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Titolo:
CD11C INTEGRIN GENE PROMOTER ACTIVITY DURING MYELOID DIFFERENTIATION
Autore:
CORBI AL; LOPEZRODRIGUEZ C;
Indirizzi:
INST PARASITOL & BIOMED,VENTANILLA 11 GRANADA 18001 SPAIN
Titolo Testata:
Leukemia & lymphoma
fascicolo: 5-6, volume: 25, anno: 1997,
pagine: 415 -
SICI:
1042-8194(1997)25:5-6<415:CIGPAD>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
HAIRY-CELL LEUKEMIA; MONOCYTIC DIFFERENTIATION; REGULATED EXPRESSION; P150,95 CD11C/CD18; ALPHA-SUBUNIT; TRANSCRIPTIONAL ACTIVATORS; TERMINAL DIFFERENTIATION; MONOCLONAL-ANTIBODIES; ADHESION MOLECULES; MESSENGER-RNA;
Keywords:
MYELOID DIFFERENTIATION; CD11C; INTEGRIN GENE; GENE PROMOTER ACTIVITY;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
67
Recensione:
Indirizzi per estratti:
Citazione:
A.L. Corbi e C. Lopezrodriguez, "CD11C INTEGRIN GENE PROMOTER ACTIVITY DURING MYELOID DIFFERENTIATION", Leukemia & lymphoma, 25(5-6), 1997, pp. 415

Abstract

The integrin CD11c/CD18 functions as a cell surface receptor for numerous soluble factors and proteins (LPS, fibrinogen, iC3b), mediates leukocyte interactions with other cell types and is a signal transducingreceptor. CD11c/CD18 is found primarily on myeloid cells, where its expression is regulated both during differentiation and during monocytematuration into tissue macrophages. To determine the transcription factors and cis-acting elements driving the developmentally-regulated expression of CD11c/CD18 the proximal regulatory region of the CD11c gene has been structurally and functionally characterized using the U1937and HL-60 cell lines as myeloid differentiation models. The tissue-specific activity of the CD11c promoter is conferred by two Sp1-binding sites and an adjacent C/EBP-binding element, with a Likely contribution from other transcription factors with a more Limited tissue distribution (PU.1, Oct-2, Myb). The participation of Sp1 in the transcriptionof the CD11c gene strongly suggests that CD11c/CD18 expression is dependent on the proliferative state of the cell, thus establishing a first level of control for the regulated expression of CD11c/CD18 during myeloid differentiation. The differentiation responsiveness of the CD11c promoter has been mapped to an AP-1-binding site whose mutation greatly decreases the inducibility of the promoter during the PMA-triggered differentiation of U937 cells. Although AP-1 mediates the responsiveness to several other differentiating agents including GM-CSF, additional elements are required for induction of the CD11c promoter activity upon Sodium Butyrate-triggered differentiation. In fact, the Sodium Butyrate-responsiveness and the presence of both AP-1- and C/EBP-binding sites suggests that the proximal regulatory region of the CD11c promoter might include an extracellular matrix-response element. As a whole, the transcription of the CD11c gene appears to be controlled by the proliferative state of the cell and is tightly coupled to progression along the myeloid differentiation pathway. The differentiation inducibility of the CD11c promoter has been further demonstrated after stable transfection into U937 cells, where the -361/+43 frag ment retains the capacity to drive luciferase expression upon PMA-, GM-CSF- or Sodium Butyrate-triggered myeloid differentiation. Thus, while the characterization of the transcription factors regulating CD11c expression is still in progress, the CD11c promoter has been shown to constitute a very useful tool for the identification of myeloid-differenting agents which might be of potential therapeutical interest.

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Documento generato il 17/01/21 alle ore 18:10:31