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Titolo:
TLS FUS, A PRO-ONCOGENE INVOLVED IN MULTIPLE CHROMOSOMAL TRANSLOCATIONS, IS A NOVEL REGULATOR OF BCR/ABL-MEDIATED LEUKEMOGENESIS/
Autore:
PERROTTI D; BONATTI S; TROTTA R; MARTINEZ R; SKORSKI T; SALOMONI P; GRASSILLI E; IOZZO RV; COOPER DR; CALABRETTA B;
Indirizzi:
THOMAS JEFFERSON UNIV,DEPT MICROBIOL & IMMUNOL,KIMMEL CANC CTR PHILADELPHIA PA 19107 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT PATHOL PHILADELPHIA PA 19107 JAMES A HALEY VET HOSP TAMPA FL 33612 UNIV S FLORIDA,COLL MED,DEPT BIOCHEM & MOL BIOL TAMPA FL 33612 UNIV MODENA,DEPT BIOMED SCI I-41100 MODENA ITALY
Titolo Testata:
EMBO journal (Print)
fascicolo: 15, volume: 17, anno: 1998,
pagine: 4442 - 4455
SICI:
0261-4189(1998)17:15<4442:TFAPII>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
RNA-BINDING-PROTEIN; BCR-ABL ONCOGENE; COLONY-STIMULATING FACTOR; RIBONUCLEOPROTEIN-C-PROTEINS; RECEPTOR MESSENGER-RNA; HUMAN MYELOID-LEUKEMIA; KINASE-C; HEMATOPOIETIC-CELLS; GRANULOCYTIC DIFFERENTIATION; PHILADELPHIA-CHROMOSOME;
Keywords:
BCR; ABL; LEUKEMOGENESIS; TLS; FUS; ZINC FINGER PROTEIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
61
Recensione:
Indirizzi per estratti:
Citazione:
D. Perrotti et al., "TLS FUS, A PRO-ONCOGENE INVOLVED IN MULTIPLE CHROMOSOMAL TRANSLOCATIONS, IS A NOVEL REGULATOR OF BCR/ABL-MEDIATED LEUKEMOGENESIS/", EMBO journal (Print), 17(15), 1998, pp. 4442-4455

Abstract

The leukemogenic potential of BCR/ABL oncoproteins depends on their tyrosine kinase activity and involves the activation of several downstream effecters, some of which are essential for cell transformation. Using electrophoretic mobility shift assays and Southwestern blot analyses with a double-stranded oligonucleotide containing a zinc finger consensus sequence, we identified a 68 kDa DNA-binding protein specifically induced by BCR/ABL, The peptide sequence of the affinity-purified protein was identical to that of the RNA-binding protein FUS (also called TLS), Binding activity of FUS required a functional BCR/ABL tyrosine kinase necessary to induce PKC beta II-dependent FUS phosphorylation, Moreover, suppression of PKC beta II activity in BCR/ABL-expressing cells by treatment with the PKC beta II inhibitor CGP53353, or by expression of a dominant-negative PKC beta II, markedly impaired the ability of FUS to bind DNA, Suppression of FUS expression in myeloid precursor 32Dc13 cells transfected with a FUS antisense construct was associated with upregulation of the granulocyte-colony stimulating factor receptor (G-CSFR) and downregulation of interleukin-3 receptor (IL-3R) beta-chain expression, and accelerated G-CSF-stimulated differentiation. Downregulation of FUS expression in BCR/ABL-expressing 32Dc13 cells was associated with suppression of growth factor-independent colony formation, restoration of G-CSF-induced granulocytic differentiation andreduced tumorigenic potential in vivo, Together, these results suggest that FUS might function as a regulator of BCR/ABL leukemogenesis, promoting growth factor independence and preventing differentiation via modulation of cytokine receptor expression.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 07:24:49