Review

◦c with smarca4 (Proteintech)

Proteintech is a verified supplier

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Proteintech ◦c with smarca4

Figure 1. <t>SMARCA4</t> is a t arget able, tumor-specific vulnerability of adrenergic neuroblastoma (NB). ( A ) Crystal violet staining of adrenergic (ADRN) and mesenchymal (MES) NB or control cell lines treated with serial titration of SWI / SNF inhibitor BRM014. Orange squares indicate MYCN amplification or 1p36 deletion. Quantified in Supplementary Figure 3A. ( B ) R epresentativ e images of NB cells treated with lethal (1 μM) and sub-lethal (1 0–1 00 nM) BRM014 or vehicle control (DMSO). ( C ) Preparation of neural crest cells (NCCs) and NCC-derived peripheral neurons from human embryonic stem cells (hESCs). ( D ) Cell growth over time upon treatment with BRM014 or DMSO. Error bars: mean ± 95% confidence interval ( N = 3 independent samples), abbreviations used as in (C). ( E ) Representative images of IMR-32 cells upon expression of shRNA mediating SMARCA4 or SMARCA2 knock-down, or non-targeting control (NTC). (F) Western blot analysis of SMARCA4 and SMARCA2 levels after SMARCA2 knock-down compared to NTC. ( G ) Western blot analysis of SMARCA4 and SMARCA2 levels in IMR-32 SMARCA4 degron-containing cell line (SMARCA4-EGFP-mAID) after 2 h of vehicle (EtOH) or auxin treatment. ( H ) Quantification of IMR-32 (WT) and SMARCA4-EGFP-mAID (mAID) cell line viability upon treatment with BRM014, auxin or vehicle controls for 96 h. Error bars: mean ± SE. ( I ) Experimental design of animal study. ( J ) Small animal MRI imaging and kidneys extracted from animals comparing BRM014- and vehicle-treated animals ( N = 11 per group). ( K ) Tumor growth time course measured by small-animal MRI. Error bars: mean ± SE. ( L ) Comparison of tumor weights of BRM014 and vehicle control treated animals. Error bars: mean ± SE. ( M ) Representative H&E staining of tumor sections comparing BRM014- and vehicle-treated animals.

◦C With Smarca4, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%E2%97%A6c+with+smarca4/pm37993417-205-7-10?v=Proteintech
Average 93 stars, based on 14 article reviews

◦c with smarca4 - by Bioz Stars, 2026-07

93/100 stars

Images

1) Product Images from "Reactivation of the G1 enhancer landscape underlies core circuitry addiction to SWI/SNF."

Article Title: Reactivation of the G1 enhancer landscape underlies core circuitry addiction to SWI/SNF.

Journal: Nucleic acids research

doi: 10.1093/nar/gkad1081

Figure 1. SMARCA4 is a t arget able, tumor-specific vulnerability of adrenergic neuroblastoma (NB). ( A ) Crystal violet staining of adrenergic (ADRN) and mesenchymal (MES) NB or control cell lines treated with serial titration of SWI / SNF inhibitor BRM014. Orange squares indicate MYCN amplification or 1p36 deletion. Quantified in Supplementary Figure 3A. ( B ) R epresentativ e images of NB cells treated with lethal (1 μM) and sub-lethal (1 0–1 00 nM) BRM014 or vehicle control (DMSO). ( C ) Preparation of neural crest cells (NCCs) and NCC-derived peripheral neurons from human embryonic stem cells (hESCs). ( D ) Cell growth over time upon treatment with BRM014 or DMSO. Error bars: mean ± 95% confidence interval ( N = 3 independent samples), abbreviations used as in (C). ( E ) Representative images of IMR-32 cells upon expression of shRNA mediating SMARCA4 or SMARCA2 knock-down, or non-targeting control (NTC). (F) Western blot analysis of SMARCA4 and SMARCA2 levels after SMARCA2 knock-down compared to NTC. ( G ) Western blot analysis of SMARCA4 and SMARCA2 levels in IMR-32 SMARCA4 degron-containing cell line (SMARCA4-EGFP-mAID) after 2 h of vehicle (EtOH) or auxin treatment. ( H ) Quantification of IMR-32 (WT) and SMARCA4-EGFP-mAID (mAID) cell line viability upon treatment with BRM014, auxin or vehicle controls for 96 h. Error bars: mean ± SE. ( I ) Experimental design of animal study. ( J ) Small animal MRI imaging and kidneys extracted from animals comparing BRM014- and vehicle-treated animals ( N = 11 per group). ( K ) Tumor growth time course measured by small-animal MRI. Error bars: mean ± SE. ( L ) Comparison of tumor weights of BRM014 and vehicle control treated animals. Error bars: mean ± SE. ( M ) Representative H&E staining of tumor sections comparing BRM014- and vehicle-treated animals.

Figure Legend Snippet: Figure 1. SMARCA4 is a t arget able, tumor-specific vulnerability of adrenergic neuroblastoma (NB). ( A ) Crystal violet staining of adrenergic (ADRN) and mesenchymal (MES) NB or control cell lines treated with serial titration of SWI / SNF inhibitor BRM014. Orange squares indicate MYCN amplification or 1p36 deletion. Quantified in Supplementary Figure 3A. ( B ) R epresentativ e images of NB cells treated with lethal (1 μM) and sub-lethal (1 0–1 00 nM) BRM014 or vehicle control (DMSO). ( C ) Preparation of neural crest cells (NCCs) and NCC-derived peripheral neurons from human embryonic stem cells (hESCs). ( D ) Cell growth over time upon treatment with BRM014 or DMSO. Error bars: mean ± 95% confidence interval ( N = 3 independent samples), abbreviations used as in (C). ( E ) Representative images of IMR-32 cells upon expression of shRNA mediating SMARCA4 or SMARCA2 knock-down, or non-targeting control (NTC). (F) Western blot analysis of SMARCA4 and SMARCA2 levels after SMARCA2 knock-down compared to NTC. ( G ) Western blot analysis of SMARCA4 and SMARCA2 levels in IMR-32 SMARCA4 degron-containing cell line (SMARCA4-EGFP-mAID) after 2 h of vehicle (EtOH) or auxin treatment. ( H ) Quantification of IMR-32 (WT) and SMARCA4-EGFP-mAID (mAID) cell line viability upon treatment with BRM014, auxin or vehicle controls for 96 h. Error bars: mean ± SE. ( I ) Experimental design of animal study. ( J ) Small animal MRI imaging and kidneys extracted from animals comparing BRM014- and vehicle-treated animals ( N = 11 per group). ( K ) Tumor growth time course measured by small-animal MRI. Error bars: mean ± SE. ( L ) Comparison of tumor weights of BRM014 and vehicle control treated animals. Error bars: mean ± SE. ( M ) Representative H&E staining of tumor sections comparing BRM014- and vehicle-treated animals.

Techniques Used: Staining, Control, Titration, Amplification, Derivative Assay, Expressing, shRNA, Knockdown, Western Blot, Imaging, Comparison

Figure 4. Temporal patterns of DNA accessibility re v eal CR C losses are enriched at G1-specific enhancers regulated b y SMAR CA4. ( A ) FACS strategy and gating to analyze genome-wide accessibility of cells in individual cell cycle phases. ( B ) Example browser tracks of cell cycle-phase dependent site sensitive to SWI / SNF inactivation. ( C ) Classification of genome-wide SMARCA4 sites based on their cell cycle-phase dependent accessibility changes, and their response to SWI / SNF inactivation. ( D ) DNA accessibility changes upon BRM014 treatment at SMARCA4-bound clusters shown in panel (C). B o x plot centers indicate median values. ( E ) Enrichment of sites with reduced CRC TF occupancy within clusters shown in panel (C). ( F ) Heatmap of cell cycle phase-specific accessibility changes of CCND1 enhancer, and browser tracks showing reduced accessibility in late G1 phase at CCND1 enhancer. Inset shows rapid loss of CRC TF binding at CCND1 enhancer within 1 h of BRM014 treatment. ( G ) Western blot analysis of CCND1 expression changes upon BRM014 treatment across NB cell lines. ( H ) Expression of CCND1 in NB patient tumors with low SMARCA4 expression compared to those with high SMARCA4 expression. Box plot centers indicate median values.

Figure Legend Snippet: Figure 4. Temporal patterns of DNA accessibility re v eal CR C losses are enriched at G1-specific enhancers regulated b y SMAR CA4. ( A ) FACS strategy and gating to analyze genome-wide accessibility of cells in individual cell cycle phases. ( B ) Example browser tracks of cell cycle-phase dependent site sensitive to SWI / SNF inactivation. ( C ) Classification of genome-wide SMARCA4 sites based on their cell cycle-phase dependent accessibility changes, and their response to SWI / SNF inactivation. ( D ) DNA accessibility changes upon BRM014 treatment at SMARCA4-bound clusters shown in panel (C). B o x plot centers indicate median values. ( E ) Enrichment of sites with reduced CRC TF occupancy within clusters shown in panel (C). ( F ) Heatmap of cell cycle phase-specific accessibility changes of CCND1 enhancer, and browser tracks showing reduced accessibility in late G1 phase at CCND1 enhancer. Inset shows rapid loss of CRC TF binding at CCND1 enhancer within 1 h of BRM014 treatment. ( G ) Western blot analysis of CCND1 expression changes upon BRM014 treatment across NB cell lines. ( H ) Expression of CCND1 in NB patient tumors with low SMARCA4 expression compared to those with high SMARCA4 expression. Box plot centers indicate median values.

Techniques Used: Genome Wide, Binding Assay, Western Blot, Expressing

Figure 5. SWI / SNF inhibition synergizes with retinoic acid to promote cell-cycle exit in G1. ( A ) Flow cytometry cell cycle analysis of NB cells upon treatment with 13- cis retinoic acid (13- cis RA), BRM014, or vehicle control (DMSO). ( B ) Model by which SWI / SNF inhibitors sensitize cells to retinoic acid-mediated cell cy cle e xit. ( C ) Metagene plots of MYCN and retinoic acid receptor alpha (RARA) chromatin binding at SMARCA4 sites in the presence of BRM014 or DMSO. ( D ) Example ChIP-seq browser track demonstrating preserved RARA binding despite loss of MYCN binding. ( E ) Experimental design. ( F ) Outgrowth of NB cell lines following cross-titration of BRM014 and 13- cis RA. ( G ) Heatmap of synergy scores for BRM014 and 13- cis RA cross-titration across NB cell lines measured by Loewe additivity ( N ≥3 independent replicates). ( H ) Isobolograms of BRM014 and 13- cis RA treatments demonstrating synergy ( N ≥3 independent replicates).

Figure Legend Snippet: Figure 5. SWI / SNF inhibition synergizes with retinoic acid to promote cell-cycle exit in G1. ( A ) Flow cytometry cell cycle analysis of NB cells upon treatment with 13- cis retinoic acid (13- cis RA), BRM014, or vehicle control (DMSO). ( B ) Model by which SWI / SNF inhibitors sensitize cells to retinoic acid-mediated cell cy cle e xit. ( C ) Metagene plots of MYCN and retinoic acid receptor alpha (RARA) chromatin binding at SMARCA4 sites in the presence of BRM014 or DMSO. ( D ) Example ChIP-seq browser track demonstrating preserved RARA binding despite loss of MYCN binding. ( E ) Experimental design. ( F ) Outgrowth of NB cell lines following cross-titration of BRM014 and 13- cis RA. ( G ) Heatmap of synergy scores for BRM014 and 13- cis RA cross-titration across NB cell lines measured by Loewe additivity ( N ≥3 independent replicates). ( H ) Isobolograms of BRM014 and 13- cis RA treatments demonstrating synergy ( N ≥3 independent replicates).

Techniques Used: Inhibition, Flow Cytometry, Cell Cycle Assay, Control, Binding Assay, ChIP-sequencing, Titration

Image Search Results

Journal: Nucleic acids research

Article Title: Reactivation of the G1 enhancer landscape underlies core circuitry addiction to SWI/SNF.

doi: 10.1093/nar/gkad1081

Figure Lengend Snippet: Figure 1. SMARCA4 is a t arget able, tumor-specific vulnerability of adrenergic neuroblastoma (NB). ( A ) Crystal violet staining of adrenergic (ADRN) and mesenchymal (MES) NB or control cell lines treated with serial titration of SWI / SNF inhibitor BRM014. Orange squares indicate MYCN amplification or 1p36 deletion. Quantified in Supplementary Figure 3A. ( B ) R epresentativ e images of NB cells treated with lethal (1 μM) and sub-lethal (1 0–1 00 nM) BRM014 or vehicle control (DMSO). ( C ) Preparation of neural crest cells (NCCs) and NCC-derived peripheral neurons from human embryonic stem cells (hESCs). ( D ) Cell growth over time upon treatment with BRM014 or DMSO. Error bars: mean ± 95% confidence interval ( N = 3 independent samples), abbreviations used as in (C). ( E ) Representative images of IMR-32 cells upon expression of shRNA mediating SMARCA4 or SMARCA2 knock-down, or non-targeting control (NTC). (F) Western blot analysis of SMARCA4 and SMARCA2 levels after SMARCA2 knock-down compared to NTC. ( G ) Western blot analysis of SMARCA4 and SMARCA2 levels in IMR-32 SMARCA4 degron-containing cell line (SMARCA4-EGFP-mAID) after 2 h of vehicle (EtOH) or auxin treatment. ( H ) Quantification of IMR-32 (WT) and SMARCA4-EGFP-mAID (mAID) cell line viability upon treatment with BRM014, auxin or vehicle controls for 96 h. Error bars: mean ± SE. ( I ) Experimental design of animal study. ( J ) Small animal MRI imaging and kidneys extracted from animals comparing BRM014- and vehicle-treated animals ( N = 11 per group). ( K ) Tumor growth time course measured by small-animal MRI. Error bars: mean ± SE. ( L ) Comparison of tumor weights of BRM014 and vehicle control treated animals. Error bars: mean ± SE. ( M ) Representative H&E staining of tumor sections comparing BRM014- and vehicle-treated animals.

Article Snippet: Chromatin was then immunoprecipitated overnight at 4 ◦C with SMARCA4 (Proteintech #21634–1-AP, RRID:AB _ 10858784 ), PHOX2B (Santa Cruz Biotechnology #sc-376997, RRID:AB _ 2813765 ), ISL1 cocktail (DSHB #40.2D6, #39.4D5, #39.3F7, and #40.3A4, RRIDs: AB_528315, AB_2314683, AB_1157901, and AB_528313), HAND2 (Abcam #ab200040, RRID:AB _ 2923502 ), GA T A3 (Thermo Fisher #MA1-028, RRID:AB _ 2536713 ), MYCN (Active Motif #61185 RRID:AB _ 2793543 ), ASCL1 (Abcam #ab74065, RRID:AB _ 1859937 ), EBF3 (Thermo Fisher #PA5-30985, RRID:AB _ 2548459 ), H3K4me1 (Abcam #ab8895, RRID:AB _ 306847 ), or RARA (Abcam #ab41934, RRID:AB _ 777683 ) antibodies bound to Protein A (Thermo Fisher #10001D) or Protein G (Thermo Fisher #10003D) Dynabeads.

Techniques: Staining, Control, Titration, Amplification, Derivative Assay, Expressing, shRNA, Knockdown, Western Blot, Imaging, Comparison

Journal: Nucleic acids research

Article Title: Reactivation of the G1 enhancer landscape underlies core circuitry addiction to SWI/SNF.

doi: 10.1093/nar/gkad1081

Figure Lengend Snippet: Figure 4. Temporal patterns of DNA accessibility re v eal CR C losses are enriched at G1-specific enhancers regulated b y SMAR CA4. ( A ) FACS strategy and gating to analyze genome-wide accessibility of cells in individual cell cycle phases. ( B ) Example browser tracks of cell cycle-phase dependent site sensitive to SWI / SNF inactivation. ( C ) Classification of genome-wide SMARCA4 sites based on their cell cycle-phase dependent accessibility changes, and their response to SWI / SNF inactivation. ( D ) DNA accessibility changes upon BRM014 treatment at SMARCA4-bound clusters shown in panel (C). B o x plot centers indicate median values. ( E ) Enrichment of sites with reduced CRC TF occupancy within clusters shown in panel (C). ( F ) Heatmap of cell cycle phase-specific accessibility changes of CCND1 enhancer, and browser tracks showing reduced accessibility in late G1 phase at CCND1 enhancer. Inset shows rapid loss of CRC TF binding at CCND1 enhancer within 1 h of BRM014 treatment. ( G ) Western blot analysis of CCND1 expression changes upon BRM014 treatment across NB cell lines. ( H ) Expression of CCND1 in NB patient tumors with low SMARCA4 expression compared to those with high SMARCA4 expression. Box plot centers indicate median values.

Techniques: Genome Wide, Binding Assay, Western Blot, Expressing

Journal: Nucleic acids research

Article Title: Reactivation of the G1 enhancer landscape underlies core circuitry addiction to SWI/SNF.

doi: 10.1093/nar/gkad1081

Figure Lengend Snippet: Figure 5. SWI / SNF inhibition synergizes with retinoic acid to promote cell-cycle exit in G1. ( A ) Flow cytometry cell cycle analysis of NB cells upon treatment with 13- cis retinoic acid (13- cis RA), BRM014, or vehicle control (DMSO). ( B ) Model by which SWI / SNF inhibitors sensitize cells to retinoic acid-mediated cell cy cle e xit. ( C ) Metagene plots of MYCN and retinoic acid receptor alpha (RARA) chromatin binding at SMARCA4 sites in the presence of BRM014 or DMSO. ( D ) Example ChIP-seq browser track demonstrating preserved RARA binding despite loss of MYCN binding. ( E ) Experimental design. ( F ) Outgrowth of NB cell lines following cross-titration of BRM014 and 13- cis RA. ( G ) Heatmap of synergy scores for BRM014 and 13- cis RA cross-titration across NB cell lines measured by Loewe additivity ( N ≥3 independent replicates). ( H ) Isobolograms of BRM014 and 13- cis RA treatments demonstrating synergy ( N ≥3 independent replicates).

Techniques: Inhibition, Flow Cytometry, Cell Cycle Assay, Control, Binding Assay, ChIP-sequencing, Titration

Journal: Cold Spring Harbor Molecular Case Studies

Article Title: Multimodal molecular analysis of an atypical small cell carcinoma of the ovary, hypercalcemic type

doi: 10.1101/mcs.a002956

Figure Lengend Snippet: Variant table

Article Snippet: A peripheral blood sample was sent to Prevention Genetics for “Ovarian Cancer and Rhabdoid Tumor Predisposition Syndrome testing via SMARCA4 NextGen Sequencing.” The results were positive for a heterozygous SMARCA4 c.1141C>T, p.Arg381Ter mutation.

Techniques: Variant Assay, Binding Assay, Dominant Negative Mutation

Review

Structured Review

Images

1) Product Images from "Reactivation of the G1 enhancer landscape underlies core circuitry addiction to SWI/SNF."

Similar Products

Image Search Results