Key features and details
- Rabbit polyclonal to BAF57/SMARCE1
- Suitable for: ICC/IF, IHC-P, WB
- Reacts with: Mouse, Rat, Human
- Isotype: IgG
Product nameAnti-BAF57/SMARCE1 antibody
See all BAF57/SMARCE1 primary antibodies
DescriptionRabbit polyclonal to BAF57/SMARCE1
Tested applicationsSuitable for: ICC/IF, IHC-P, WBmore details
Species reactivityReacts with: Mouse, Rat, Human
Recombinant full length protein corresponding to Human BAF57/SMARCE1 aa 1-411.
Database link: Q969G3
- WB: HL60, K562, SHSY-5Y. SW620 and SKOV3 cell line extracts. IHC-P: Human liver cancer; IF: U2OS cells.
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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.
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.30
Preservative: 0.02% Sodium azide
Constituents: 50% Glycerol, 49% PBS
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab186824 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ICC/IF||Use at an assay dependent concentration.|
|IHC-P||1/50 - 1/200.|
|WB||1/500 - 1/2000. Predicted molecular weight: 47 kDa.|
FunctionInvolved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a post-mitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to post-mitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron-specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth (By similarity). Required for the coactivation of estrogen responsive promoters by Swi/Snf complexes and the SRC/p160 family of histone acetyltransferases (HATs). Also specifically interacts with the CoREST corepressor resulting in repression of neuronal specific gene promoters in non-neuronal cells. Also involved in vitamin D-coupled transcription regulation via its association with the WINAC complex, a chromatin-remodeling complex recruited by vitamin D receptor (VDR), which is required for the ligand-bound VDR-mediated transrepression of the CYP27B1 gene.
Sequence similaritiesContains 1 HMG box DNA-binding domain.
DomainThe HMG domain is essential for CD4 silencing and CD8 activation; mutation of this domain blocks thymus development.
- Information by UniProt
- BAF57 antibody
- BRG1 associated factor 57 antibody
- BRG1-associated factor 57 antibody
Immunohistochemistry of paraffin-embedded mouse brain tissue labelling BAF57/SMARCE1 usinf ab186824 at 1/200 dilution (40x lens).
Immunocytochemistry/Immunofluorescence analysis of U2OS cells using ab186824. Blue DAPI for nuclear staining.
All lanes : Anti-BAF57/SMARCE1 antibody (ab186824) at 1/500 dilution
Lane 1 : HL60 cell line extract
Lane 2 : K562 cell line extract
Lane 3 : SHSY-5Y cell line extract
Lane 4 : SW620 cell line extract
Lane 5 : SKOV3 cell line extract
Predicted band size: 47 kDa
ab186824 has not yet been referenced specifically in any publications.