Linked Life Data

8786306

Source:http://linkedlifedata.com/resource/pubmed/id/8786306

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1996-9-20
pubmed:abstractText
Membrane lymphotoxin (LT) complex is a trimer composed of two subunits , LT-alpha and LT-beta of which the latter is a 33-kDa transmembrane protein. The LT-beta gene is expressed in lymphoid cells and organs, but little is known about its inducible regulation. Previously, the surface expression of LT-beta in Jurkat cells has been shown to increase in response to PMA. In this report, we used this model to study the transcriptional control of the human and murine LT-beta genes. PMA strongly induced the expression of LT-beta mRNA, and the level of induction was not changed markedly by cycloheximide (CHX) treatment. The LT-beta promoter region contains conserved Egr-1, nuclear factor (NF)-kappaB, and Ets binding sites, and PMA-inducible factors bound to these sites were detected by the gel-retardation technique (electrophoretic mobility shift assay (EMSA)). To identify sequences involved in transcriptional control, sets of human and mouse promoter-chloramphenicol acetyltransferase (CAT) constructs were generated and assayed by transient transfections. The PMA response was lost after deletion of the distal Ets binding site at -110. Mutations at either the Ets or NF-kappaB sites that prevented factor binding dramatically reduced PMA-inducible promoter activity, suggesting cooperative interaction between corresponding transcription factors in PMA activation. Mutation at the Egr-1 site also resulted in substantial loss of promoter activity, and the residual activity may be attributed to binding of constitutively expressed Sp-1 to the same site. We propose that the interaction between the members of NF-kappaB and Ets families of transcription factors and their cognate sites in the promoter is the major determinant of inducible expression of the LT-beta gene in Jurkat cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
156
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2465-72
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:8786306-Animals, pubmed-meshheading:8786306-Base Sequence, pubmed-meshheading:8786306-Binding Sites, pubmed-meshheading:8786306-Cell Line, pubmed-meshheading:8786306-Cycloheximide, pubmed-meshheading:8786306-DNA, pubmed-meshheading:8786306-DNA Probes, pubmed-meshheading:8786306-Gene Expression Regulation, pubmed-meshheading:8786306-Humans, pubmed-meshheading:8786306-Lymphotoxin-alpha, pubmed-meshheading:8786306-Lymphotoxin-beta, pubmed-meshheading:8786306-Membrane Proteins, pubmed-meshheading:8786306-Mice, pubmed-meshheading:8786306-Molecular Sequence Data, pubmed-meshheading:8786306-Promoter Regions, Genetic, pubmed-meshheading:8786306-Protein Binding, pubmed-meshheading:8786306-RNA, Messenger, pubmed-meshheading:8786306-Sequence Deletion, pubmed-meshheading:8786306-Tetradecanoylphorbol Acetate, pubmed-meshheading:8786306-Transcription Factors
pubmed:year
1996
pubmed:articleTitle
Functional analysis of the lymphotoxin-beta promoter. Sequence requirements for PMA activation.
pubmed:affiliation
Labortory of Cytokine Molecular Biology, Engelhart Insitute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
pubmed:publicationType
Journal Article