Anti-Lamin B Receptor/LBR antibody (ab122919)
Key features and details
- Rabbit polyclonal to Lamin B Receptor/LBR
- Suitable for: IP, ICC/IF
- Reacts with: Mouse, Human
- Isotype: IgG
Overview
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Product name
Anti-Lamin B Receptor/LBR antibody
See all Lamin B Receptor/LBR primary antibodies -
Description
Rabbit polyclonal to Lamin B Receptor/LBR -
Host species
Rabbit -
Tested applications
Suitable for: IP, ICC/IFmore details -
Species reactivity
Reacts with: Mouse, Human -
Immunogen
Recombinant fragment corresponding to Mouse Lamin B Receptor/LBR aa 1-81.
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General notes
This product was previously labelled as Lamin B Receptor
Reproducibility is key to advancing scientific discovery and accelerating scientists’ next breakthrough.
Abcam is leading the way with our range of recombinant antibodies, knockout-validated antibodies and knockout cell lines, all of which support improved reproducibility.
We are also planning to innovate the way in which we present recommended applications and species on our product datasheets, so that only applications & species that have been tested in our own labs, our suppliers or by selected trusted collaborators are covered by our Abpromise™ guarantee.
In preparation for this, we have started to update the applications & species that this product is Abpromise guaranteed for.
We are also updating the applications & species that this product has been “predicted to work with,” however this information is not covered by our Abpromise guarantee.
Applications & species from publications and Abreviews that have not been tested in our own labs or in those of our suppliers are not covered by the Abpromise guarantee.
Please check that this product meets your needs before purchasing. If you have any questions, special requirements or concerns, please send us an inquiry and/or contact our Support team ahead of purchase. Recommended alternatives for this product can be found below, as well as customer reviews and Q&As.
Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles. -
Storage buffer
pH: 6
Preservative: 0.05% Sodium azide
Constituents: 49% PBS, 50% Glycerol (glycerin, glycerine)
Ammonium sulphate - trace. -
Concentration information loading... -
Purity
Immunogen affinity purified -
Purification notes
ab122919 is affinity purified using recombinant immunogen. -
Clonality
Polyclonal -
Isotype
IgG -
Research areas
Associated products
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Compatible Secondaries
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Isotype control
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Recombinant Protein
Applications
Our Abpromise guarantee covers the use of ab122919 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
| Application | Abreviews | Notes |
|---|---|---|
| IP | Use at an assay dependent concentration. | |
| ICC/IF | Use at an assay dependent concentration. |
Target
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Function
Anchors the lamina and the heterochromatin to the inner nuclear membrane. -
Involvement in disease
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. -
Sequence similarities
Belongs to the ERG4/ERG24 family. -
Post-translational
modificationsPhosphorylated 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. -
Cellular localization
Nucleus inner membrane. - Information by UniProt
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Database links
- Entrez Gene: 3930 Human
- Entrez Gene: 98386 Mouse
- Omim: 600024 Human
- SwissProt: Q14739 Human
- SwissProt: Q3U9G9 Mouse
- Unigene: 435166 Human
- Unigene: 4538 Mouse
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Alternative names
- DHCR 14B antibody
- DHCR14B antibody
- Integral nuclear envelope inner membrane protein antibody
see all
Images
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Immunoprecipitation - Anti-Lamin B Receptor/LBR antibody (ab122919)
Identification of Lamin B Receptor/LBR in crude extract of HeLa cells by immuno-precipitation using ab122919, followed by Western blotting.
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Immunocytochemistry/ Immunofluorescence - Anti-Lamin B Receptor/LBR antibody (ab122919)Indirect immuno-fluorescence staining of HeLa cells using ab122919.
Protocols
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
Datasheets and documents
References (4)
ab122919 has been referenced in 4 publications.
- Zhang C et al. Chrysin protects human osteoarthritis chondrocytes by inhibiting inflammatory mediator expression via HMGB1 suppression. Mol Med Rep 19:1222-1229 (2019). PubMed: 30535473
- Pappas SS et al. TorsinA dysfunction causes persistent neuronal nuclear pore defects. Hum Mol Genet 27:407-420 (2018). PubMed: 29186574
- Tajik A et al. Transcription upregulation via force-induced direct stretching of chromatin. Nat Mater 15:1287-1296 (2016). PubMed: 27548707
- Kilinc S et al. Sequestration within nuclear chromocenters is not a requirement for silencing olfactory receptor transcription in a placode-derived cell line. Nucleus 5:318-30 (0). IF . PubMed: 25482121
