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ORMDL/serine palmitoyltransferase stoichiometry determines effects of ORMDL3 expression on sphingolipid biosynthesis
Deanna Siow1, Manjula Sunkara2, Teresa M Dunn3
1James Graham Brown Cancer Center University of Louisville School of Medicine, Louisville, KY 40202.
Journal of Lipid Research
|February 19, 2015
Summary
Elevated ORMDL3, linked to asthma risk, surprisingly does not suppress sphingolipid biosynthesis. However, it does lead to a marginal decrease in overall sphingolipid levels, suggesting a complex metabolic link to asthma.
Area of Science:
- Biochemistry
- Cell Biology
- Genetics
Background:
- ORMDL proteins regulate sphingolipid biosynthesis by inhibiting serine palmitoyltransferase (SPT).
- ORMDL3 overexpression is correlated with childhood asthma risk.
- The precise mechanism linking ORMDL3 to asthma pathogenesis remains unclear.
Purpose of the Study:
- To investigate if elevated ORMDL3 expression suppresses de novo sphingolipid biosynthesis.
- To explore the relationship between ORMDL3 levels, SPT activity, and sphingolipid metabolism.
Main Methods:
- Experiments were conducted in cultured human bronchial epithelial cells (HBECs) and HeLa cells.
- Assessed the impact of ORMDL3 overexpression on sphingolipid biosynthesis and steady-state mass levels.
Main Results:
- Elevated ORMDL3 did not suppress de novo sphingolipid biosynthesis.
- ORMDL proteins are expressed in functional excess relative to SPT.
- ORMDL3 overexpression led to a marginal decrease in the steady-state mass levels of major sphingolipids.
Conclusions:
- The link between ORMDL3 and asthma risk may involve alterations in sphingolipid metabolism.
- The relationship between ORMDL3, sphingolipid metabolism, and asthma is complex and warrants further investigation.
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