Site-directed deletions of Abelson murine leukemia virus define 3' sequences essential for transformation and lethality.
about
The cytostatic function of c-Abl is controlled by multiple nuclear localization signals and requires the p53 and Rb tumor suppressor gene productsBCR first exon sequences specifically activate the BCR/ABL tyrosine kinase oncogene of Philadelphia chromosome-positive human leukemias.Abelson murine leukemia virus variants with increased oncogenic potential.Oncogenic v-Abl tyrosine kinase can inhibit or stimulate growth, depending on the cell context.Isolation of temperature-sensitive Abelson virus mutants by site-directed mutagenesisComplete c-mos (rat) nucleotide sequence: presence of conserved domains in c-mos proteinsInsertional mutagenesis of the Abelson murine leukemia virus genome: identification of mutants with altered kinase activity and defective transformation ability.BCR-ABL and v-abl oncogenes induce distinct patterns of thymic lymphoma involving different lymphocyte subsets.The Ets-related transcription factor PU.1 immortalizes erythroblastsMutated alpha subunit of the Gq protein induces malignant transformation in NIH 3T3 cellsHigh incidence of lung, bone, and lymphoid tumors in transgenic mice overexpressing mutant alleles of the p53 oncogene.Temperature-sensitive mutants of Abelson murine leukemia virus deficient in protein tyrosine kinase activity.Carboxyl-terminal determinants of Abelson protein important for lymphoma induction.The transforming domain alone of the latent membrane protein of Epstein-Barr virus is toxic to cells when expressed at high levelsActivation of the c-abl oncogene by viral transduction or chromosomal translocation generates altered c-abl proteins with similar in vitro kinase propertiesOnly site-directed antibodies reactive with the highly conserved src-homologous region of the v-abl protein neutralize kinase activity.Protein stabilization explains the gag requirement for transformation of lymphoid cells by Abelson murine leukemia virusA membrane-associated, carbohydrate-modified form of the v-abl protein that cannot be phosphorylated in vivo or in vitroNormal cellular and transformation-associated abl proteins share common sites for protein kinase C phosphorylation.The location of v-src in a retrovirus vector determines whether the virus is toxic or transforming.Targeted gene disruption of the endogenous c-abl locus by homologous recombination with DNA encoding a selectable fusion protein.Ras complements the carboxyl terminus of v-Abl protein in lymphoid transformation.Abelson murine leukemia virus induces platelet-derived growth factor-independent fibroblast growth: correlation with kinase activity and dissociation from full morphologic transformation
P2860
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P2860
Site-directed deletions of Abelson murine leukemia virus define 3' sequences essential for transformation and lethality.
description
1983 nî lūn-bûn
@nan
1983年の論文
@ja
1983年論文
@yue
1983年論文
@zh-hant
1983年論文
@zh-hk
1983年論文
@zh-mo
1983年論文
@zh-tw
1983年论文
@wuu
1983年论文
@zh
1983年论文
@zh-cn
name
Site-directed deletions of Abe ...... transformation and lethality.
@en
type
label
Site-directed deletions of Abe ...... transformation and lethality.
@en
prefLabel
Site-directed deletions of Abe ...... transformation and lethality.
@en
P2860
P1433
P1476
Site-directed deletions of Abe ...... transformation and lethality.
@en
P2093
S M Watanabe
P2860
P304
P407
P577
1983-03-01T00:00:00Z