Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1999-8-23
pubmed:abstractText
The major histocompatibility complex (MHC)-associated invariant chain (Ii) associates with the class II alpha/beta heterodimer during its biosynthesis, inhibiting association of endogenous peptides with the peptide-binding cleft. It is therefore not surprising that there are significant similarities in regulatory mechanisms controlling the expression of the structural class II MHC and Ii genes. One important similarity is that both classes of genes can be expressed via CIITA-dependent or -independent mechanisms. In this report, we have dissected CIITA-dependent and -independent transcription of the Ii gene using an isogenic B-LCL cell pair (Jijoye and clone-13) which do or do not express the class II MHC transactivator (CIITA), respectively. Experiments using mutant or deletion constructs of the Ii gene promoter indicate that while both the X-box and li-kappaB1 elements are critical for CIITA-dependent transcription in B lymphocytes, the Ii-kappaBI element is of greater importance for CIITA-independent Ii gene transcription, with the X-box playing a secondary role. Despite these clear differences in cis-element dependence of CIITA-dependent and -independent Ii transcription, there are only subtle differences in the occupancy of these elements in vivo as assessed by genomic footprinting. These differences are restricted to occupancy of the X-box and Y-box, with which the RF-X and NF-Y complexes interact in Ii-positive cells. This difference in the occupancy of the X-box and Y-box in this cell pair indicates that while protein/protein interactions between CIITA and promoter-bound factors stabilize promoter occupancy, these interactions are not absolutely required for occupancy and transcription of the invariant chain gene.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0161-5890
pubmed:author
pubmed:issnType
Print
pubmed:volume
36
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
447-60
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10449097-Antigens, Differentiation, B-Lymphocyte, pubmed-meshheading:10449097-Base Sequence, pubmed-meshheading:10449097-Cell Line, pubmed-meshheading:10449097-Chloramphenicol O-Acetyltransferase, pubmed-meshheading:10449097-Enhancer Elements, Genetic, pubmed-meshheading:10449097-Gene Deletion, pubmed-meshheading:10449097-Genes, Reporter, pubmed-meshheading:10449097-Histocompatibility Antigens Class II, pubmed-meshheading:10449097-Humans, pubmed-meshheading:10449097-Models, Biological, pubmed-meshheading:10449097-Models, Genetic, pubmed-meshheading:10449097-Models, Molecular, pubmed-meshheading:10449097-Molecular Sequence Data, pubmed-meshheading:10449097-NF-kappa B, pubmed-meshheading:10449097-Nuclear Proteins, pubmed-meshheading:10449097-Promoter Regions, Genetic, pubmed-meshheading:10449097-RNA, pubmed-meshheading:10449097-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:10449097-Trans-Activators, pubmed-meshheading:10449097-Transcription, Genetic, pubmed-meshheading:10449097-Transfection
pubmed:year
1999
pubmed:articleTitle
Cis-element dependence and occupancy of the human invariant chain promoter in CIITA-dependent and -independent transcription.
pubmed:affiliation
The Schepens Eye Research Institute, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02114, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't