Angiogenesis and c-Jun
نویسندگان
چکیده
منابع مشابه
Angiogenesis and c-Jun.
A new pathway for tumor angiogenesis, and possibly for other forms of pathologic angiogenesis, is reported in this issue of the Journal by Zhang et al. (1). They showed that when expression of the basic region-leucine zipper protein c-Jun was suppressed in human endothelial cells by transfection with a DNAzyme targeting the c-Jun mRNA, the cells could no longer form new blood vessels in vitro o...
متن کاملDifferential and antagonistic effects of v-Jun and c-Jun.
We compared the ability of cellular and viral Jun (c-Jun and v-Jun) to transactivate target genes. c-Jun and v-Jun bind specifically to 12-O-tetradecanoylphorbol-13-acetate responsive elements [TREs, also called activator protein 1 (AP-1) motifs]. However, whereas c-Jun activates TRE-controlled promoters, v-Jun represses them. Cotransfection of the two Jun proteins reduces c-Jun-dependent trans...
متن کاملEffect of deoxyribozymes targeting c-Jun on solid tumor growth and angiogenesis in rodents.
BACKGROUND The basic region-leucine zipper protein c-Jun has been linked to cell proliferation, transformation, and apoptosis. However, a direct role for c-Jun in angiogenesis has not been shown. METHODS We used human microvascular endothelial cells (HMEC-1) transfected with a DNAzyme targeting the c-Jun mRNA (Dz13), related oligonucleotides, or vehicle in in vitro models of microvascular end...
متن کاملCOOH-terminal Src kinase-mediated c-Jun phosphorylation promotes c-Jun degradation and inhibits cell transformation.
The oncoprotein c-Jun is a component of the activator protein-1 transcription factor complex, which is involved in cellular proliferation, transformation, and death. The stabilization of c-Jun is critically important for its function. The phosphorylation of c-Jun by c-Jun NH(2)-terminal kinase 1 and extracellular signal-regulated protein kinases reduces c-Jun ubiquitination resulting in increas...
متن کاملC-Jun N-terminal kinases/c-Jun and p38 pathways cooperate in ceramide-induced neuronal apoptosis.
Understanding the regulation of the apoptotic program in neurons by intracellular pathways is currently a subject of great interest. Recent results suggest that c-Jun N-terminal kinases (JNK), mitogen-activated protein kinases and the transcription factor c-Jun are important regulators of this cell death program in post-mitotic neurons following survival-factor withdrawal. Our study demonstrate...
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ژورنال
عنوان ژورنال: JNCI Journal of the National Cancer Institute
سال: 2004
ISSN: 0027-8874,1460-2105
DOI: 10.1093/jnci/djh148