primary antibodies arid1a  (Cell Signaling Technology Inc)

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: Immunohistochemical staining for ARID1A expression in EGFR-mutant LUAD tissues (50×and 200×). (A) ARID1A low expression. (B) ARID1A high expression.

Article Snippet: Immunodetection involved overnight 4°C incubation with anti-ARID1A primary antibody (Proteintech, 1:500) and subsequent HRP-conjugated secondary antibody for 60 min. Chromogenic development utilized DAB substrate under standardized conditions.

Techniques: Immunohistochemical staining, Staining, Expressing, Mutagenesis

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: The role of SWI/SNF subunit mutations in the prognosis of EGFR-mutant LUAD. (A-F) ARID1A, ARID1B, ARID2, ARID5B, SMARCA4, and SMARCB1.

Article Snippet: Immunodetection involved overnight 4°C incubation with anti-ARID1A primary antibody (Proteintech, 1:500) and subsequent HRP-conjugated secondary antibody for 60 min. Chromogenic development utilized DAB substrate under standardized conditions.

Techniques: Mutagenesis

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: Comparison of clinical features between patients with ARID1A mutations and patients with wild-type ARID1A. (A) The number of patients with distant metastases. (B) Tumour purity. (C) The frequency of gene alterations. (D) Mutation count. (E) Fractions of genome alterations. (F) TMB. (G) MSI score. (H) The rate of PDL1 positivity. * P < 0.05, **** P < 0.0001.

Article Snippet: Immunodetection involved overnight 4°C incubation with anti-ARID1A primary antibody (Proteintech, 1:500) and subsequent HRP-conjugated secondary antibody for 60 min. Chromogenic development utilized DAB substrate under standardized conditions.

Techniques: Comparison, Mutagenesis

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: ARID1A mutation confers a poor prognosis for patients with EGFR-mutant LUAD. (A) The frequencies of genes exhibiting coexisting mutations with EGFR. Survival analysis for patients with the EGFR mutation, ARID1A/EGFR comutation and (B) TP53/EGFR, (C) KRAS/EGFR, (D) CDKN2A/EGFR, (E) PIK3CA/EGFR, (F) RB1/EGFR, and (G) PTEN/EGFR comutations.

Article Snippet: Immunodetection involved overnight 4°C incubation with anti-ARID1A primary antibody (Proteintech, 1:500) and subsequent HRP-conjugated secondary antibody for 60 min. Chromogenic development utilized DAB substrate under standardized conditions.

Techniques: Mutagenesis

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: The role of ARID1A expression in the prognosis of EGFR-mutant LUAD patients receiving EGFR-TKIs as a first-line treatment after postoperative progression. (A) Comparison of PFS between patients with low ARID1A expression and patients with high ARID1A expression. (B) Forest plots for the univariate and multivariate analyses of PFS.

Article Snippet: Immunodetection involved overnight 4°C incubation with anti-ARID1A primary antibody (Proteintech, 1:500) and subsequent HRP-conjugated secondary antibody for 60 min. Chromogenic development utilized DAB substrate under standardized conditions.

Techniques: Expressing, Mutagenesis, Comparison

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: The role of ARID1A in the prognosis of EGFR-mutant LUAD patients receiving postoperative adjuvant EGFR-TKI treatments. (A) Comparison of DFS between patients with low ARID1A expression and patients with high ARID1A expression. (B) Forest plots for univariate and multivariate analyses of DFS. (C) Nomogram for the prediction of 1-, 2- and 3-year survival. (D) Calibration curves of the nomogram.

Article Snippet: Immunodetection involved overnight 4°C incubation with anti-ARID1A primary antibody (Proteintech, 1:500) and subsequent HRP-conjugated secondary antibody for 60 min. Chromogenic development utilized DAB substrate under standardized conditions.

Techniques: Mutagenesis, Adjuvant, Comparison, Expressing

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: Loss of ARID1A expression confers resistance to Osimertinib in PC9 cell. (A) Western blot analysis of ARID1A protein expression in the control group (shNC) and the knockdown group (shARID1A). (B) The IC50 for osimertinib in the control group and the knockdown group. (C) Flow cytometry analysis of ARID1A konckdown effect on apoptosis with and without osimertinib treatment. (D) Transwell migration analysis of ARID1A konckdown effect on migration with and without osimertinib treatment. * * P < 0.01, **** P < 0.0001.

Article Snippet: Immunodetection involved overnight 4°C incubation with anti-ARID1A primary antibody (Proteintech, 1:500) and subsequent HRP-conjugated secondary antibody for 60 min. Chromogenic development utilized DAB substrate under standardized conditions.

Techniques: Expressing, Western Blot, Control, Knockdown, Flow Cytometry, Migration

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: ARID1A knockdown confers resistance to EGFR-TKI by activating the EGFR/AKT/mTOR signalling pathway. (A) Genes coexpressed with ARID1A. (B) The top 50 genes that were positively associated with ARID1A. (C) The top 50 genes that were negatively associated with ARID1A. (D) GO analysis of ARID1A coexpressed genes. CC: cellular component, BP: biological process, MF: molecular function. (E) KEGG analysis of ARID1A coexpressed genes. (F) GSEA analysis of ARID1A via TCGA database. (G) Western blot analysis of ARID1A konckdown effect on EGFR/AKT/mTOR pathway-related protein. * P < 0.05.

Article Snippet: Immunodetection involved overnight 4°C incubation with anti-ARID1A primary antibody (Proteintech, 1:500) and subsequent HRP-conjugated secondary antibody for 60 min. Chromogenic development utilized DAB substrate under standardized conditions.

Techniques: Knockdown, Western Blot

Journal: BioTechniques

Article Title: Generation of genetically tailored porcine liver cancer cells by CRISPR/Cas9 editing.

doi: 10.2144/btn-2020-0119

Figure Lengend Snippet: Figure 3. CRISPR/Cas9-mediated disruption of the porcine ARID1A gene. (A) Schematic representation of the porcine ARID1A locus, showing the location of spacer sequences crRNA#1 and crRNA#2 (underlined blue font). Protospacer-adjacent motif sequences are marked in red. The introns are represented by lines, coding regions of exons are shaded in black and the untranslated region is white. (B) Comparing the CRISPR/Cas9-mediated editing efficiency of two ARID1A-targeting gRNAs. Porcine HCC line-1 cells were transfected with 15 nM RNP comprising Cas9 and gRNA#1 or gRNA#2. Nontransfected cells were used as control. Genomic DNA was collected 2 days post-transfection and analyzed by targeted NGS. The bar graph depicts the percentages (%) of total reads that displayed indels at the gRNA target site occurring as a result of nonhomologous end joining. (C & D) Top 15 reads detected by targeted NGS analysis, mapped to the reference sequence. The percentages of reads for each sequence are shown on the right. The asterisk indicates non-edited reads. Dashed line: predicted Cas9 cleavage position; red box: insertion; dash: deleted base. HCC: Hepatocellular carcinoma; NGS: Next-generation sequencing; RNP: Ribonucleoprotein.

Article Snippet: The following anti-ARID1A primary antibodies were used: #sc-373784 and #sc-32761 (Santa Cruz Biotechnolog, TX, USA) and #A301-041A (Bethyl Laboratories, TX, USA).

Techniques: CRISPR, Disruption, Transfection, Control, Sequencing, Next-Generation Sequencing

Journal: BioTechniques

Article Title: Generation of genetically tailored porcine liver cancer cells by CRISPR/Cas9 editing.

doi: 10.2144/btn-2020-0119

Figure Lengend Snippet: Figure 5. Increased CRISPR-Cas9 editing efficiency of ARID1A at higher ribonucleoprotein concentration. (A) ARID1A editing efficiency in four porcine HCC cell lines following transfection with 25 nM ribonucleoprotein comprising Cas9 and gRNA#1. Genomic DNA was collected 2 days post-transfection and analyzed by targeted NGS. The bar graph depicts the percentages (%) of total reads that displayed indels at the gRNA target site occurring as a result of nonhomologous end joining. (B) Top 15 reads detected by targeted NGS analysis in the four porcine HCC lines, mapped to the reference sequence. The identity and frequency of indels in the four cell lines is consistent. The percentages of reads of each sequence are shown on the right. The location of the indel relative to the expected cleavage site is shown on the left, followed by a colon and the number of nucleotides inserted (i) or deleted (d). The asterisk denotes non-edited reads. Dashed line: predicted Cas9 cleavage position; red box: insertion; dash: deleted base. HCC: Hepatocellular carcinoma; NGS: Next-generation sequencing.

Article Snippet: The following anti-ARID1A primary antibodies were used: #sc-373784 and #sc-32761 (Santa Cruz Biotechnolog, TX, USA) and #A301-041A (Bethyl Laboratories, TX, USA).

Techniques: CRISPR, Concentration Assay, Transfection, Sequencing, Next-Generation Sequencing

Journal: BioTechniques

Article Title: Generation of genetically tailored porcine liver cancer cells by CRISPR/Cas9 editing.

doi: 10.2144/btn-2020-0119

Figure Lengend Snippet: Figure 6. Comparing analysis of CRISPR/Cas9 mediated disruption of ARID1A by next-generation and Sanger sequencing. (A) Sanger sequencing chromatograms of porcine HCC cells transfected with Cas9 and ARID1A gRNA#1 and control nontransfected cells. Overlapping peaks near the gRNA target site are observed for the sample subjected to CRISPR/Cas9 editing. Dashed line: predicted Cas9 cleavage position; underlined nucleotides: crRNA spacer sequence. (B) Top 5 reads detected by ICE software analysis of Sanger sequencing data in three porcine HCC lines transfected with Cas9 and ARID1A gRNA#1. The type and frequency of indels is shown on the left and is consistent among the three cell lines. (C) The editing efficiency (%) and frequency of the top five frequent reads (%) identified by ICE software analysis of Sanger sequencing data as compared with NGS analysis in three ARID1A-edited porcine HCC cells. The location of the indel relative to the expected cleavage site is shown on the left, followed by a colon and the number of nucleotides inserted (i) or deleted (d). Overall similarity was noted between the two analysis methods. HCC: Hepatocellular carcinoma; NGS: Next-generation sequencing.

Article Snippet: The following anti-ARID1A primary antibodies were used: #sc-373784 and #sc-32761 (Santa Cruz Biotechnolog, TX, USA) and #A301-041A (Bethyl Laboratories, TX, USA).

Techniques: CRISPR, Disruption, Sequencing, Transfection, Control, Software, Next-Generation Sequencing

Journal: BioTechniques

Article Title: Generation of genetically tailored porcine liver cancer cells by CRISPR/Cas9 editing.

doi: 10.2144/btn-2020-0119

Figure Lengend Snippet: Figure 7. Representative single cell clones isolated from porcine hepatocellular carcinoma cells subject to CRISPR/Cas9-mediated ARID1A disruption. (A) Possible editing outcomes of CRISPR/Cas9 include the following: an identical indel is introduced in both alleles (homozygous mutation), different indels occur in each allele (biallelic mutation) or an indel is observed in an allele while the other allele remains unedited (heterozygous mutation). (B–D) Analysis of representative single cells clones isolated from porcine HCC cells transfected with Cas9 and ARID1A gRNA#1. (B) Reads detected by targeted NGS analysis mapped to the reference sequence (top) for three single cell clones. Dashed line: predicted Cas9 cleavage position; red box: insertion; dash: deleted base. (C) The predicted translation of ARID1A protein for the representative clones. The dotted region represents amino acids with frameshift mutation. (D) Arginase-1 staining (green) merged with DAPI staining (blue) for parental porcine HCC cell line and the representative single-cell clones (scale bar = 200 μm). All clones show positive arginase-1 staining, confirming their hepatocellular origin. HCC: Hepatocellular carcinoma; NGS: Next-generation sequencing.

Article Snippet: The following anti-ARID1A primary antibodies were used: #sc-373784 and #sc-32761 (Santa Cruz Biotechnolog, TX, USA) and #A301-041A (Bethyl Laboratories, TX, USA).

Techniques: Clone Assay, Isolation, CRISPR, Disruption, Mutagenesis, Transfection, Sequencing, Staining, Next-Generation Sequencing

Journal: Asian Pacific Journal of Cancer Prevention : APJCP

Article Title: Histopathology and ARID1A Expression in Endometriosis-Associated Ovarian Carcinoma (EAOC) Carcinogenesis Model with Endometrial Autoimplantation and DMBA Induction

doi: 10.31557/APJCP.2021.22.2.553

Figure Lengend Snippet: ARID1A Expression. A. Negative control. B. Positive control from intestinal tissue. C. ARID1A expression in normal endometrium in the sham group. D. ARID1A expression in non-atypical endometriosis. E. ARID1A expression in atypical endometriosis. F. Endometrioid carcinoma showed patchy negative ARID1A expression (A-E, HE 400x).

Article Snippet: It was then made into Hematoxylin-Eosin (HE) preparations and immunohistochemical staining was performed using ARID1A-PSG3 Santa Cruz biotechnology primary antibodies and seen under a light microscope.

Techniques: Expressing, Negative Control, Positive Control