R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
Lamin B2 (E1S1Q) Rabbit mAb #13823
Filter:
- WB
Supporting Data
| REACTIVITY | H M |
| SENSITIVITY | Endogenous |
| MW (kDa) | 68-70 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
Lamin B2 (E1S1Q) Rabbit mAb recognizes endogenous levels of total lamin B2 protein.
Species Reactivity:
Human, Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu75 of human lamin B2 protein.
Background
Lamins are nuclear membrane structural components that are important in maintaining normal cell functions, such as cell cycle control, DNA replication, and chromatin organization (1-3). Lamins have been subdivided into types A and B. Type-A lamins consist of lamin A and C, which arise from alternative splicing of the lamin A gene LMNA. Lamin A and C are cleaved by caspases into large (41-50 kDa) and small (28 kDa) fragments, which can be used as markers for apoptosis (4,5). Type-B lamins consist of lamin B1 and B2, encoded by separate genes (6-8). Lamin B1 is also cleaved by caspases during apoptosis (9). Research studies have shown that duplication of the lamin B1 gene LMNB1 is correlated with pathogenesis of the neurological disorder adult-onset leukodystrophy (10).
Research studies show that both lamin B2 and lamin B1 knockout mice exhibit neuronal developmental defects and that both proteins are essential for typical brain development. Lamin B1 and B2 deficiencies result in changes in nuclear morphology, with lamin B1 playing a role in regulating nuclear lamina integrity and lamin B2 inhibiting elongation of neuronal nuclei (11,12). Mutations in the corresponding lamin B2 gene (LMNB2) can result in a susceptibility to developing acquired partial lipodystrophy, a rare disorder characterized by the progressive loss of subcutaneous fat in a bilaterally symmetrical fashion (13).
Research studies show that both lamin B2 and lamin B1 knockout mice exhibit neuronal developmental defects and that both proteins are essential for typical brain development. Lamin B1 and B2 deficiencies result in changes in nuclear morphology, with lamin B1 playing a role in regulating nuclear lamina integrity and lamin B2 inhibiting elongation of neuronal nuclei (11,12). Mutations in the corresponding lamin B2 gene (LMNB2) can result in a susceptibility to developing acquired partial lipodystrophy, a rare disorder characterized by the progressive loss of subcutaneous fat in a bilaterally symmetrical fashion (13).
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- Goldberg, M. et al. (1999) Crit Rev Eukaryot Gene Expr 9, 285-93.
- Yabuki, M. et al. (1999) Physiol Chem Phys Med NMR 31, 77-84.
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- Biamonti, G. et al. (1992) Mol Cell Biol 12, 3499-506.
- Lin, F. and Worman, H.J. (1995) Genomics 27, 230-6.
- Pollard, K.M. et al. (1990) Mol Cell Biol 10, 2164-75.
- Chandler, J.M. et al. (1997) Biochem J 322 ( Pt 1), 19-23.
- Padiath, Q.S. et al. (2006) Nat Genet 38, 1114-23.
- Coffinier, C. et al. (2010) Proc Natl Acad Sci U S A 107, 5076-81.
- Coffinier, C. et al. (2011) Mol Biol Cell 22, 4683-93.
- Hegele, R.A. et al. (2006) Am J Hum Genet 79, 383-9.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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