Abstract:
:The 5'-flanking sequences of the human macrophage inflammatory protein-3alpha/CCL20 gene were cloned and transfected into G-361 human melanoma cells in a luciferase reporter construct. Tumor necrosis factor-alpha (TNF-alpha) treatment stimulated luciferase expression, and promoter truncations demonstrated that TNF-alpha inducibility is conferred by a region between nt -111 and -77, which contains a non-standard nuclear factor-kappaB (NF-kappaB) binding site. The requirement for NF-kappaB was demonstrated as follows: (i) mutations in this NF-kappaB site abrogated TNF-alpha responsiveness; (ii) TNF-alpha activated a construct containing two copies of the CCL20 NF-kappaB binding site; (iii) overexpression of NF-kappaB p65 activated the CCL20 promoter; (iv) NF-kappaB from nuclear extracts of TNF-alpha-stimulated cells bound specifically to this NF-kappaB site.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Harant H,Eldershaw SA,Lindley IJdoi
10.1016/s0014-5793(01)03138-6keywords:
subject
Has Abstractpub_date
2001-12-14 00:00:00pages
439-45issue
3eissn
0014-5793issn
1873-3468pii
S0014-5793(01)03138-6journal_volume
509pub_type
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