Key result
Liver polysomes from guinea pigs genetically deficient in C4 failed to synthesize pro-C4 but synthesized nascent C4 polypeptides that remained polysome bound.
Highlights potential translational defect in C4 deficiency; leaves open relevance to human complement disorders.
Under cell-free conditions, liver polysomes from guinea pigs genetically deficient in the fourth component of complement (C4) did not synthesize pro-C4 (the precursor of C4), but did synthesize nascent C4 polypeptides which remained polysome bound. The defect was specific for pro-C4 synthesis since the amounts of total protein and albumin synthesis and release from C4-deficient polysomes were similar to that in normal guinea pig liver polysomes.
No takes yet. Share an insight, caveat, or question.
Hall et al. (1978) studied Genetic deficiency in the fourth component of complement (C4). Genetic deficiency in C4 vs. Normal guinea pig liver polysomes was evaluated on Synthesis of pro-C4. Liver polysomes from guinea pigs genetically deficient in C4 failed to synthesize pro-C4 but synthesized nascent C4 polypeptides that remained polysome bound.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: