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General Comment |
The ANGPTL3 protein is synthesized by the liver and secreted into the bloodstream11. It inhibits lipoprotein lipase12, thus delaying clearance of TRLs from the blood and increasing TRL blood concentrations (Fig. 1). These observations from mice suggested that complete lack of ANGPTL3 should lead to lower levels of TRLs and LDLs. In support of this idea, a family has been identified13 whose members have exceptionally low levels of TRLs and LDLs in their blood as a result of the complete absence of ANGPTL3.
NCBI Summary:
This gene encodes a member of a family of secreted proteins that function in angiogenesis. The encoded protein, which is expressed predominantly in the liver, is further processed into an N-terminal coiled-coil domain-containing chain and a C-terminal fibrinogen chain. The N-terminal chain is important for lipid metabolism, while the C-terminal chain may be involved in angiogenesis. Mutations in this gene cause familial hypobetalipoproteinemia type 2. [provided by RefSeq, Aug 2015]
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