功能: nucleus organization, nuclear envelope organization, gamete generation, spermatogenesis, muscle organ development, endomembrane organization, membrane organization, sexual reproduction, multicellular organism reproduction, male gamete generation, reproductive process in a multicellular organism,
细胞定位: Nucleus . Nucleus envelope . Nucleus lamina. Nucleus, nucleoplasm. Nucleus matrix . Farnesylation of prelamin-A/C facilitates nuclear envelope targeting and subsequent cleavage by ZMPSTE24/FACE1 to remove the farnesyl group produces mature lamin-A/C, which can then be inserted into the nuclear lamina. EMD is required for proper localization of non-farnesylated prelamin-A/C.; [Isoform C]: Nucleus speckle .
组织表达: In the arteries, prelamin-A/C accumulation is not observed in young healthy vessels but is prevalent in medial vascular smooth muscle cells (VSMCs) from aged individuals and in atherosclerotic lesions, where it often colocalizes with senescent and degenerate VSMCs. Prelamin-A/C expression increases with age and disease. In normal aging, the accumulation of prelamin-A/C is caused in part by the down-regulation of ZMPSTE24/FACE1 in response to oxidative stress.
功能: nucleus organization, nuclear envelope organization, gamete generation, spermatogenesis, muscle organ development, endomembrane organization, membrane organization, sexual reproduction, multicellular organism reproduction, male gamete generation, reproductive process in a multicellular organism,
细胞定位: Nucleus . Nucleus envelope . Nucleus lamina. Nucleus, nucleoplasm. Nucleus matrix . Farnesylation of prelamin-A/C facilitates nuclear envelope targeting and subsequent cleavage by ZMPSTE24/FACE1 to remove the farnesyl group produces mature lamin-A/C, which can then be inserted into the nuclear lamina. EMD is required for proper localization of non-farnesylated prelamin-A/C.; [Isoform C]: Nucleus speckle .
组织表达: In the arteries, prelamin-A/C accumulation is not observed in young healthy vessels but is prevalent in medial vascular smooth muscle cells (VSMCs) from aged individuals and in atherosclerotic lesions, where it often colocalizes with senescent and degenerate VSMCs. Prelamin-A/C expression increases with age and disease. In normal aging, the accumulation of prelamin-A/C is caused in part by the down-regulation of ZMPSTE24/FACE1 in response to oxidative stress.