Molecular mechanisms for synchronized transcription of three complement C1q subunit genes in dendritic cells and macrophages.

ABSTRACT: Hereditary homozygous C1q deficiency is rare, but it almost certainly causes systemic lupus erythematosus. On the other hand, C1q levels can decline in systemic lupus erythematosus patients without apparent C1q gene defects and the versatility in C1q production is a likely cause. As an 18-subunit protein, C1q is assembled in a 1:1:1 ratio from three different subunits. The three human C1q genes are closely bundled on chromosome 1 (C1qA-C1qC-C1qB) and their basal and IFNγ-stimulated expression, largely restricted to macrophages and dendritic cells, is apparently synchronized. We cloned the three gene promoters and observed that although the C1qB promoter exhibited basal and IFNγ-stimulated activities consistent with the endogenous C1qB gene, the activities of the cloned C1qA and C1qC promot

SUBMITTER: Chen G 

PROVIDER: S-EPMC3186423 | biostudies-literature | 2011 Oct

REPOSITORIES: biostudies-literature