Mechanism for transcriptional gain of function resulting from chromosomal translocation in alveolar rhabdomyosarcoma.
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Transcriptional modulation of the anti-apoptotic protein BCL-XL by the paired box transcription factors PAX3 and PAX3/FKHRForkhead homologue in rhabdomyosarcoma functions as a bifunctional nuclear receptor-interacting protein with both coactivator and corepressor functionsThe human forkhead protein FREAC-2 contains two functionally redundant activation domains and interacts with TBP and TFIIBInhibition of nuclear import by protein kinase B (Akt) regulates the subcellular distribution and activity of the forkhead transcription factor AFX.MLL-AFX requires the transcriptional effector domains of AFX to transform myeloid progenitors and transdominantly interfere with forkhead protein functionPAX3-FOXO1 fusion gene in rhabdomyosarcomaPAX7 expression in embryonal rhabdomyosarcoma suggests an origin in muscle satellite cellsTargeted Cancer Therapy: Vital Oncogenes and a New Molecular Genetic Paradigm for Cancer Initiation Progression and TreatmentOverexpression of murine Pax3 increases NCAM polysialylation in a human medulloblastoma cell lineInducible short-term and stable long-term cell culture systems reveal that the PAX3-FKHR fusion oncoprotein regulates CXCR4, PAX3, and PAX7 expressionCell-type-specific regulation of distinct sets of gene targets by Pax3 and Pax3/FKHRThe transcriptional activator PAX3-FKHR rescues the defects of Pax3 mutant mice but induces a myogenic gain-of-function phenotype with ligand-independent activation of Met signaling in vivo.Embryonic expression of the tumor-associated PAX3-FKHR fusion protein interferes with the developmental functions of Pax3Effect of inhibition of the ubiquitin-proteasome system and Hsp90 on growth and survival of rhabdomyosarcoma cells in vitro.Gene fusions involving PAX and FOX family members in alveolar rhabdomyosarcoma.Pax3-FKHR knock-in mice show developmental aberrations but do not develop tumors.Differential cooperation of oncogenes with p53 and Bax to induce apoptosis in rhabdomyosarcoma.Myogenin and MyoD1 expression in paediatric rhabdomyosarcomas.Mechanisms of sarcoma development.Amplification of the t(2; 13) and t(1; 13) translocations of alveolar rhabdomyosarcoma in small formalin-fixed biopsies using a modified reverse transcriptase polymerase chain reaction.AKT and PAX3-FKHR cooperation enforces myogenic differentiation blockade in alveolar rhabdomyosarcoma cellPAX3-FOXO1 controls expression of the p57Kip2 cell-cycle regulator through degradation of EGR1.Fusion genes resulting from alternative chromosomal translocations are overexpressed by gene-specific mechanisms in alveolar rhabdomyosarcoma.cDNA microarrays detect activation of a myogenic transcription program by the PAX3-FKHR fusion oncogene.Molecular alterations in pediatric sarcomas: potential targets for immunotherapyRegulated expression of the diphtheria toxin A chain by a tumor-specific chimeric transcription factor results in selective toxicity for alveolar rhabdomyosarcoma cells.Diagnostic and prognostic sarcoma signatures.Small molecule inhibition of PAX3-FOXO1 through AKT activation suppresses malignant phenotypes of alveolar rhabdomyosarcomaMolecular and cellular biology of rhabdomyosarcoma.Marking the tempo for myogenesis: Pax7 and the regulation of muscle stem cell fate decisionsCaveolins in rhabdomyosarcomaA call to ARMS: targeting the PAX3-FOXO1 gene in alveolar rhabdomyosarcoma.Microarray analysis detects novel Pax3 downstream target genes.The COOH-terminal transactivation domain plays a key role in regulating the in vitro and in vivo function of Pax3 homeodomain.Identification of a new binding motif for the paired domain of Pax-3 and unusual characteristics of spacing of bipartite recognition elements on binding and transcription activation.Identification of target genes of PAX3-FOXO1 in alveolar rhabdomyosarcoma.Chromosomal Rearrangements in Cancer: Detection and potential causal mechanisms.JARID2 is a direct target of the PAX3-FOXO1 fusion protein and inhibits myogenic differentiation of rhabdomyosarcoma cells.The synthetic retinoid ST1926 as a novel therapeutic agent in rhabdomyosarcoma.The over-expression of cell migratory genes in alveolar rhabdomyosarcoma could contribute to metastatic spread.
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Mechanism for transcriptional gain of function resulting from chromosomal translocation in alveolar rhabdomyosarcoma.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on May 1996
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Mechanism for transcriptional ...... in alveolar rhabdomyosarcoma.
@en
Mechanism for transcriptional ...... in alveolar rhabdomyosarcoma.
@nl
type
label
Mechanism for transcriptional ...... in alveolar rhabdomyosarcoma.
@en
Mechanism for transcriptional ...... in alveolar rhabdomyosarcoma.
@nl
prefLabel
Mechanism for transcriptional ...... in alveolar rhabdomyosarcoma.
@en
Mechanism for transcriptional ...... in alveolar rhabdomyosarcoma.
@nl
P2093
P2860
P356
P1476
Mechanism for transcriptional ...... in alveolar rhabdomyosarcoma.
@en
P2093
J L Bennicelli
R H Edwards
P2860
P304
P356
10.1073/PNAS.93.11.5455
P407
P577
1996-05-01T00:00:00Z