|Calculated MW||74139 Da|
|Application & Usage||The peptide is used for blocking the antibody activity of active Lamin A. It usually blocks the antibody activity completely in Western blot analysis by incubating the peptide with equal volume of antibody for 30 minutes at 37°C|
|Other Names||Prelamin-A/C, Lamin-A/C, 70 kDa lamin, Renal carcinoma antigen NY-REN-32, LMNA, LMN1|
|Formulation||50 µg (0.2 mg/ml) in phosphate buffered saline (PBS), pH 7.2, containing 50% glycerol, 0.1% BSA and 0.02% thimerosal.|
|Reconstitution & Storage||-20 °C|
|Precautions||Lamin A Blocking Peptide is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Lamins are components of the nuclear lamina, a fibrous layer on the nucleoplasmic side of the inner nuclear membrane, which is thought to provide a framework for the nuclear envelope and may also interact with chromatin. Lamin A and C are present in equal amounts in the lamina of mammals. Plays an important role in nuclear assembly, chromatin organization, nuclear membrane and telomere dynamics. Required for normal development of peripheral nervous system and skeletal muscle and for muscle satellite cell proliferation. Required for osteoblastogenesis and bone formation. Also prevents fat infiltration of muscle and bone marrow, helping to maintain the volume and strength of skeletal muscle and bone.|
|Cellular Location||Nucleus. Nucleus envelope. Nucleus lamina. Nucleus, nucleoplasm. Note=Farnesylation of prelamin-A/C facilitates nuclear envelope targeting and subsequent cleaveage 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|
|Tissue Location||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.|
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