tailieunhanh - Báo cáo khoa học: A human-specific TNF-responsive promoter for Goodpasture antigen-binding protein

The Goodpasture antigen-binding protein, GPBP, is a serine⁄threonine kinase whose relative expression increases in autoimmune processes. Tumor necrosis factor (TNF) is a pro-inflammatory cytokine implicated in auto-immune pathogenesis. Here we show that COL4A3BP, the gene encoding GPBP, maps head-to-head withPOLK, the gene encoding for DNA polymerase kappa (polj), and shares with it a 140-bp promoter containing a Sp1 site, a TATA-like element, and a nuclear factor kappa B (NFjB)-like site | ềFEBS Journal A human-specific TNF-responsive promoter for Goodpasture antigen-binding protein Froilan Granero Fernando Revert Francisco Revert-Ros Sergio Lainez Pilar Martinez-Martinez and Juan Saus Centro de Investigacion Príncipe Felipe Valencia Spain Keywords Goodpasture antigen-binding protein tumor necrosis factor Goodpasture disease bidirectionalpromoter DNA polymerase K Correspondence J. Saus Centro de Investigacion Príncipe Felipe Avenida de la Autopista delSaler 16 C En Proyecto 3 Camino de las Moreras 46013 Valencia Spain Fax 34 96 3289701 Tel 34 96 3289680 E-mail jsaus@ Present address Center for Matrix Biology Vanderbilt University MedicalCenter Nashville TN USA Received 8 July 2005 accepted 19 August 2005 doi The Goodpasture antigen-binding protein GPBP is a serine threonine kinase whose relative expression increases in autoimmune processes. Tumor necrosis factor TNF is a pro-inflammatory cytokine implicated in autoimmune pathogenesis. Here we show that COL4A3BP the gene encoding GPBP maps head-to-head with POLK the gene encoding for DNA polymerase kappa pol k and shares with it a 140-bp promoter containing a Sp1 site a TATA-like element and a nuclear factor kappa B NFKB -like site. These three elements cooperate in the assembly of a bidirectional transcription complex containing abundant Sp1 and little NFKB that is more efficient in the POLK direction. Tumour necrosis factor cell induction is associated with Sp1 release NFKB recruitment and assembly of a complex comparatively more efficient in the COL4A3BP direction. This is accomplished by competitive binding of Sp1 and NFKB to a DNA element encompassing a NFKB-like site that is pivotal for the 140-bp promoter to function. Consistently a murine homologous DNA region which contains the Sp1 site and the TATA-like element but is devoid of the NFKB-like site does not show transcriptional activity in transient gene expression assays. Our findings identify a .

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