BCR/ABL induces multiple abnormalities of cytoskeletal function.
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Bcr-Abl induces abnormal cytoskeleton remodeling, beta1 integrin clustering and increased cell adhesion to fibronectin through the Abl interactor 1 pathwayPhosphoregulation of the WAVE regulatory complex and signal integrationAssociation of tyrosine phosphatase SHP-2 with F-actin at low cell densitiesMultiple signaling interactions of Abl and Arg kinases with the EphB2 receptorPSTPIP 2, a second tyrosine phosphorylated, cytoskeletal-associated protein that binds a PEST-type protein-tyrosine phosphataseBCR/ABL-mediated downregulation of genes implicated in cell adhesion and motility leads to impaired migration toward CCR7 ligands CCL19 and CCL21 in primary BCR/ABL-positive cellsThe Abl-related gene (Arg) nonreceptor tyrosine kinase uses two F-actin-binding domains to bundle F-actinInhibition of class II phosphoinositide 3-kinase gamma expression by p185(Bcr-Abl) contributes to impaired chemotaxis and aberrant homing of leukemic cellsSHIP1, an SH2 domain containing polyinositol-5-phosphatase, regulates migration through two critical tyrosine residues and forms a novel signaling complex with DOK1 and CRKLC3G forms complexes with Bcr-Abl and p38α MAPK at the focal adhesions in chronic myeloid leukemia cells: implication in the regulation of leukemic cell adhesion.Signal transduction and cellular functions of the TEL/ARG oncoprotein.c-Abl is activated by growth factors and Src family kinases and has a role in the cellular response to PDGFUsing Bcr-Abl to examine mechanisms by which abl kinase regulates morphogenesis in Drosophila.Genetically encoded fluorescent reporters of protein tyrosine kinase activities in living cells.Changes in cell adhesivity and cytoskeleton-related proteins during imatinib-induced apoptosis of leukemic JURL-MK1 cells.Rac2 GTPase deficiency depletes BCR-ABL+ leukemic stem cells and progenitors in vivo.Differential expression and signaling of CBL and CBL-B in BCR/ABL transformed cells.Recent advances in the molecular and cellular biology of chronic myeloid leukaemia: lessons to be learned from the laboratory.BCR-ABL as a target for novel therapeutic interventions.BCR/ABL: from molecular mechanisms of leukemia induction to treatment of chronic myelogenous leukemia.Chronic myelogenous leukemia as a paradigm of early cancer and possible curative strategies.Oncogenic Abl and Src tyrosine kinases elicit the ubiquitin-dependent degradation of target proteins through a Ras-independent pathwayReal-time analysis of imatinib- and dasatinib-induced effects on chronic myelogenous leukemia cell interaction with fibronectin.CDK1-mediated phosphorylation of Abi1 attenuates Bcr-Abl-induced F-actin assembly and tyrosine phosphorylation of WAVE complex during mitosis.SHP-2 phosphatase is required for hematopoietic cell transformation by Bcr-Abl.Abi1 gene silencing by short hairpin RNA impairs Bcr-Abl-induced cell adhesion and migration in vitro and leukemogenesis in vivo.The RhoGEF domain of p210 Bcr-Abl activates RhoA and is required for transformation.A chimeric receptor/oncogene that can be regulated by a ligand in vitro and in vivoBCR-ABL1 kinase-dependent alteration of mRNA metabolism: potential alternatives for therapeutic intervention.Signal Transduction by the Philadelphia Chromosome-encoded BCR/ABL Oncoproteins: Therapeutic Implications for Chronic Myeloid Leukemia and Philadelphia-positive Acute Lymphoblastic Leukemia.BCR/ABL directly inhibits expression of SHIP, an SH2-containing polyinositol-5-phosphatase involved in the regulation of hematopoiesis.Abl tyrosine kinases are required for infection by Shigella flexneri.Differential motility of p190bcr-abl- and p210bcr-abl-expressing cells: respective roles of Vav and Bcr-Abl GEFs.Eight-channel iTRAQ enables comparison of the activity of six leukemogenic tyrosine kinases.Dose-dependent effects of Bcr-Abl in cell line models of different stages of chronic myeloid leukemia.Global effects of BCR/ABL and TEL/PDGFRbeta expression on the proteome and phosphoproteome: identification of the Rho pathway as a target of BCR/ABL.MEK kinase 1 mediates the antiapoptotic effect of the Bcr-Abl oncogene through NF-kappaB activation.A member of Forkhead transcription factor FKHRL1 is a downstream effector of STI571-induced cell cycle arrest in BCR-ABL-expressing cells.Deletion of the Src homology 3 domain and C-terminal proline-rich sequences in Bcr-Abl prevents Abl interactor 2 degradation and spontaneous cell migration and impairs leukemogenesis.Functional analysis of a single chain chimeric alpha/beta-granulocyte-macrophage colony-stimulating factor receptor. Importance of a glutamate residue in the transmembrane region.
P2860
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P2860
BCR/ABL induces multiple abnormalities of cytoskeletal function.
description
1997 nî lūn-bûn
@nan
1997年の論文
@ja
1997年論文
@yue
1997年論文
@zh-hant
1997年論文
@zh-hk
1997年論文
@zh-mo
1997年論文
@zh-tw
1997年论文
@wuu
1997年论文
@zh
1997年论文
@zh-cn
name
BCR/ABL induces multiple abnormalities of cytoskeletal function.
@en
BCR/ABL induces multiple abnormalities of cytoskeletal function.
@nl
type
label
BCR/ABL induces multiple abnormalities of cytoskeletal function.
@en
BCR/ABL induces multiple abnormalities of cytoskeletal function.
@nl
prefLabel
BCR/ABL induces multiple abnormalities of cytoskeletal function.
@en
BCR/ABL induces multiple abnormalities of cytoskeletal function.
@nl
P2093
P2860
P356
P1476
BCR/ABL induces multiple abnormalities of cytoskeletal function.
@en
P2093
D S Ewaniuk
J D Griffin
P2860
P356
10.1172/JCI119520
P407
P577
1997-07-01T00:00:00Z