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Titolo:
Retinoic acid-induced blr1 expression requires RAR alpha, RXR, and MAPK activation and uses ERK2 but not JNK/SAPK to accelerate cell differentiation
Autore:
Battle, TE; Roberson, MS; Zhang, T; Varvayanis, S; Yen, A;
Indirizzi:
Cornell Univ, Coll Vet Med, Dept Biomed Sci, Sect Pathol, Ithaca, NY 14853USA Cornell Univ Ithaca NY USA 14853 ed Sci, Sect Pathol, Ithaca, NY 14853USA Cornell Univ, Coll Vet Med, Dept Biomed Sci, Physiol Sect, Ithaca, NY 14853 USA Cornell Univ Ithaca NY USA 14853 Sci, Physiol Sect, Ithaca, NY 14853 USA
Titolo Testata:
EUROPEAN JOURNAL OF CELL BIOLOGY
fascicolo: 1, volume: 80, anno: 2001,
pagine: 59 - 67
SICI:
0171-9335(200101)80:1<59:RABERR>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-COUPLED RECEPTOR; ACUTE PROMYELOCYTIC LEUKEMIA; RESPONSIVE ELEMENT; ALL-TRANS; MYELOID DIFFERENTIATION; BETA-GENE; B-CELLS; INDUCTION; CHEMOKINE; PROMOTER;
Keywords:
BLR1; retinoids; leukemic monocytic cell differentiation; MAPK;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Battle, TE Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Adult Oncol,Mayer 549,44 Binney St, Boston, MA 02115 USA Harvard Univ Mayer 549,44 Binney St Boston MA USA 02115 115 USA
Citazione:
T.E. Battle et al., "Retinoic acid-induced blr1 expression requires RAR alpha, RXR, and MAPK activation and uses ERK2 but not JNK/SAPK to accelerate cell differentiation", EUR J CELL, 80(1), 2001, pp. 59-67

Abstract

Upstream signaling requirements of retinoic acid (RA)induced blr1 expression and downstream signaling consequences of blr1 over-expression in a humanmyeloid leukemia cell line demonstrate that mitogen-activated protein kinase (MAPK) signaling complexes are involved in both avenues. RA-induced myeloid differentiation and G(1)/G(0) growth arrest of HL-60 cells is known to require the activation of the RAR alpha and RXR retinoid receptors, as wellas activation of the MAPK, ERK2. Transcriptional activation of the Burkitt's lymphoma receptor 1 (blr1) gene occurs early during RA-induced differentiation of HL-60 cells and requires these same three activating processes. The use of retinoid ligands that activate either the RAR alpha or the RXR retinoid receptors revealed that blr1 mRNA induction was detectable only whenboth RAR alpha and RXR were activated. Neither the RAR alpha nor RXR selective ligands alone induced expression of blr1, but the combination of the two ligands induced the expression of blr1 to the same extent as RA. The MAPKK (MEK) inhibitor, PD98059, was used to determine whether extracellular signal-regulated kinase (ERK2) activation was necessary for induction of blr1mRNA, PD98059 inhibited induced blr1 mRNA expression, due to RA or activated RAR alpha plus RXR ligands, indicating that ERK2 activation is necessaryfor blr1 mRNA expression. Previous studies showed that ectopic expression of blr1 also caused increased MAPK activation, in particular ERK2, and subsequently accelerated RA-induced differentiation and G(1)/G(0) growth arrest. Inhibition of ERK2 activation inhibited differentiation of blr1 transfectants, suggesting that the accelerated differentiation reflected blr1-enhanced ERK2 activation. The present data also demonstrate that ectopic expression of blr1 increased JNK/SAPK activity, but JNK/SAPK activation was not needed for accelerated RA-induced differentiation and growth arrest. The results show that the signals known to be required for HL-60 differentiation, activated RAR alpha, RXR, and ERK2, are necessary for blr1 mRNA expression. Downstream consequences of blr1 overexpression include enhanced MAPK signaling.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 10:32:53