The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
1/500. Detects a band of approximately 67 kDa (predicted molecular weight: 71 kDa).
Use at an assay dependent concentration.
ab172730-Rabbit monoclonal IgG, is suitable for use as an isotype control with this antibody.
Use a concentration of 5 µg/ml. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.
Anchors the lamina and the heterochromatin to the inner nuclear membrane.
Defects in LBR are a cause of Pelger-Huet anomaly (PHA) [MIM:169400]. PHA is an autosomal dominant inherited abnormality of neutrophils, characterized by reduced nuclear segmentation and an apparently looser chromatin structure. Heterozygotes show hypolobulated neutrophil nuclei with coarse chromatin. Presumed homozygous individuals have ovoid neutrophil nuclei, as well as varying degrees of developmental delay, epilepsy, and skeletal abnormalities. Defects in LBR are the cause of hydrops-ectopic calcification-moth-eaten skeletal dysplasia (HEM) [MIM:215140]; also known as Greenberg skeletal dysplasia. HEM is a rare autosomal recessive chondrodystrophy characterized by early in utero lethality and, therefore, considered to be nonviable. Affected fetuses typically present with fetal hydrops, short-limbed dwarfism, and a marked disorganization of chondro-osseous calcification and may present with polydactyly and additional nonskeletal malformations. Defects in LBR may be a cause of Reynolds syndrome (REYNS) [MIM:613471]. It is a syndrome specifically associating limited cutaneous systemic sclerosis and primary biliray cirrhosis. It is characterized by liver disease, telangiectasia, abrupt onset of digital paleness or cyanosis in response to cold exposure or stress (Raynaud phenomenon), and variable features of scleroderma. The liver disease is characterized by pruritis, jaundice, hepatomegaly, increased serum alkaline phosphatase and positive serum mitochondrial autoantibodies, all consistent with primary biliary cirrhosis.
Belongs to the ERG4/ERG24 family.
Phosphorylated by CDK1 protein kinase in mitosis when the inner nuclear membrane breaks down into vesicles that dissociate from the lamina and the chromatin. It is phosphorylated by different protein kinases in interphase when the membrane is associated with these structures. Phosphorylation of LBR and HP1 proteins may be responsible for some of the alterations in chromatin organization and nuclear structure which occur at various times during the cell cycle.
Flow Cytometry - Anti-Lamin B Receptor antibody [E398L] (ab32535)
Flow Cytometry analysis of HeLa (human cervix adenocarcinoma) cells labeling Lamin B Receptor with unpurified ab32535 at 1/20 dilutionc(10ug/ml) (red). Cells were fixed with 4% paraformaldehyde and permeabilised with 90% methanol. A Goat anti rabbit IgG (Alexa Fluor® 488) (1/2000 dilution) was used as the secondary antibody. Rabbit monoclonal IgG (Black) was used as the isotype control, cells without incubation with primary antibody and secondary antibody (Blue) were used as the unlabeled control.
IHC image of ab32535 staining in human breast cancer formalin fixed paraffin embedded tissue section, performed on a Leica BondTM system using the standard protocol F. The section was pre-treated using heat mediated antigen retrieval with sodium citrate buffer (pH6, epitope retrieval solution 1) for 20 mins. The section was then incubated with ab32535, 5µg/ml, for 15 mins at room temperature and detected using an HRP conjugated compact polymer system. DAB was used as the chromogen. The section was then counterstained with haematoxylin and mounted with DPX.
For other IHC staining systems (automated and non-automated) customers should optimize variable parameters such as antigen retrieval conditions, primary antibody concentration and antibody incubation times.
Anti-Lamin B Receptor antibody [E398L] (ab32535) 使用論文
This product has been referenced in:
Cundell MJ et al. A PP2A-B55 recognition signal controls substrate dephosphorylation kinetics during mitotic exit. J Cell Biol214:539-54 (2016).
Read more (PubMed: 27551054) »
Mimura Y et al. ELYS regulates the localization of LBR by modulating its phosphorylation state. J Cell Sci129:4200-4212 (2016).
Read more (PubMed: 27802161) »