Abstract:
OBJECTIVE:A common gain-of-function LPL variant, LPLS447X, has favorable clinical features and involves a C→G base change at nucleotide 1595 of the LPL cDNA, along with a haplotype, which includes other non-coding SNPs. The mechanism for the LPL gain-in-function is not clear. LPL translation is regulated by epinephrine by an RNA-protein complex, consisting of PKA subunits and an A kinase anchoring protein (AKAP), which targets the 3'UTR. METHODS:To examine LPL translation of the LPLS447X variant, in vitro translation of LPL mRNA constructs was studied in the presence of cytoplasmic extracts from 3T3-F442A adipocytes treated with/without epinephrine. RESULTS:When the C→G base change at nucleotide 1595 was introduced, LPL mRNA was less susceptible to inhibition by the adipocyte extract. Similarly, a lessened susceptibility to translation inhibition occurred when the complete haplotype was constructed in the full-length 3.6 kb LPL mRNA, when an irrelevant coding sequence was introduced into the LPL mRNA construct, and in response to the use of components of the RNA binding complex (PKA C and R subunits, and KH region of AKAP149). CONCLUSION:These studies suggest that the LPLS447X gain of function may be due to the base change in the LPL mRNA resulting in a decreased susceptibility to translational inhibition.
journal_name
Atherosclerosisjournal_title
Atherosclerosisauthors
Ranganathan G,Unal R,Pokrovskaya ID,Tripathi P,Rotter JI,Goodarzi MO,Kern PAdoi
10.1016/j.atherosclerosis.2011.12.028subject
Has Abstractpub_date
2012-03-01 00:00:00pages
143-7issue
1eissn
0021-9150issn
1879-1484pii
S0021-9150(11)01175-0journal_volume
221pub_type
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