SH1 domain autophosphorylation of P210 BCR/ABL is required for transformation but not growth factor independence.
about
DNA sequence and analysis of human chromosome 9A direct binding site for Grb2 contributes to transformation and leukemogenesis by the Tel-Abl (ETV6-Abl) tyrosine kinaseTranscriptional activation of a ras-like gene (kir) by oncogenic tyrosine kinasesThe PAG gene product, a stress-induced protein with antioxidant properties, is an Abl SH3-binding protein and a physiological inhibitor of c-Abl tyrosine kinase activityThe Philadelphia chromosome in leukemogenesisBcr-Abl is a "molecular switch" for the decision for growth and differentiation in hematopoietic stem cellsIntracellular retention of ABL kinase inhibitors determines commitment to apoptosis in CML cellsProgressive changes in the leukemogenic signaling in BCR/ABL-transformed cells.Structural requirements for function of the Crkl adapter protein in fibroblasts and hematopoietic cells.Deletion of the ABL SH3 domain reactivates de-oligomerized BCR-ABL for growth factor independence.Structure-function relationships in Src family and related protein tyrosine kinases.En bloc substitution of the Src homology region 2 domain activates the transforming potential of the c-Abl protein tyrosine kinase.Abl kinase inhibits the engulfment of apoptotic [corrected] cells in Caenorhabditis elegansThe carboxyl terminus of v-Abl protein can augment SH2 domain function.Temperature-sensitive transformation by an Abelson virus mutant encoding an altered SH2 domain.BUB3 that dissociates from BUB1 activates caspase-independent mitotic death (CIMD).Mechanisms of transformation by the BCR/ABL oncogene.Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3k/Akt-dependent pathway.Modeling Philadelphia chromosome positive leukemias.Aptameric inhibition of p210bcr-abl tyrosine kinase autophosphorylation by oligodeoxynucleotides of defined sequence and backbone structurePhiladelphia-positive leukemia: a personal perspective.Studying the pathogenesis of BCR-ABL+ leukemia in mice.A requirement for NF-kappaB activation in Bcr-Abl-mediated transformationBCR/ABL inhibition by an escort/phosphatase fusion proteinTyrosine kinase inhibitors as cancer therapy.PD166326, a novel tyrosine kinase inhibitor, has greater antileukemic activity than imatinib mesylate in a murine model of chronic myeloid leukemia.IL-3 receptor signaling is dispensable for BCR-ABL-induced myeloproliferative disease.The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase Inhibitors conferred by the BIM deletion polymorphism in chronic myeloid leukemia.FoxO tumor suppressors and BCR-ABL-induced leukemia: a matter of evasion of apoptosis.Genetic requirement for Ras in the transformation of fibroblasts and hematopoietic cells by the Bcr-Abl oncogene.Leukemia treatment in severe combined immunodeficiency mice by antisense oligodeoxynucleotides targeting cooperating oncogenesStructural and signaling requirements for BCR-ABL-mediated transformation and inhibition of apoptosis.Targeting ABL and SRC kinases in chronic myeloid leukemia: experience with dasatinib.Oncogenic activation of c-ABL by mutation within its last exon.Active Akt and functional p53 modulate apoptosis in Abelson virus-transformed pre-B cells.Sole BCR-ABL inhibition is insufficient to eliminate all myeloproliferative disorder cell populations.p140/c-Abl that binds DNA is preferentially phosphorylated at tyrosine residues.Molecular and cellular bases of chronic myeloid leukemia.Development of novel benzotriazines for drug discovery.Oligomerization of the ABL tyrosine kinase by the Ets protein TEL in human leukemia.
P2860
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P2860
SH1 domain autophosphorylation of P210 BCR/ABL is required for transformation but not growth factor independence.
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
SH1 domain autophosphorylation ...... ot growth factor independence.
@ast
SH1 domain autophosphorylation ...... ot growth factor independence.
@en
type
label
SH1 domain autophosphorylation ...... ot growth factor independence.
@ast
SH1 domain autophosphorylation ...... ot growth factor independence.
@en
prefLabel
SH1 domain autophosphorylation ...... ot growth factor independence.
@ast
SH1 domain autophosphorylation ...... ot growth factor independence.
@en
P2093
P2860
P356
P1476
SH1 domain autophosphorylation ...... ot growth factor independence.
@en
P2093
Gishizky ML
Pendergast AM
P2860
P304
P356
10.1128/MCB.13.3.1728
P407
P577
1993-03-01T00:00:00Z