Overview

  • Product name

    Anti-BRG1 antibody [EPNCIR111A] (HRP)
    See all BRG1 primary antibodies
  • Description

    Rabbit monoclonal [EPNCIR111A] to BRG1 (HRP)
  • Host species

    Rabbit
  • Conjugation

    HRP
  • Tested applications

    Suitable for: WBmore details
  • Species reactivity

    Reacts with: Mouse, Rat, Human
  • Immunogen

    Synthetic peptide within Mouse BRG1 aa 200-300. The exact sequence is proprietary.

  • Positive control

    • WB: K562, HeLa, NIH3T3, and PC12 whole cell lysates.
  • General notes

     

     

     

    Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents.

Properties

Applications

Our Abpromise guarantee covers the use of ab196315 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
WB 1/5000. Detects a band of approximately 185 kDa (predicted molecular weight: 185 kDa).

Target

  • Function

    Transcriptional coactivator cooperating with nuclear hormone receptors to potentiate transcriptional activation. Component of the CREST-BRG1 complex, a multiprotein complex that regulates promoter activation by orchestrating a calcium-dependent release of a repressor complex and a recruitment of an activator complex. In resting neurons, transcription of the c-FOS promoter is inhibited by BRG1-dependent recruitment of a phospho-RB1-HDAC repressor complex. Upon calcium influx, RB1 is dephosphorylated by calcineurin, which leads to release of the repressor complex. At the same time, there is increased recruitment of CREBBP to the promoter by a CREST-dependent mechanism, which leads to transcriptional activation. The CREST-BRG1 complex also binds to the NR2B promoter, and activity-dependent induction of NR2B expression involves a release of HDAC1 and recruitment of CREBBP. 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. SMARCA4/BAF190A may promote neural stem cell self-renewal/proliferation by enhancing Notch-dependent proliferative signals, while concurrently making the neural stem cell insensitive to SHH-dependent differentiating cues (By similarity). 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. Acts as a corepressor of ZEB1 to regulate E-cadherin transcription and is required for induction of epithelial-mesenchymal transition (EMT) by ZEB1.
  • Tissue specificity

    Colocalizes with ZEB1 in E-cadherin-negative cells from established lines, and stroma of normal colon as well as in de-differentiated epithelial cells at the invasion front of colorectal carcinomas (at protein level).
  • Involvement in disease

    Defects in SMARCA4 are the cause of rhabdoid tumor predisposition syndrome type 2 (RTPS2) [MIM:613325]. RTPS2 is a familial cancer syndrome predisposing to renal or extrarenal malignant rhabdoid tumors and to a variety of tumors of the central nervous system, including choroid plexus carcinoma, medulloblastoma, and central primitive neuroectodermal tumors. Rhabdoid tumors are the most aggressive and lethal malignancies occurring in early childhood.
  • Sequence similarities

    Belongs to the SNF2/RAD54 helicase family.
    Contains 1 bromo domain.
    Contains 1 helicase ATP-binding domain.
    Contains 1 helicase C-terminal domain.
    Contains 1 HSA domain.
  • Post-translational
    modifications

    Phosphorylated upon DNA damage, probably by ATM or ATR.
  • Cellular localization

    Nucleus.
  • Information by UniProt
  • Database links

  • Alternative names

    • ATP dependent helicase SMARCA4 antibody
    • ATP-dependent helicase SMARCA4 antibody
    • BAF 190 antibody
    • BAF190 antibody
    • BAF190A antibody
    • Brahma protein like 1 antibody
    • BRG1 antibody
    • BRG1 associated factor 190A antibody
    • BRG1 protein antibody
    • BRG1-associated factor 190A antibody
    • BRM/SWI2 related gene 1 antibody
    • Global transcription activator homologous sequence antibody
    • global transcription activator snf2l4 antibody
    • Homeotic gene regulator antibody
    • hSNF2b antibody
    • Mitotic growth and transcription activator antibody
    • MRD16 antibody
    • Nuclear protein GRB1 antibody
    • Protein brahma homolog 1 antibody
    • Protein BRG-1 antibody
    • Protein BRG1 antibody
    • RTPS2 antibody
    • SMARC A4 antibody
    • SMARCA4 antibody
    • SMCA4_HUMAN antibody
    • SNF2 antibody
    • SNF2 beta antibody
    • SNF2 like 4 antibody
    • SNF2-beta antibody
    • SNF2B antibody
    • SNF2L4 antibody
    • SNF2LB antibody
    • Sucrose nonfermenting like 4 antibody
    • SWI/SNF related matrix associated actin dependent regulator of chromatin subfamily A member 4 antibody
    • SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 antibody
    • SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 4 antibody
    • SWI2 antibody
    • Transcription activator BRG1 antibody
    see all

Images

  • All lanes : Anti-BRG1 antibody [EPNCIR111A] (HRP) (ab196315) at 1/5000 dilution

    Lane 1 : Wild-type HAP1 whole cell lysate
    Lane 2 : Smarca4 (BRG1) knockout HAP1 whole cell lysate

    Lysates/proteins at 20 µg per lane.

    Predicted band size: 185 kDa
    Observed band size: 185 kDa


    Exposure time: 8 minutes


    ab196315 was shown to specifically react with BRG1 in wild-type HAP1 cells as signal was lost in Smarca4 (BRG1) knockout cells. Wild-type and Smarca4 (BRG1) knockout samples were subjected to SDS-PAGE. Ab196315 and ab184095 (Mouse monoclonal [mAbcam 9484] to GAPDH - Loading Control (Alexa Fluor® 680) loading control) were incubated overnight at 4°C at 1/5000 dilution and 1/20000 dilution respectively. The loading control was imaged using the Licor Odyssey CLx prior to blots being developed with ECL technique.

  • All lanes : Anti-BRG1 antibody [EPNCIR111A] (HRP) (ab196315) at 1/5000 dilution

    Lane 1 : K562 (Human erythromyeloblastoid leukemia cell line) Whole Cell Lysate
    Lane 2 : HeLa whole cell lysate (ab150035)
    Lane 3 : NIH 3T3 (Mouse embryonic fibroblast cell line) Whole Cell Lysate
    Lane 4 : PC12 (Rat adrenal pheochromocytoma cell line) Whole Cell Lysate

    Lysates/proteins at 10 µg per lane.

    Developed using the ECL technique.

    Performed under reducing conditions.

    Predicted band size: 185 kDa
    Observed band size: 185 kDa


    Exposure time: 20 minutes


    This blot was produced using a 3-8% Tris Acetate gel under the TA buffer system. The gel was run at 150V for 60 minutes before being transferred onto a Nitrocellulose membrane at 30V for 70 minutes. The membrane was then blocked for an hour using 2% Bovine Serum Albumin before being incubated with ab196315 overnight at 4°C. Antibody binding was visualised using ECL development solution ab133406.

References

ab196315 has not yet been referenced specifically in any publications.

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