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tide analysis webtool  (Brinkmann Instruments)

 
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    Brinkmann Instruments tide analysis webtool
    Tide Analysis Webtool, supplied by Brinkmann Instruments, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tide/analysis+tide/pm42315647-443-8-13
    Average 86 stars, based on 1 article reviews
    tide analysis webtool - by Bioz Stars, 2026-10
    86/100 stars

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    Related Articles

    Software:

    Article Title: SACF and GILA assays on AML12 cells show limited predictive value for mouse liver genotoxicity
    Article Snippet: Hepatocellular carcinoma (HCC) has been observed in neonatal mice following the integration of recombinant Adeno-Associated Viruses (rAAV) into the Rian locus. rAAV-related oncogenic risk for patients remains unclear, and the lack of relevant in vitro methods hinders its proper assessment.. The soft agar colony-forming (SACF) assay and the growth in low attachment assay (GILA) monitor anchorage-independent growth, a hallmark of transformed adherent cells, and have been previously proposed to assess the tumorigenicity of CRISPR/Cas9edited human MCF10A cells.. Here, we introduce murine versions of SACF and GILA as surrogate in vitro systems to evaluate the risk of HCC development following genome editing or rAAV induced insertional mutagenesis.

    Polymerase Chain Reaction:

    Article Title: High-efficiency and multi-locus targeted integration in CHO cells using CRISPR-mediated donor nicking and DNA repair inhibitors
    Article Snippet: Golden gate assemblies were performed using PaqCI with PaqCI activator (NEB) in CutSmart buffer supplemented with ATP. .. The sequences of DNA oligos used to perform T7 endonuclease I (T7E1) mismatch detection assays, TIDE (Tracking of Indels by DEcomposition) analyses ( Brinkman et al., 2014 ), integration junction PCR, and amplification of homology arms from genomic DNA (gDNA) are provided in Supporting Information : Table S2 . ..

    Amplification:

    Article Title: High-efficiency and multi-locus targeted integration in CHO cells using CRISPR-mediated donor nicking and DNA repair inhibitors
    Article Snippet: Golden gate assemblies were performed using PaqCI with PaqCI activator (NEB) in CutSmart buffer supplemented with ATP. .. The sequences of DNA oligos used to perform T7 endonuclease I (T7E1) mismatch detection assays, TIDE (Tracking of Indels by DEcomposition) analyses ( Brinkman et al., 2014 ), integration junction PCR, and amplification of homology arms from genomic DNA (gDNA) are provided in Supporting Information : Table S2 . ..



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    CRISPR-Cas9 loss-of-function validation of the SMARCAL1–ferroptosis–chemokine axis and integrated mechanistic model. (a) SMARCAL1 knockout validation in A549 and H1299 NSCLC cell lines: anti-SMARCAL1 immunoblot (115 kDa; GAPDH loading control 37 kDa) demonstrating absence of SMARCAL1 protein in sgSMARCAL1-1 and sgSMARCAL1-2 versus sgScramble; Sanger sequencing chromatograms of indel-introduced sgSMARCAL1 target locus within SMARCAL1 exon 3 region (~150 bp) versus wild-type reference; <t>TIDE</t> indel size distribution (sgSMARCAL1-1 38% efficiency, sgSMARCAL1-2 22% efficiency at predominant indel sizes −5 to −1, +1, +5). (b) Ferroptosis phenotyping after erastin (5 µM, 24 h) in A549 (left) and H1299 (right), expressed as relative value (% sgScramble): cell viability, BODIPY-C11 oxidized/reduced ratio, intracellular Fe 2+ (FerroOrange MFI), malondialdehyde (MDA), reduced glutathione (GSH), and TEM ferroptotic mitochondrial percent. SMARCAL1-KO cells (sgSMARCAL1-1, -2) show resistance to erastin-induced ferroptosis; ***P < 0.001 versus sgScramble. Lower rescue panel (A549): wild-type SMARCAL1 reconstitution fully rescues ferroptosis susceptibility (viability 31% sgScramble baseline); helicase-dead R764Q mutant fails to rescue (viability 74%, no rescue). (c) Chemokine secretion assays. ELISA of CXCL9 and CXCL10 (pg/mL) <t>and</t> <t>qRT-PCR</t> mRNA fold-change versus baseline in sgScramble (sgScr) versus sgSMARCAL1 (sgSMAR) ± wild-type or R764Q rescue: SMARCAL1 knockout reduces CXCL9 by 62% (1240 → 471 pg/mL) and CXCL10 by 57% (842 → 362 pg/mL) under IFN-γ stimulation; full rescue by wild-type, partial rescue (45% efficiency) by R764Q. ***P < 0.001, **P < 0.01, ns = not significant. (d) Western blot of cGAS-STING-IRF3 pathway activation: phospho-STING Ser366, phospho-TBK1 Ser172, phospho-IRF3 Ser396, with total STING/TBK1/IRF3 and GAPDH loading controls, in sgScr versus sgSMAR ± IFN-γ; quantified bar plots (arbitrary units): p-STING 4.7 → 1.5, p-TBK1 3.9 → 1.4, p-IRF3 5.2 → 1.5, all ***P < 0.001. diABZI rescue panel (10 µM, 6 h): STING agonist diABZI partially restores CXCL9 (64% recovery, 471 → 792 pg/mL) and CXCL10 (58% recovery, 362 → 591 pg/mL) secretion in SMARCAL1-KO cells. (e) Primary human CD8 + T cell transwell chemotaxis (transmigrated CXCR3 + CD8 + cells × 10 3 , mean ± SD across three donors): condition 1 unstimulated (2.1); condition 2 IFN-γ-stimulated sgScramble supernatant (9.8); condition 3 IFN-γ-stimulated sgSMARCAL1 supernatant (4.1, 58% reduction, ***P < 0.001); condition 4 sgScramble supernatant + AMG 487 (1 µM CXCR3 antagonist, 0.9, > 90% blockade); condition 5 isotype control (2); condition 6 H1299 IFN-γ sgScramble (8.2); condition 7 H1299 IFN-γ sgSMARCAL1 (3.9, 52% reduction, ***P < 0.001). ***P < 0.001, ns = not significant. (f) Integrated mechanistic model schematic: replication stress in APOBEC-enriched (high Rad-Score) tumors → SMARCAL1 upregulation (helicase activity-dependent) → ACSL4-dependent phospholipid remodeling and ferroptotic susceptibility → cGAS-STING-IRF3 axis activation amplifying IFN-γ-induced CXCL9/CXCL10 transcription → chemokine gradient recruiting CXCR3 + CD8 + T cells to peritumoral invasive margin → systemic immune priming and sustained post-operative MRD-negative surveillance. Evidence sources annotated per arrow: bulk RNA-seq (transcriptomic), Visium spatial, mIF/IHC (protein), CRISPR (causal), chemotaxis (functional).
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    CRISPR-Cas9 loss-of-function validation of the SMARCAL1–ferroptosis–chemokine axis and integrated mechanistic model. (a) SMARCAL1 knockout validation in A549 and H1299 NSCLC cell lines: anti-SMARCAL1 immunoblot (115 kDa; GAPDH loading control 37 kDa) demonstrating absence of SMARCAL1 protein in sgSMARCAL1-1 and sgSMARCAL1-2 versus sgScramble; Sanger sequencing chromatograms of indel-introduced sgSMARCAL1 target locus within SMARCAL1 exon 3 region (~150 bp) versus wild-type reference; <t>TIDE</t> indel size distribution (sgSMARCAL1-1 38% efficiency, sgSMARCAL1-2 22% efficiency at predominant indel sizes −5 to −1, +1, +5). (b) Ferroptosis phenotyping after erastin (5 µM, 24 h) in A549 (left) and H1299 (right), expressed as relative value (% sgScramble): cell viability, BODIPY-C11 oxidized/reduced ratio, intracellular Fe 2+ (FerroOrange MFI), malondialdehyde (MDA), reduced glutathione (GSH), and TEM ferroptotic mitochondrial percent. SMARCAL1-KO cells (sgSMARCAL1-1, -2) show resistance to erastin-induced ferroptosis; ***P < 0.001 versus sgScramble. Lower rescue panel (A549): wild-type SMARCAL1 reconstitution fully rescues ferroptosis susceptibility (viability 31% sgScramble baseline); helicase-dead R764Q mutant fails to rescue (viability 74%, no rescue). (c) Chemokine secretion assays. ELISA of CXCL9 and CXCL10 (pg/mL) <t>and</t> <t>qRT-PCR</t> mRNA fold-change versus baseline in sgScramble (sgScr) versus sgSMARCAL1 (sgSMAR) ± wild-type or R764Q rescue: SMARCAL1 knockout reduces CXCL9 by 62% (1240 → 471 pg/mL) and CXCL10 by 57% (842 → 362 pg/mL) under IFN-γ stimulation; full rescue by wild-type, partial rescue (45% efficiency) by R764Q. ***P < 0.001, **P < 0.01, ns = not significant. (d) Western blot of cGAS-STING-IRF3 pathway activation: phospho-STING Ser366, phospho-TBK1 Ser172, phospho-IRF3 Ser396, with total STING/TBK1/IRF3 and GAPDH loading controls, in sgScr versus sgSMAR ± IFN-γ; quantified bar plots (arbitrary units): p-STING 4.7 → 1.5, p-TBK1 3.9 → 1.4, p-IRF3 5.2 → 1.5, all ***P < 0.001. diABZI rescue panel (10 µM, 6 h): STING agonist diABZI partially restores CXCL9 (64% recovery, 471 → 792 pg/mL) and CXCL10 (58% recovery, 362 → 591 pg/mL) secretion in SMARCAL1-KO cells. (e) Primary human CD8 + T cell transwell chemotaxis (transmigrated CXCR3 + CD8 + cells × 10 3 , mean ± SD across three donors): condition 1 unstimulated (2.1); condition 2 IFN-γ-stimulated sgScramble supernatant (9.8); condition 3 IFN-γ-stimulated sgSMARCAL1 supernatant (4.1, 58% reduction, ***P < 0.001); condition 4 sgScramble supernatant + AMG 487 (1 µM CXCR3 antagonist, 0.9, > 90% blockade); condition 5 isotype control (2); condition 6 H1299 IFN-γ sgScramble (8.2); condition 7 H1299 IFN-γ sgSMARCAL1 (3.9, 52% reduction, ***P < 0.001). ***P < 0.001, ns = not significant. (f) Integrated mechanistic model schematic: replication stress in APOBEC-enriched (high Rad-Score) tumors → SMARCAL1 upregulation (helicase activity-dependent) → ACSL4-dependent phospholipid remodeling and ferroptotic susceptibility → cGAS-STING-IRF3 axis activation amplifying IFN-γ-induced CXCL9/CXCL10 transcription → chemokine gradient recruiting CXCR3 + CD8 + T cells to peritumoral invasive margin → systemic immune priming and sustained post-operative MRD-negative surveillance. Evidence sources annotated per arrow: bulk RNA-seq (transcriptomic), Visium spatial, mIF/IHC (protein), CRISPR (causal), chemotaxis (functional).
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    CRISPR-Cas9 loss-of-function validation of the SMARCAL1–ferroptosis–chemokine axis and integrated mechanistic model. (a) SMARCAL1 knockout validation in A549 and H1299 NSCLC cell lines: anti-SMARCAL1 immunoblot (115 kDa; GAPDH loading control 37 kDa) demonstrating absence of SMARCAL1 protein in sgSMARCAL1-1 and sgSMARCAL1-2 versus sgScramble; Sanger sequencing chromatograms of indel-introduced sgSMARCAL1 target locus within SMARCAL1 exon 3 region (~150 bp) versus wild-type reference; <t>TIDE</t> indel size distribution (sgSMARCAL1-1 38% efficiency, sgSMARCAL1-2 22% efficiency at predominant indel sizes −5 to −1, +1, +5). (b) Ferroptosis phenotyping after erastin (5 µM, 24 h) in A549 (left) and H1299 (right), expressed as relative value (% sgScramble): cell viability, BODIPY-C11 oxidized/reduced ratio, intracellular Fe 2+ (FerroOrange MFI), malondialdehyde (MDA), reduced glutathione (GSH), and TEM ferroptotic mitochondrial percent. SMARCAL1-KO cells (sgSMARCAL1-1, -2) show resistance to erastin-induced ferroptosis; ***P < 0.001 versus sgScramble. Lower rescue panel (A549): wild-type SMARCAL1 reconstitution fully rescues ferroptosis susceptibility (viability 31% sgScramble baseline); helicase-dead R764Q mutant fails to rescue (viability 74%, no rescue). (c) Chemokine secretion assays. ELISA of CXCL9 and CXCL10 (pg/mL) <t>and</t> <t>qRT-PCR</t> mRNA fold-change versus baseline in sgScramble (sgScr) versus sgSMARCAL1 (sgSMAR) ± wild-type or R764Q rescue: SMARCAL1 knockout reduces CXCL9 by 62% (1240 → 471 pg/mL) and CXCL10 by 57% (842 → 362 pg/mL) under IFN-γ stimulation; full rescue by wild-type, partial rescue (45% efficiency) by R764Q. ***P < 0.001, **P < 0.01, ns = not significant. (d) Western blot of cGAS-STING-IRF3 pathway activation: phospho-STING Ser366, phospho-TBK1 Ser172, phospho-IRF3 Ser396, with total STING/TBK1/IRF3 and GAPDH loading controls, in sgScr versus sgSMAR ± IFN-γ; quantified bar plots (arbitrary units): p-STING 4.7 → 1.5, p-TBK1 3.9 → 1.4, p-IRF3 5.2 → 1.5, all ***P < 0.001. diABZI rescue panel (10 µM, 6 h): STING agonist diABZI partially restores CXCL9 (64% recovery, 471 → 792 pg/mL) and CXCL10 (58% recovery, 362 → 591 pg/mL) secretion in SMARCAL1-KO cells. (e) Primary human CD8 + T cell transwell chemotaxis (transmigrated CXCR3 + CD8 + cells × 10 3 , mean ± SD across three donors): condition 1 unstimulated (2.1); condition 2 IFN-γ-stimulated sgScramble supernatant (9.8); condition 3 IFN-γ-stimulated sgSMARCAL1 supernatant (4.1, 58% reduction, ***P < 0.001); condition 4 sgScramble supernatant + AMG 487 (1 µM CXCR3 antagonist, 0.9, > 90% blockade); condition 5 isotype control (2); condition 6 H1299 IFN-γ sgScramble (8.2); condition 7 H1299 IFN-γ sgSMARCAL1 (3.9, 52% reduction, ***P < 0.001). ***P < 0.001, ns = not significant. (f) Integrated mechanistic model schematic: replication stress in APOBEC-enriched (high Rad-Score) tumors → SMARCAL1 upregulation (helicase activity-dependent) → ACSL4-dependent phospholipid remodeling and ferroptotic susceptibility → cGAS-STING-IRF3 axis activation amplifying IFN-γ-induced CXCL9/CXCL10 transcription → chemokine gradient recruiting CXCR3 + CD8 + T cells to peritumoral invasive margin → systemic immune priming and sustained post-operative MRD-negative surveillance. Evidence sources annotated per arrow: bulk RNA-seq (transcriptomic), Visium spatial, mIF/IHC (protein), CRISPR (causal), chemotaxis (functional).
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    CRISPR-Cas9 loss-of-function validation of the SMARCAL1–ferroptosis–chemokine axis and integrated mechanistic model. (a) SMARCAL1 knockout validation in A549 and H1299 NSCLC cell lines: anti-SMARCAL1 immunoblot (115 kDa; GAPDH loading control 37 kDa) demonstrating absence of SMARCAL1 protein in sgSMARCAL1-1 and sgSMARCAL1-2 versus sgScramble; Sanger sequencing chromatograms of indel-introduced sgSMARCAL1 target locus within SMARCAL1 exon 3 region (~150 bp) versus wild-type reference; <t>TIDE</t> indel size distribution (sgSMARCAL1-1 38% efficiency, sgSMARCAL1-2 22% efficiency at predominant indel sizes −5 to −1, +1, +5). (b) Ferroptosis phenotyping after erastin (5 µM, 24 h) in A549 (left) and H1299 (right), expressed as relative value (% sgScramble): cell viability, BODIPY-C11 oxidized/reduced ratio, intracellular Fe 2+ (FerroOrange MFI), malondialdehyde (MDA), reduced glutathione (GSH), and TEM ferroptotic mitochondrial percent. SMARCAL1-KO cells (sgSMARCAL1-1, -2) show resistance to erastin-induced ferroptosis; ***P < 0.001 versus sgScramble. Lower rescue panel (A549): wild-type SMARCAL1 reconstitution fully rescues ferroptosis susceptibility (viability 31% sgScramble baseline); helicase-dead R764Q mutant fails to rescue (viability 74%, no rescue). (c) Chemokine secretion assays. ELISA of CXCL9 and CXCL10 (pg/mL) <t>and</t> <t>qRT-PCR</t> mRNA fold-change versus baseline in sgScramble (sgScr) versus sgSMARCAL1 (sgSMAR) ± wild-type or R764Q rescue: SMARCAL1 knockout reduces CXCL9 by 62% (1240 → 471 pg/mL) and CXCL10 by 57% (842 → 362 pg/mL) under IFN-γ stimulation; full rescue by wild-type, partial rescue (45% efficiency) by R764Q. ***P < 0.001, **P < 0.01, ns = not significant. (d) Western blot of cGAS-STING-IRF3 pathway activation: phospho-STING Ser366, phospho-TBK1 Ser172, phospho-IRF3 Ser396, with total STING/TBK1/IRF3 and GAPDH loading controls, in sgScr versus sgSMAR ± IFN-γ; quantified bar plots (arbitrary units): p-STING 4.7 → 1.5, p-TBK1 3.9 → 1.4, p-IRF3 5.2 → 1.5, all ***P < 0.001. diABZI rescue panel (10 µM, 6 h): STING agonist diABZI partially restores CXCL9 (64% recovery, 471 → 792 pg/mL) and CXCL10 (58% recovery, 362 → 591 pg/mL) secretion in SMARCAL1-KO cells. (e) Primary human CD8 + T cell transwell chemotaxis (transmigrated CXCR3 + CD8 + cells × 10 3 , mean ± SD across three donors): condition 1 unstimulated (2.1); condition 2 IFN-γ-stimulated sgScramble supernatant (9.8); condition 3 IFN-γ-stimulated sgSMARCAL1 supernatant (4.1, 58% reduction, ***P < 0.001); condition 4 sgScramble supernatant + AMG 487 (1 µM CXCR3 antagonist, 0.9, > 90% blockade); condition 5 isotype control (2); condition 6 H1299 IFN-γ sgScramble (8.2); condition 7 H1299 IFN-γ sgSMARCAL1 (3.9, 52% reduction, ***P < 0.001). ***P < 0.001, ns = not significant. (f) Integrated mechanistic model schematic: replication stress in APOBEC-enriched (high Rad-Score) tumors → SMARCAL1 upregulation (helicase activity-dependent) → ACSL4-dependent phospholipid remodeling and ferroptotic susceptibility → cGAS-STING-IRF3 axis activation amplifying IFN-γ-induced CXCL9/CXCL10 transcription → chemokine gradient recruiting CXCR3 + CD8 + T cells to peritumoral invasive margin → systemic immune priming and sustained post-operative MRD-negative surveillance. Evidence sources annotated per arrow: bulk RNA-seq (transcriptomic), Visium spatial, mIF/IHC (protein), CRISPR (causal), chemotaxis (functional).
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    CRISPR-Cas9 loss-of-function validation of the SMARCAL1–ferroptosis–chemokine axis and integrated mechanistic model. (a) SMARCAL1 knockout validation in A549 and H1299 NSCLC cell lines: anti-SMARCAL1 immunoblot (115 kDa; GAPDH loading control 37 kDa) demonstrating absence of SMARCAL1 protein in sgSMARCAL1-1 and sgSMARCAL1-2 versus sgScramble; Sanger sequencing chromatograms of indel-introduced sgSMARCAL1 target locus within SMARCAL1 exon 3 region (~150 bp) versus wild-type reference; <t>TIDE</t> indel size distribution (sgSMARCAL1-1 38% efficiency, sgSMARCAL1-2 22% efficiency at predominant indel sizes −5 to −1, +1, +5). (b) Ferroptosis phenotyping after erastin (5 µM, 24 h) in A549 (left) and H1299 (right), expressed as relative value (% sgScramble): cell viability, BODIPY-C11 oxidized/reduced ratio, intracellular Fe 2+ (FerroOrange MFI), malondialdehyde (MDA), reduced glutathione (GSH), and TEM ferroptotic mitochondrial percent. SMARCAL1-KO cells (sgSMARCAL1-1, -2) show resistance to erastin-induced ferroptosis; ***P < 0.001 versus sgScramble. Lower rescue panel (A549): wild-type SMARCAL1 reconstitution fully rescues ferroptosis susceptibility (viability 31% sgScramble baseline); helicase-dead R764Q mutant fails to rescue (viability 74%, no rescue). (c) Chemokine secretion assays. ELISA of CXCL9 and CXCL10 (pg/mL) <t>and</t> <t>qRT-PCR</t> mRNA fold-change versus baseline in sgScramble (sgScr) versus sgSMARCAL1 (sgSMAR) ± wild-type or R764Q rescue: SMARCAL1 knockout reduces CXCL9 by 62% (1240 → 471 pg/mL) and CXCL10 by 57% (842 → 362 pg/mL) under IFN-γ stimulation; full rescue by wild-type, partial rescue (45% efficiency) by R764Q. ***P < 0.001, **P < 0.01, ns = not significant. (d) Western blot of cGAS-STING-IRF3 pathway activation: phospho-STING Ser366, phospho-TBK1 Ser172, phospho-IRF3 Ser396, with total STING/TBK1/IRF3 and GAPDH loading controls, in sgScr versus sgSMAR ± IFN-γ; quantified bar plots (arbitrary units): p-STING 4.7 → 1.5, p-TBK1 3.9 → 1.4, p-IRF3 5.2 → 1.5, all ***P < 0.001. diABZI rescue panel (10 µM, 6 h): STING agonist diABZI partially restores CXCL9 (64% recovery, 471 → 792 pg/mL) and CXCL10 (58% recovery, 362 → 591 pg/mL) secretion in SMARCAL1-KO cells. (e) Primary human CD8 + T cell transwell chemotaxis (transmigrated CXCR3 + CD8 + cells × 10 3 , mean ± SD across three donors): condition 1 unstimulated (2.1); condition 2 IFN-γ-stimulated sgScramble supernatant (9.8); condition 3 IFN-γ-stimulated sgSMARCAL1 supernatant (4.1, 58% reduction, ***P < 0.001); condition 4 sgScramble supernatant + AMG 487 (1 µM CXCR3 antagonist, 0.9, > 90% blockade); condition 5 isotype control (2); condition 6 H1299 IFN-γ sgScramble (8.2); condition 7 H1299 IFN-γ sgSMARCAL1 (3.9, 52% reduction, ***P < 0.001). ***P < 0.001, ns = not significant. (f) Integrated mechanistic model schematic: replication stress in APOBEC-enriched (high Rad-Score) tumors → SMARCAL1 upregulation (helicase activity-dependent) → ACSL4-dependent phospholipid remodeling and ferroptotic susceptibility → cGAS-STING-IRF3 axis activation amplifying IFN-γ-induced CXCL9/CXCL10 transcription → chemokine gradient recruiting CXCR3 + CD8 + T cells to peritumoral invasive margin → systemic immune priming and sustained post-operative MRD-negative surveillance. Evidence sources annotated per arrow: bulk RNA-seq (transcriptomic), Visium spatial, mIF/IHC (protein), CRISPR (causal), chemotaxis (functional).
    Dna Tide Sequencing Analysis, supplied by Brinkmann Instruments, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    tide  (Brinkmann Instruments)
    86
    Brinkmann Instruments tide
    CRISPR-Cas9 loss-of-function validation of the SMARCAL1–ferroptosis–chemokine axis and integrated mechanistic model. (a) SMARCAL1 knockout validation in A549 and H1299 NSCLC cell lines: anti-SMARCAL1 immunoblot (115 kDa; GAPDH loading control 37 kDa) demonstrating absence of SMARCAL1 protein in sgSMARCAL1-1 and sgSMARCAL1-2 versus sgScramble; Sanger sequencing chromatograms of indel-introduced sgSMARCAL1 target locus within SMARCAL1 exon 3 region (~150 bp) versus wild-type reference; <t>TIDE</t> indel size distribution (sgSMARCAL1-1 38% efficiency, sgSMARCAL1-2 22% efficiency at predominant indel sizes −5 to −1, +1, +5). (b) Ferroptosis phenotyping after erastin (5 µM, 24 h) in A549 (left) and H1299 (right), expressed as relative value (% sgScramble): cell viability, BODIPY-C11 oxidized/reduced ratio, intracellular Fe 2+ (FerroOrange MFI), malondialdehyde (MDA), reduced glutathione (GSH), and TEM ferroptotic mitochondrial percent. SMARCAL1-KO cells (sgSMARCAL1-1, -2) show resistance to erastin-induced ferroptosis; ***P < 0.001 versus sgScramble. Lower rescue panel (A549): wild-type SMARCAL1 reconstitution fully rescues ferroptosis susceptibility (viability 31% sgScramble baseline); helicase-dead R764Q mutant fails to rescue (viability 74%, no rescue). (c) Chemokine secretion assays. ELISA of CXCL9 and CXCL10 (pg/mL) <t>and</t> <t>qRT-PCR</t> mRNA fold-change versus baseline in sgScramble (sgScr) versus sgSMARCAL1 (sgSMAR) ± wild-type or R764Q rescue: SMARCAL1 knockout reduces CXCL9 by 62% (1240 → 471 pg/mL) and CXCL10 by 57% (842 → 362 pg/mL) under IFN-γ stimulation; full rescue by wild-type, partial rescue (45% efficiency) by R764Q. ***P < 0.001, **P < 0.01, ns = not significant. (d) Western blot of cGAS-STING-IRF3 pathway activation: phospho-STING Ser366, phospho-TBK1 Ser172, phospho-IRF3 Ser396, with total STING/TBK1/IRF3 and GAPDH loading controls, in sgScr versus sgSMAR ± IFN-γ; quantified bar plots (arbitrary units): p-STING 4.7 → 1.5, p-TBK1 3.9 → 1.4, p-IRF3 5.2 → 1.5, all ***P < 0.001. diABZI rescue panel (10 µM, 6 h): STING agonist diABZI partially restores CXCL9 (64% recovery, 471 → 792 pg/mL) and CXCL10 (58% recovery, 362 → 591 pg/mL) secretion in SMARCAL1-KO cells. (e) Primary human CD8 + T cell transwell chemotaxis (transmigrated CXCR3 + CD8 + cells × 10 3 , mean ± SD across three donors): condition 1 unstimulated (2.1); condition 2 IFN-γ-stimulated sgScramble supernatant (9.8); condition 3 IFN-γ-stimulated sgSMARCAL1 supernatant (4.1, 58% reduction, ***P < 0.001); condition 4 sgScramble supernatant + AMG 487 (1 µM CXCR3 antagonist, 0.9, > 90% blockade); condition 5 isotype control (2); condition 6 H1299 IFN-γ sgScramble (8.2); condition 7 H1299 IFN-γ sgSMARCAL1 (3.9, 52% reduction, ***P < 0.001). ***P < 0.001, ns = not significant. (f) Integrated mechanistic model schematic: replication stress in APOBEC-enriched (high Rad-Score) tumors → SMARCAL1 upregulation (helicase activity-dependent) → ACSL4-dependent phospholipid remodeling and ferroptotic susceptibility → cGAS-STING-IRF3 axis activation amplifying IFN-γ-induced CXCL9/CXCL10 transcription → chemokine gradient recruiting CXCR3 + CD8 + T cells to peritumoral invasive margin → systemic immune priming and sustained post-operative MRD-negative surveillance. Evidence sources annotated per arrow: bulk RNA-seq (transcriptomic), Visium spatial, mIF/IHC (protein), CRISPR (causal), chemotaxis (functional).
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    intelligence red tide early warning  (Qinhuangdao Lihua Starch Co Ltd)
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    Qinhuangdao Lihua Starch Co Ltd intelligence red tide early warning
    CRISPR-Cas9 loss-of-function validation of the SMARCAL1–ferroptosis–chemokine axis and integrated mechanistic model. (a) SMARCAL1 knockout validation in A549 and H1299 NSCLC cell lines: anti-SMARCAL1 immunoblot (115 kDa; GAPDH loading control 37 kDa) demonstrating absence of SMARCAL1 protein in sgSMARCAL1-1 and sgSMARCAL1-2 versus sgScramble; Sanger sequencing chromatograms of indel-introduced sgSMARCAL1 target locus within SMARCAL1 exon 3 region (~150 bp) versus wild-type reference; <t>TIDE</t> indel size distribution (sgSMARCAL1-1 38% efficiency, sgSMARCAL1-2 22% efficiency at predominant indel sizes −5 to −1, +1, +5). (b) Ferroptosis phenotyping after erastin (5 µM, 24 h) in A549 (left) and H1299 (right), expressed as relative value (% sgScramble): cell viability, BODIPY-C11 oxidized/reduced ratio, intracellular Fe 2+ (FerroOrange MFI), malondialdehyde (MDA), reduced glutathione (GSH), and TEM ferroptotic mitochondrial percent. SMARCAL1-KO cells (sgSMARCAL1-1, -2) show resistance to erastin-induced ferroptosis; ***P < 0.001 versus sgScramble. Lower rescue panel (A549): wild-type SMARCAL1 reconstitution fully rescues ferroptosis susceptibility (viability 31% sgScramble baseline); helicase-dead R764Q mutant fails to rescue (viability 74%, no rescue). (c) Chemokine secretion assays. ELISA of CXCL9 and CXCL10 (pg/mL) <t>and</t> <t>qRT-PCR</t> mRNA fold-change versus baseline in sgScramble (sgScr) versus sgSMARCAL1 (sgSMAR) ± wild-type or R764Q rescue: SMARCAL1 knockout reduces CXCL9 by 62% (1240 → 471 pg/mL) and CXCL10 by 57% (842 → 362 pg/mL) under IFN-γ stimulation; full rescue by wild-type, partial rescue (45% efficiency) by R764Q. ***P < 0.001, **P < 0.01, ns = not significant. (d) Western blot of cGAS-STING-IRF3 pathway activation: phospho-STING Ser366, phospho-TBK1 Ser172, phospho-IRF3 Ser396, with total STING/TBK1/IRF3 and GAPDH loading controls, in sgScr versus sgSMAR ± IFN-γ; quantified bar plots (arbitrary units): p-STING 4.7 → 1.5, p-TBK1 3.9 → 1.4, p-IRF3 5.2 → 1.5, all ***P < 0.001. diABZI rescue panel (10 µM, 6 h): STING agonist diABZI partially restores CXCL9 (64% recovery, 471 → 792 pg/mL) and CXCL10 (58% recovery, 362 → 591 pg/mL) secretion in SMARCAL1-KO cells. (e) Primary human CD8 + T cell transwell chemotaxis (transmigrated CXCR3 + CD8 + cells × 10 3 , mean ± SD across three donors): condition 1 unstimulated (2.1); condition 2 IFN-γ-stimulated sgScramble supernatant (9.8); condition 3 IFN-γ-stimulated sgSMARCAL1 supernatant (4.1, 58% reduction, ***P < 0.001); condition 4 sgScramble supernatant + AMG 487 (1 µM CXCR3 antagonist, 0.9, > 90% blockade); condition 5 isotype control (2); condition 6 H1299 IFN-γ sgScramble (8.2); condition 7 H1299 IFN-γ sgSMARCAL1 (3.9, 52% reduction, ***P < 0.001). ***P < 0.001, ns = not significant. (f) Integrated mechanistic model schematic: replication stress in APOBEC-enriched (high Rad-Score) tumors → SMARCAL1 upregulation (helicase activity-dependent) → ACSL4-dependent phospholipid remodeling and ferroptotic susceptibility → cGAS-STING-IRF3 axis activation amplifying IFN-γ-induced CXCL9/CXCL10 transcription → chemokine gradient recruiting CXCR3 + CD8 + T cells to peritumoral invasive margin → systemic immune priming and sustained post-operative MRD-negative surveillance. Evidence sources annotated per arrow: bulk RNA-seq (transcriptomic), Visium spatial, mIF/IHC (protein), CRISPR (causal), chemotaxis (functional).
    Intelligence Red Tide Early Warning, supplied by Qinhuangdao Lihua Starch Co Ltd, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    CRISPR-Cas9 loss-of-function validation of the SMARCAL1–ferroptosis–chemokine axis and integrated mechanistic model. (a) SMARCAL1 knockout validation in A549 and H1299 NSCLC cell lines: anti-SMARCAL1 immunoblot (115 kDa; GAPDH loading control 37 kDa) demonstrating absence of SMARCAL1 protein in sgSMARCAL1-1 and sgSMARCAL1-2 versus sgScramble; Sanger sequencing chromatograms of indel-introduced sgSMARCAL1 target locus within SMARCAL1 exon 3 region (~150 bp) versus wild-type reference; TIDE indel size distribution (sgSMARCAL1-1 38% efficiency, sgSMARCAL1-2 22% efficiency at predominant indel sizes −5 to −1, +1, +5). (b) Ferroptosis phenotyping after erastin (5 µM, 24 h) in A549 (left) and H1299 (right), expressed as relative value (% sgScramble): cell viability, BODIPY-C11 oxidized/reduced ratio, intracellular Fe 2+ (FerroOrange MFI), malondialdehyde (MDA), reduced glutathione (GSH), and TEM ferroptotic mitochondrial percent. SMARCAL1-KO cells (sgSMARCAL1-1, -2) show resistance to erastin-induced ferroptosis; ***P < 0.001 versus sgScramble. Lower rescue panel (A549): wild-type SMARCAL1 reconstitution fully rescues ferroptosis susceptibility (viability 31% sgScramble baseline); helicase-dead R764Q mutant fails to rescue (viability 74%, no rescue). (c) Chemokine secretion assays. ELISA of CXCL9 and CXCL10 (pg/mL) and qRT-PCR mRNA fold-change versus baseline in sgScramble (sgScr) versus sgSMARCAL1 (sgSMAR) ± wild-type or R764Q rescue: SMARCAL1 knockout reduces CXCL9 by 62% (1240 → 471 pg/mL) and CXCL10 by 57% (842 → 362 pg/mL) under IFN-γ stimulation; full rescue by wild-type, partial rescue (45% efficiency) by R764Q. ***P < 0.001, **P < 0.01, ns = not significant. (d) Western blot of cGAS-STING-IRF3 pathway activation: phospho-STING Ser366, phospho-TBK1 Ser172, phospho-IRF3 Ser396, with total STING/TBK1/IRF3 and GAPDH loading controls, in sgScr versus sgSMAR ± IFN-γ; quantified bar plots (arbitrary units): p-STING 4.7 → 1.5, p-TBK1 3.9 → 1.4, p-IRF3 5.2 → 1.5, all ***P < 0.001. diABZI rescue panel (10 µM, 6 h): STING agonist diABZI partially restores CXCL9 (64% recovery, 471 → 792 pg/mL) and CXCL10 (58% recovery, 362 → 591 pg/mL) secretion in SMARCAL1-KO cells. (e) Primary human CD8 + T cell transwell chemotaxis (transmigrated CXCR3 + CD8 + cells × 10 3 , mean ± SD across three donors): condition 1 unstimulated (2.1); condition 2 IFN-γ-stimulated sgScramble supernatant (9.8); condition 3 IFN-γ-stimulated sgSMARCAL1 supernatant (4.1, 58% reduction, ***P < 0.001); condition 4 sgScramble supernatant + AMG 487 (1 µM CXCR3 antagonist, 0.9, > 90% blockade); condition 5 isotype control (2); condition 6 H1299 IFN-γ sgScramble (8.2); condition 7 H1299 IFN-γ sgSMARCAL1 (3.9, 52% reduction, ***P < 0.001). ***P < 0.001, ns = not significant. (f) Integrated mechanistic model schematic: replication stress in APOBEC-enriched (high Rad-Score) tumors → SMARCAL1 upregulation (helicase activity-dependent) → ACSL4-dependent phospholipid remodeling and ferroptotic susceptibility → cGAS-STING-IRF3 axis activation amplifying IFN-γ-induced CXCL9/CXCL10 transcription → chemokine gradient recruiting CXCR3 + CD8 + T cells to peritumoral invasive margin → systemic immune priming and sustained post-operative MRD-negative surveillance. Evidence sources annotated per arrow: bulk RNA-seq (transcriptomic), Visium spatial, mIF/IHC (protein), CRISPR (causal), chemotaxis (functional).

    Journal: Frontiers in Immunology

    Article Title: Non-invasive radiogenomic mapping of the SMARCAL1-driven ferroptotic niche is associated with longitudinal MRD-negative surveillance in early-stage NSCLC

    doi: 10.3389/fimmu.2026.1835413

    Figure Lengend Snippet: CRISPR-Cas9 loss-of-function validation of the SMARCAL1–ferroptosis–chemokine axis and integrated mechanistic model. (a) SMARCAL1 knockout validation in A549 and H1299 NSCLC cell lines: anti-SMARCAL1 immunoblot (115 kDa; GAPDH loading control 37 kDa) demonstrating absence of SMARCAL1 protein in sgSMARCAL1-1 and sgSMARCAL1-2 versus sgScramble; Sanger sequencing chromatograms of indel-introduced sgSMARCAL1 target locus within SMARCAL1 exon 3 region (~150 bp) versus wild-type reference; TIDE indel size distribution (sgSMARCAL1-1 38% efficiency, sgSMARCAL1-2 22% efficiency at predominant indel sizes −5 to −1, +1, +5). (b) Ferroptosis phenotyping after erastin (5 µM, 24 h) in A549 (left) and H1299 (right), expressed as relative value (% sgScramble): cell viability, BODIPY-C11 oxidized/reduced ratio, intracellular Fe 2+ (FerroOrange MFI), malondialdehyde (MDA), reduced glutathione (GSH), and TEM ferroptotic mitochondrial percent. SMARCAL1-KO cells (sgSMARCAL1-1, -2) show resistance to erastin-induced ferroptosis; ***P < 0.001 versus sgScramble. Lower rescue panel (A549): wild-type SMARCAL1 reconstitution fully rescues ferroptosis susceptibility (viability 31% sgScramble baseline); helicase-dead R764Q mutant fails to rescue (viability 74%, no rescue). (c) Chemokine secretion assays. ELISA of CXCL9 and CXCL10 (pg/mL) and qRT-PCR mRNA fold-change versus baseline in sgScramble (sgScr) versus sgSMARCAL1 (sgSMAR) ± wild-type or R764Q rescue: SMARCAL1 knockout reduces CXCL9 by 62% (1240 → 471 pg/mL) and CXCL10 by 57% (842 → 362 pg/mL) under IFN-γ stimulation; full rescue by wild-type, partial rescue (45% efficiency) by R764Q. ***P < 0.001, **P < 0.01, ns = not significant. (d) Western blot of cGAS-STING-IRF3 pathway activation: phospho-STING Ser366, phospho-TBK1 Ser172, phospho-IRF3 Ser396, with total STING/TBK1/IRF3 and GAPDH loading controls, in sgScr versus sgSMAR ± IFN-γ; quantified bar plots (arbitrary units): p-STING 4.7 → 1.5, p-TBK1 3.9 → 1.4, p-IRF3 5.2 → 1.5, all ***P < 0.001. diABZI rescue panel (10 µM, 6 h): STING agonist diABZI partially restores CXCL9 (64% recovery, 471 → 792 pg/mL) and CXCL10 (58% recovery, 362 → 591 pg/mL) secretion in SMARCAL1-KO cells. (e) Primary human CD8 + T cell transwell chemotaxis (transmigrated CXCR3 + CD8 + cells × 10 3 , mean ± SD across three donors): condition 1 unstimulated (2.1); condition 2 IFN-γ-stimulated sgScramble supernatant (9.8); condition 3 IFN-γ-stimulated sgSMARCAL1 supernatant (4.1, 58% reduction, ***P < 0.001); condition 4 sgScramble supernatant + AMG 487 (1 µM CXCR3 antagonist, 0.9, > 90% blockade); condition 5 isotype control (2); condition 6 H1299 IFN-γ sgScramble (8.2); condition 7 H1299 IFN-γ sgSMARCAL1 (3.9, 52% reduction, ***P < 0.001). ***P < 0.001, ns = not significant. (f) Integrated mechanistic model schematic: replication stress in APOBEC-enriched (high Rad-Score) tumors → SMARCAL1 upregulation (helicase activity-dependent) → ACSL4-dependent phospholipid remodeling and ferroptotic susceptibility → cGAS-STING-IRF3 axis activation amplifying IFN-γ-induced CXCL9/CXCL10 transcription → chemokine gradient recruiting CXCR3 + CD8 + T cells to peritumoral invasive margin → systemic immune priming and sustained post-operative MRD-negative surveillance. Evidence sources annotated per arrow: bulk RNA-seq (transcriptomic), Visium spatial, mIF/IHC (protein), CRISPR (causal), chemotaxis (functional).

    Article Snippet: Knockout was validated by: (i) Sanger sequencing of the target locus (PCR-amplified genomic DNA); (ii) Western blot demonstrating absence of SMARCAL1 protein; (iii) TIDE analysis (Brinkman et al., NAR 2014) of indel profiles.

    Techniques: CRISPR, Biomarker Discovery, Knock-Out, Western Blot, Control, Sequencing, Mutagenesis, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Activation Assay, Chemotaxis Assay, Activity Assay, RNA Sequencing, Functional Assay