosum group B proteinThe amphiphysin-like protein 1 (ALP1) interacts functionally with the cABL tyrosine kinase and may play a role in cytoskeletal regulationRole of tyrosine-kinase inhibitors in myeloproliferative neoplasms: comparative lessons learnedKinase-independent mechanisms of resistance of leukemia stem cells to tyrosine kinase inhibitorsThe interaction of the Bcr-Abl tyrosine kinase with the Src kinase Hck is mediated by multiple binding domainsEffective killing of Gleevec-resistant CML cells with T315I mutation by a natural compound PEITC through redox-mediated mechanismThe cytostatic function of c-Abl is controlled by multiple nuclear localization signals and requires the p53 and Rb tumor suppressor gene productsZNF198-FGFR1 transforms Ba/F3 cells to growth factor independence and results in high level tyrosine phosphorylation of STATS 1 and 5Phosphorylation of Enabled by the Drosophila Abelson tyrosine kinase regulates the in vivo function and protein-protein interactions of EnabledThe murine AIDS virus Gag precursor protein binds to the SH3 domain of c-AblMisfolding, Aggregation, and Disordered Segments in c-Abl and p53 in Human Cancer.Light microscopic detection of BCR-ABL transcripts after in-cell RT-PCR: fusion gene expression might correlate with clinical evolution of chronic myeloid leukemia.Subcellular distribution of p210(BCR-ABL) in CML cell lines and primary CD34+ CML cells.Acute myeloblastic leukemia with associated BCR-ABL translocation in a dog.Expression and function of the megakaryocyte growth and development factor receptor in acute myeloid leukemia blasts.Clinical targeting of mutated and wild-type protein tyrosine kinases in cancer.Interplay between kinase domain autophosphorylation and F-actin binding domain in regulating imatinib sensitivity and nuclear import of BCR-ABL.Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loopInterferon-alpha restores normal adhesion of chronic myelogenous leukemia hematopoietic progenitors to bone marrow stroma by correcting impaired beta 1 integrin receptor function.Cell cycle-related shifts in subcellular localization of BCR: association with mitotic chromosomes and with heterochromatin.Effector caspases and leukemiaTyrosine kinase inhibitors as cancer therapy.Treatment of marrow stroma with interferon-alpha restores normal beta 1 integrin-dependent adhesion of chronic myelogenous leukemia hematopoietic progenitors. Role of MIP-1 alpha.Gag influences transformation by Abelson murine leukemia virus and suppresses nuclear localization of the v-Abl proteinTargeting Filarial Abl-like Kinases: Orally Available, Food and Drug Administration-Approved Tyrosine Kinase Inhibitors Are Microfilaricidal and Macrofilaricidal.T cell survival and function requires the c-Abl tyrosine kinaseMolecular approach to diagnose BCR/ABL negative chronic myeloproliferative neoplasms.The COOH terminus of the c-Abl tyrosine kinase contains distinct F- and G-actin binding domains with bundling activity.Comparison of mutated ABL1 and JAK2 as oncogenes and drug targets in myeloproliferative disordersEffective killing of leukemia cells by the natural product OSW-1 through disruption of cellular calcium homeostasisMAPK15 mediates BCR-ABL1-induced autophagy and regulates oncogene-dependent cell proliferation and tumor formation.Normal ABL1 is a tumor suppressor and therapeutic target in human and mouse leukemias expressing oncogenic ABL1 kinases.Expression of BCR/ABL p210 from a knockin allele enhances bone marrow engraftment without inducing neoplasiaBlockade of Y177 and Nuclear Translocation of Bcr-Abl Inhibits Proliferation and Promotes Apoptosis in Chronic Myeloid Leukemia Cells.c-Abl in neurodegenerative diseaseBCR-ABL1 tyrosine kinase sustained MECOM expression in chronic myeloid leukaemia.Changing the subcellular location of the oncoprotein Bcr-Abl using rationally designed capture motifsBCR/ABL induces multiple abnormalities of cytoskeletal function.Treatment of intracerebral glioblastomas with G422 tumour cell vaccine in a mouse model.
P2860
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P2860
Subcellular localization of Bcr, Abl, and Bcr-Abl proteins in normal and leukemic cells and correlation of expression with myeloid differentiation.
description
1993 nî lūn-bûn
@nan
1993年の論文
@ja
1993年論文
@yue
1993年論文
@zh-hant
1993年論文
@zh-hk
1993年論文
@zh-mo
1993年論文
@zh-tw
1993年论文
@wuu
1993年论文
@zh
1993年论文
@zh-cn
name
Subcellular localization of Bc ...... with myeloid differentiation.
@en
type
label
Subcellular localization of Bc ...... with myeloid differentiation.
@en
prefLabel
Subcellular localization of Bc ...... with myeloid differentiation.
@en
P2093
P2860
P356
P1476
Subcellular localization of Bc ...... with myeloid differentiation.
@en
P2093
Hirsh-Ginsberg C
Kurzrock R
Van Etten RA
P2860
P304
P356
10.1172/JCI116786
P407
P577
1993-10-01T00:00:00Z