Rabbit Polyclonal Antibody to Lamin A+C(Discontinued)
Figure-1 : Western blot analysis of Lamin A+C Antibody at 1 µg/ml on HeLa, A431, HepG2, LOVO, NIH/3T3 cell lysates, IRDye 800 Conjugated Goat Anti-Rabbit IgG was used as secondary antibody.
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| Format : | Purified |
| Amount : | 100 µg |
| Isotype : | Rabbit IgG |
| Purification : | Immunoaffinity chromatography |
| Content : | 0.5 mg/ml, lyophilized with PBS, pH 7.4, containing 0.02% sodium azide |
| Storage condition : | The antibody is stable in lyophilized form if stored at -20°C or below. The reconstituted antibody can be stored for 2-3 weeks at 2-8°C. For long term storage, aliquot and store at -20°C or below. Avoid repeated freezing and thawing cycles. |
Lamins are structural protein components of the nuclear lamina which contains 3 members: Lamin A, B and C in mammalian cells. Lamin A and lamin C are generated by alternative splicing from the same gene and share complete identity for the first 566 amino acids. Lamin A interacts with transcription factor SREBP1 via its C-terminal domain. The lamin A/C deficiency is probably associated with both defective nuclear mechanics and impaired transcriptional activation. The lamin A/C is cleaved by caspase-6 and serves as a marker for caspase-6 activation. Rabbit Anti-Lamin A+C Polyclonal Antibody is developed in rabbit using a KLH-coupled synthetic peptide within residues 400-450 of human Lamin A (Swiss Prot: P02545).
ELISA Capture: 0.5-10 µg/ml
ELISA Detection: 0.05-0.2 µg/ml
Western Blot: 1-2 µg/ml
Flowcytometry analysis: 1-2 µg/10^6Cells
For Research Use Only. Not for use in diagnostic/therapeutics procedures.
| Subcellular location: | Nucleus speckle |
| Post transnational modification: | Farnesylation of prelamin-A/C facilitates nuclear envelope targeting. |
| Tissue Specificity: | 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. |
| BioGrid: | 110186. 661 interactions. |
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