Recombinant Mouse SWI/SNF complex subunit SMARCC2 (Smarcc2), partial
Description
Functional Characteristics
Key Roles in Chromatin Remodeling
The partial protein retains functionality in:
Research Applications
Experimental Uses
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Chromatin Accessibility Studies: Used to reconstitute SWI/SNF complexes for nucleosome remodeling assays
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Cancer Research: Investigated in glioma and prostate cancer models to assess EMT regulation and drug resistance
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Protein Interaction Mapping: Identified binding partners like SMARCA4 and β-catenin via co-immunoprecipitation
Validation Data
Key Research Findings
Oncogenic Regulation
Product Specs
Note: We prioritize shipping the format currently in stock. However, if you have specific format requirements, please specify them in your order notes. We will fulfill your request if possible.
Note: All proteins are shipped with standard blue ice packs. If you require dry ice shipping, please communicate this in advance, as additional fees will apply.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Target Background
- These findings demonstrate the involvement of BAF170-dependent chromatin remodeling in hippocampal neurogenesis. PMID: 27392482
- BAF170 mediates the interaction between BAF complexes and H3K27demethylases, controlling the global level of H3K27me2/3 and ultimately the gene expression program in cortical development. PMID: 26655900
- Data show that knockdown of components of the chromatin remodeling complex Brm or Baf170 at different stages promotes reprogramming. PMID: 26121422
- BAF170 acts within a precise time window to repress indirect cortical neurogenesis and control cortical size. PMID: 23643363
Q&A
The SWI/SNF complex subunit SMARCC2 plays critical roles in chromatin remodeling and transcriptional regulation. Below are structured FAQs addressing key research considerations, supported by experimental evidence from recent studies:
What functional roles does SMARCC2 serve in SWI/SNF complexes?
SMARCC2 stabilizes the SWI/SNF complex architecture and mediates interactions with chromatin/DNA through its SWIRM domain . Methodological insights:
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Co-immunoprecipitation (Co-IP) validates interactions with core subunits (e.g., BRG1, SMARCB1) .
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CRISPR knockout models show SMARCC2 depletion disrupts nucleosome repositioning and pluripotency in mESCs .
Which experimental models effectively study SMARCC2 function?
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Mouse embryonic stem cells (mESCs): Retain esBAF complexes with SMARCC1 but lack SMARCC2, enabling isoform-specific studies .
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Synchronized cell cycles: Reveal cell cycle-dependent SMARCC2 degradation via L3MBTL3 during S/G2 phases .
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Primary neuronal cultures: Detect cytoplasmic SMARCC2 truncations (60 kDa, 25 kDa) in Parkinson’s disease models .
How to address antibody specificity challenges for SMARCC2 detection?
How do SMARCC2 lysine methylation states regulate complex stability?
SMARCC2 undergoes LSD1-mediated demethylation at K475, preventing L3MBTL3-CRL4DCAF5–mediated proteasomal degradation . Experimental approaches:
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Site-directed mutagenesis: K475R mutations stabilize SMARCC2 in LSD1-deficient cells .
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Methylation assays: Use anti-methyl lysine antibodies (e.g., anti-K615me) to track cell cycle-dependent modifications .
What mechanisms explain SMARCC2 cytoplasmic mislocalization in neurodegeneration?
In Parkinson’s disease, truncated SMARCC2 (25 kDa) forms cytoplasmic aggregates colocalizing with p62, suggesting autophagic clearance defects . Key methods:
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CHIER (Controlled Heat-Induced Epitope Retrieval): Enhances detection of cytoplasmic SMARCC2 in FFPE brain sections .
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Proteomic profiling: Identifies SWIRM domain retention in aggregates, impairing nuclear reimport .
How does SMARCC2 interact with non-SWI/SNF proteins like IPMK?
IPMK binds SMARCC2 via the SMARCB1 subunit, modulating chromatin accessibility at bivalent promoters . Key findings:
Data Contradiction Analysis
Conflict: Studies report conflicting SMARCC2 isoforms (150 kDa vs. 60 kDa/25 kDa) .
Resolution:
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Truncated isoforms arise from tissue-specific proteolysis (e.g., neuronal vs. embryonic cells) .
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Antibody selection biases (e.g., SMARCC2-1A3 vs. AP06744PU-N) affect detection .
Recommendation: Perform Pulse-chase assays to track isoform turnover and RNAi validation to confirm antibody specificity .
