Anti-Lamin A/C Polyclonal Antibody
Figure 1: Anti-Lamin A+C antibody(39-2070). Western blotting : Lane 1: HELA Cell Lysate, Lane 2: A431 Cell Lysate.
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Format : | Lyophilized |
Amount : | 100 μg/vial |
Isotype : | Rabbit IgG |
Purification : | Immunogen affinity purified. |
Content : | Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg Thimerosal, 0.05mg NaN3. Reconstitute : Add 0.2ml of distilled water will yield a concentration of 500ug/ml. |
Storage condition : | At -20˚C for one year. After reconstitution, at 4˚C for one month. It can also be aliquotted and stored frozen at -20˚C for a longer time. Avoid repeated freezing and thawing. |
Gene : | LMNA |
Gene ID : | 4000 |
Uniprot ID : | P02545 |
Alternative Name : | Prelamin-A/C; Lamin-A/C; 70 kDa lamin; Renal carcinoma antigen NY-REN-32; LMNA; LMN1 |
Immunogen Information : | A synthetic peptide corresponding to a sequence at the C-terminus of Human Lamin A/C(455-469aa RNKSNEDQSMGNWQI), identical to the related Rat and Mouse sequences. |
Lamins are structural protein components of the nuclear lamina, a protein network underlying the inner nuclear membrane that determines nuclear shape and size. There are three types of lamins, A,B and C. The lamin A/C(LMNA) gene contains 12 exons. Alternative splicing within exon 10 gives rise to two different mRNAs that code for pre-lamin A and lamin C. Lamin A/C mapped to 1q21.2-q21.3 and mutations in this gene cause a variety of human diseases including Emery-Dreifuss muscular dystrophy, dilated cardiomyopathy, and Hutchinson-Gilford progeria syndrome. Lamin A/C deficiency is thus associated with both defective nuclear mechanics and impaired mechanically activated gene transcription.
Western blot : 0.1-0.5μg/ml; Immunohistochemistry(Paraffin-embedded Section) : 0.5-1μg/ml; Immunocytochemistry : 0.5-1μg/ml
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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