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anti atf3  (Novus Biologicals)


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    Structured Review

    Novus Biologicals anti atf3
    Anti Atf3, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 37 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti atf3/product/Novus Biologicals
    Average 93 stars, based on 37 article reviews
    anti atf3 - by Bioz Stars, 2026-05
    93/100 stars

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    (A-B) Volcano plots of whole-transcriptome differentially expressed genes (DEGs) identified by RNAseq in ST88-14 and NF90.8 cells following siRNA-mediated depletion of ZNF423 ( n =3) compared to control ( n =3). Dashed vertical lines reflect log 2 FC of −1 and 1. Dashed horizontal line reflects false discovery rate (FDR) of 0.05. Downregulated genes with log 2 FC≤-1 and -log 10 adjusted p-value above FDR threshold are denoted in blue. Upregulated genes log 2 FC≥1 and -log 10 adjusted p-value above FDR threshold are denoted in red. Raw RNAseq hit counts for ZNF423 in NF90.8 cells transfected with control siRNA ( n =3) or siZNF423 ( n =3). P-values represent unpaired, two-tailed t-tests between groups. (C) Venn diagram showing overlap of significantly downregulated DEGs common among ST88-14 and NF90.8 cell lines. Downregulated DEGs were defined as log 2 FC≥-1 and adjusted p-value of ≤0.05. (D) Dot plot of top enriched Hallmark gene signatures of shared downregulated genes (FDR≤0.05). (E) Venn diagram showing overlap of significantly upregulated DEGs common among ST88-14 and NF90.8 cell lines. Upregulated DEGs were defined as log 2 FC≥1 and adjusted p-value of ≤0.05. (F) Dot plot of top enriched Hallmark gene signatures of shared upregulated genes (FDR≤0.05). (G-H) Volcano plots of differentially expressed transcription factors and kinases in ST88-14 and NF90.8 cells following siRNA-mediated depletion of ZNF423 compared to control. (I-J) Immunoblots showing cleavage of PARP, <t>ATF3,</t> ATF4 and ZNF423 protein expression following siRNA-mediated depletion of ZNF423 ( n =3) compared to controls ( n =3). GAPDH serves as loading control. Protein expression was normalized to total protein and quantified using ImageJ. Error bars reflect SEM. P-values represent unpaired, two-tailed t test with Welch’s correction. ****=p-value ≤0.0001, ***=p-value≤0.001, **=p-value≤0.01, *=p-value≤0.05, ns=not significant.
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    (A-B) Volcano plots of whole-transcriptome differentially expressed genes (DEGs) identified by RNAseq in ST88-14 and NF90.8 cells following siRNA-mediated depletion of ZNF423 ( n =3) compared to control ( n =3). Dashed vertical lines reflect log 2 FC of −1 and 1. Dashed horizontal line reflects false discovery rate (FDR) of 0.05. Downregulated genes with log 2 FC≤-1 and -log 10 adjusted p-value above FDR threshold are denoted in blue. Upregulated genes log 2 FC≥1 and -log 10 adjusted p-value above FDR threshold are denoted in red. Raw RNAseq hit counts for ZNF423 in NF90.8 cells transfected with control siRNA ( n =3) or siZNF423 ( n =3). P-values represent unpaired, two-tailed t-tests between groups. (C) Venn diagram showing overlap of significantly downregulated DEGs common among ST88-14 and NF90.8 cell lines. Downregulated DEGs were defined as log 2 FC≥-1 and adjusted p-value of ≤0.05. (D) Dot plot of top enriched Hallmark gene signatures of shared downregulated genes (FDR≤0.05). (E) Venn diagram showing overlap of significantly upregulated DEGs common among ST88-14 and NF90.8 cell lines. Upregulated DEGs were defined as log 2 FC≥1 and adjusted p-value of ≤0.05. (F) Dot plot of top enriched Hallmark gene signatures of shared upregulated genes (FDR≤0.05). (G-H) Volcano plots of differentially expressed transcription factors and kinases in ST88-14 and NF90.8 cells following siRNA-mediated depletion of ZNF423 compared to control. (I-J) Immunoblots showing cleavage of PARP, <t>ATF3,</t> ATF4 and ZNF423 protein expression following siRNA-mediated depletion of ZNF423 ( n =3) compared to controls ( n =3). GAPDH serves as loading control. Protein expression was normalized to total protein and quantified using ImageJ. Error bars reflect SEM. P-values represent unpaired, two-tailed t test with Welch’s correction. ****=p-value ≤0.0001, ***=p-value≤0.001, **=p-value≤0.01, *=p-value≤0.05, ns=not significant.
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    The results of western blotting (A) . The protein levels of <t>ATF3</t> (B) , p-p53 (C) , p-p21 (D) , and cas3 (E) were represented in the studied groups. β-actin was used as an internal control. cas3: caspase-3, ip: intraperitoneal, I/R: ischemia/reperfusion, NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells, Rem: Remdesivir, sc: subcutaneous.
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    SSD induces ferroptosis via downregulation of GPX4 through ER stress. (A) Western blot analysis of GPX4 in PDO and A549 cells treated with 2 µM SSD and control groups, β-Actin was used as a loading control. (B) Statistical analysis of GPX4 expression levels from three independent experiments ( n = 3). (C) Molecular docking of SSD and <t>ATF3</t> protein. (D) DARTS-Western blot analysis showed the resistance of ATF to pronase E digestion under the treatment of SSD (10 µM), n = 3. (E) RT-qPCR analysis of mRNA expression levels of PDO-related genes ATF3 , CHOP , and CHAC1 treatment with SSD ( n = 3). (F , G) Western blot analysis of protein expression (ATF3, CHOP, CHAC1) in A549 cells and PDOs after treatment with 2 µM SSD( n = 3). (H) Mechanism of SSD acting on lung adenocarcinoma. (Data are presented as mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001). ER, endoplasmic reticulum; PDO, patient-derived organoids; SSD, saikosaponin D. SD, standard deviation.
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    SSD induces ferroptosis via downregulation of GPX4 through ER stress. (A) Western blot analysis of GPX4 in PDO and A549 cells treated with 2 µM SSD and control groups, β-Actin was used as a loading control. (B) Statistical analysis of GPX4 expression levels from three independent experiments ( n = 3). (C) Molecular docking of SSD and <t>ATF3</t> protein. (D) DARTS-Western blot analysis showed the resistance of ATF to pronase E digestion under the treatment of SSD (10 µM), n = 3. (E) RT-qPCR analysis of mRNA expression levels of PDO-related genes ATF3 , CHOP , and CHAC1 treatment with SSD ( n = 3). (F , G) Western blot analysis of protein expression (ATF3, CHOP, CHAC1) in A549 cells and PDOs after treatment with 2 µM SSD( n = 3). (H) Mechanism of SSD acting on lung adenocarcinoma. (Data are presented as mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001). ER, endoplasmic reticulum; PDO, patient-derived organoids; SSD, saikosaponin D. SD, standard deviation.
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    Image Search Results


    (A-B) Volcano plots of whole-transcriptome differentially expressed genes (DEGs) identified by RNAseq in ST88-14 and NF90.8 cells following siRNA-mediated depletion of ZNF423 ( n =3) compared to control ( n =3). Dashed vertical lines reflect log 2 FC of −1 and 1. Dashed horizontal line reflects false discovery rate (FDR) of 0.05. Downregulated genes with log 2 FC≤-1 and -log 10 adjusted p-value above FDR threshold are denoted in blue. Upregulated genes log 2 FC≥1 and -log 10 adjusted p-value above FDR threshold are denoted in red. Raw RNAseq hit counts for ZNF423 in NF90.8 cells transfected with control siRNA ( n =3) or siZNF423 ( n =3). P-values represent unpaired, two-tailed t-tests between groups. (C) Venn diagram showing overlap of significantly downregulated DEGs common among ST88-14 and NF90.8 cell lines. Downregulated DEGs were defined as log 2 FC≥-1 and adjusted p-value of ≤0.05. (D) Dot plot of top enriched Hallmark gene signatures of shared downregulated genes (FDR≤0.05). (E) Venn diagram showing overlap of significantly upregulated DEGs common among ST88-14 and NF90.8 cell lines. Upregulated DEGs were defined as log 2 FC≥1 and adjusted p-value of ≤0.05. (F) Dot plot of top enriched Hallmark gene signatures of shared upregulated genes (FDR≤0.05). (G-H) Volcano plots of differentially expressed transcription factors and kinases in ST88-14 and NF90.8 cells following siRNA-mediated depletion of ZNF423 compared to control. (I-J) Immunoblots showing cleavage of PARP, ATF3, ATF4 and ZNF423 protein expression following siRNA-mediated depletion of ZNF423 ( n =3) compared to controls ( n =3). GAPDH serves as loading control. Protein expression was normalized to total protein and quantified using ImageJ. Error bars reflect SEM. P-values represent unpaired, two-tailed t test with Welch’s correction. ****=p-value ≤0.0001, ***=p-value≤0.001, **=p-value≤0.01, *=p-value≤0.05, ns=not significant.

    Journal: bioRxiv

    Article Title: ZNF423 depletion induces the integrated stress response and represents a potential vulnerability in NF1-associated MPNST

    doi: 10.64898/2026.03.03.709360

    Figure Lengend Snippet: (A-B) Volcano plots of whole-transcriptome differentially expressed genes (DEGs) identified by RNAseq in ST88-14 and NF90.8 cells following siRNA-mediated depletion of ZNF423 ( n =3) compared to control ( n =3). Dashed vertical lines reflect log 2 FC of −1 and 1. Dashed horizontal line reflects false discovery rate (FDR) of 0.05. Downregulated genes with log 2 FC≤-1 and -log 10 adjusted p-value above FDR threshold are denoted in blue. Upregulated genes log 2 FC≥1 and -log 10 adjusted p-value above FDR threshold are denoted in red. Raw RNAseq hit counts for ZNF423 in NF90.8 cells transfected with control siRNA ( n =3) or siZNF423 ( n =3). P-values represent unpaired, two-tailed t-tests between groups. (C) Venn diagram showing overlap of significantly downregulated DEGs common among ST88-14 and NF90.8 cell lines. Downregulated DEGs were defined as log 2 FC≥-1 and adjusted p-value of ≤0.05. (D) Dot plot of top enriched Hallmark gene signatures of shared downregulated genes (FDR≤0.05). (E) Venn diagram showing overlap of significantly upregulated DEGs common among ST88-14 and NF90.8 cell lines. Upregulated DEGs were defined as log 2 FC≥1 and adjusted p-value of ≤0.05. (F) Dot plot of top enriched Hallmark gene signatures of shared upregulated genes (FDR≤0.05). (G-H) Volcano plots of differentially expressed transcription factors and kinases in ST88-14 and NF90.8 cells following siRNA-mediated depletion of ZNF423 compared to control. (I-J) Immunoblots showing cleavage of PARP, ATF3, ATF4 and ZNF423 protein expression following siRNA-mediated depletion of ZNF423 ( n =3) compared to controls ( n =3). GAPDH serves as loading control. Protein expression was normalized to total protein and quantified using ImageJ. Error bars reflect SEM. P-values represent unpaired, two-tailed t test with Welch’s correction. ****=p-value ≤0.0001, ***=p-value≤0.001, **=p-value≤0.01, *=p-value≤0.05, ns=not significant.

    Article Snippet: Immunoblots were performed using primary antibodies against ZNF423 (ABN410, Sigma-Aldrich), GAPDH (sc-365062, Santa Cruz Biotechnology), SUZ12 (3737S, Cell Signaling Technology), ATF3 (18665S, Cell Signaling Technology), ATF4 (11815S, Cell Signaling Technology), PARP (9542S, Cell Signaling Technology), and γH2A.x (9718S, Cell Signaling Technology).

    Techniques: RNA sequencing, Control, Transfection, Two Tailed Test, Western Blot, Expressing

    The results of western blotting (A) . The protein levels of ATF3 (B) , p-p53 (C) , p-p21 (D) , and cas3 (E) were represented in the studied groups. β-actin was used as an internal control. cas3: caspase-3, ip: intraperitoneal, I/R: ischemia/reperfusion, NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells, Rem: Remdesivir, sc: subcutaneous.

    Journal: PLOS One

    Article Title: Remdesivir may exacerbate ischemic acute kidney injury through molecular alterations in PGC-1α and apoptosis pathways: An in vivo study

    doi: 10.1371/journal.pone.0336221

    Figure Lengend Snippet: The results of western blotting (A) . The protein levels of ATF3 (B) , p-p53 (C) , p-p21 (D) , and cas3 (E) were represented in the studied groups. β-actin was used as an internal control. cas3: caspase-3, ip: intraperitoneal, I/R: ischemia/reperfusion, NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells, Rem: Remdesivir, sc: subcutaneous.

    Article Snippet: Monoclonal antibodies were against PGC-1α (ab54481, Abcam), NF-κB p65 (ab16502, Abcam), Drp-1 (sc-271583), ATF3 (sc-518032), p-p53 (sc-377553), p-p21 (sc-377569), and caspase-3 (sc-7272) (Santa Cruz Biotechnology, Inc).

    Techniques: Western Blot, Control

    SSD induces ferroptosis via downregulation of GPX4 through ER stress. (A) Western blot analysis of GPX4 in PDO and A549 cells treated with 2 µM SSD and control groups, β-Actin was used as a loading control. (B) Statistical analysis of GPX4 expression levels from three independent experiments ( n = 3). (C) Molecular docking of SSD and ATF3 protein. (D) DARTS-Western blot analysis showed the resistance of ATF to pronase E digestion under the treatment of SSD (10 µM), n = 3. (E) RT-qPCR analysis of mRNA expression levels of PDO-related genes ATF3 , CHOP , and CHAC1 treatment with SSD ( n = 3). (F , G) Western blot analysis of protein expression (ATF3, CHOP, CHAC1) in A549 cells and PDOs after treatment with 2 µM SSD( n = 3). (H) Mechanism of SSD acting on lung adenocarcinoma. (Data are presented as mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001). ER, endoplasmic reticulum; PDO, patient-derived organoids; SSD, saikosaponin D. SD, standard deviation.

    Journal: Scientific Reports

    Article Title: Mechanism of Saikosaponin D in regulating ferroptosis in patient-derived lung adenocarcinoma organoids via upregulation of ATF3/CHOP/CHAC1 signaling

    doi: 10.1038/s41598-025-27251-y

    Figure Lengend Snippet: SSD induces ferroptosis via downregulation of GPX4 through ER stress. (A) Western blot analysis of GPX4 in PDO and A549 cells treated with 2 µM SSD and control groups, β-Actin was used as a loading control. (B) Statistical analysis of GPX4 expression levels from three independent experiments ( n = 3). (C) Molecular docking of SSD and ATF3 protein. (D) DARTS-Western blot analysis showed the resistance of ATF to pronase E digestion under the treatment of SSD (10 µM), n = 3. (E) RT-qPCR analysis of mRNA expression levels of PDO-related genes ATF3 , CHOP , and CHAC1 treatment with SSD ( n = 3). (F , G) Western blot analysis of protein expression (ATF3, CHOP, CHAC1) in A549 cells and PDOs after treatment with 2 µM SSD( n = 3). (H) Mechanism of SSD acting on lung adenocarcinoma. (Data are presented as mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001). ER, endoplasmic reticulum; PDO, patient-derived organoids; SSD, saikosaponin D. SD, standard deviation.

    Article Snippet: Then blocked with 5% BSA for 1 h. Reaction with specific antibodies against the following proteins: β-Actin (A00730, Genscript, China), ATF3 (DF3110, Affinity, USA), GPX4 (ET1706-45, HUABIO, China), CHOP (15204-AF6277, Affinity, USA), and CHAC1 (15207-1-AP, Proteintech, China).

    Techniques: Western Blot, Control, Expressing, Quantitative RT-PCR, Derivative Assay, Standard Deviation