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Lymphocyte HEV adhesion variants differ in the expression of multiple gene sequences.
C Nottenburg1, W M Gallatin, T St John
1Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98104.
Gene
|November 15, 1990
Summary
Researchers investigated lymphocyte adhesion molecules, identifying a novel gene, DIFF6, potentially co-regulated with the gp90MEL-14 adhesion receptor. This suggests a link between cell surface adhesion and intracellular regulatory factors.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- Lymphocyte adhesion to high endothelial venules is crucial for immune cell trafficking.
- This adhesion is mediated by cell-surface glycoproteins, including gp90MEL-14, detected by the MEL-14 monoclonal antibody (mAb).
- Variations in gp90MEL-14 expression exist, as seen in EL4 cell line variants (EL4MEL-14-hi and EL4-MEL-14-lo).
Purpose of the Study:
- To identify genes differentially expressed in cells with high versus low surface expression of the gp90MEL-14 adhesion receptor.
- To investigate potential co-regulation between the gp90MEL-14 molecule and other cellular factors.
Main Methods:
- Construction and enrichment of a cDNA library from EL4MEL-14-hi cells.
- Quantitative analysis of differential gene expression using RNA probe protection assays.
- Nucleotide sequencing and protein characteristic prediction for candidate clones.
Main Results:
- Five cDNA clones showed increased mRNA levels in EL4MEL-14-hi cells compared to EL4-MEL-14-lo cells.
- One clone, DIFF6, exhibited higher expression in cells with abundant MEL-14-reactive gp90 and lower expression in cells with low gp90 levels.
- DIFF6 does not encode gp90MEL-14 but predicts a cytoplasmic or nuclear protein.
Conclusions:
- The expression of the cell-surface adhesion receptor gp90MEL-14 may be co-regulated with intracellular factors.
- The identified gene, DIFF6, represents a potential co-regulated factor, possibly a cytoplasmic or nuclear protein.
- Further research is needed to elucidate the precise role of DIFF6 in relation to gp90MEL-14 function.