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anti atf6 d4z8v rabbit monoclonal antibody (Cell Signaling Technology Inc)

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Cell Signaling Technology Inc anti atf6 d4z8v rabbit monoclonal antibody
Anti Atf6 D4z8v Rabbit Monoclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 383 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+atf+6/ATF-6+Rabbit+mAb/10__1007_slash_s13273___026___00616___8-87-5-10
Average 96 stars, based on 383 article reviews

anti atf6 d4z8v rabbit monoclonal antibody - by Bioz Stars, 2026-10

96/100 stars

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Article Title: Subcellular localization and ER-mediated cytotoxic function of α1A and α1ACT in spinocerebellar ataxia type 6.
Article Snippet: Spinocerebellar ataxia type 6 (SCA6) is a polyglutamine (polyQ) disease, which is caused by the elongation of CAG repeats encoding polyQ in the CACNA1A gene.. The CACNA1A gene encodes two proteins, namely, α1A (a subunit of the plasma membrane calcium channel), which is translated in its entire length, and α1ACT, which is translated from the second cistron, and both proteins have a polyQ tract.. The α1A-polyQ and α1ACT-polyQ proteins with an elongated polyQ stretch have been reported to form aggregates in cells and induce neuronal cell death, but the subcellular localization of these proteins and their cytotoxic properties remain unclear.

Article Title: Covalent inhibition of endoplasmic reticulum chaperone GRP78 disconnects the transduction of ER stress signals to inflammation and lipid accumulation in diet-induced obese mice
Article Snippet: Antibody , Anti-Calnexin (goat polyclonal) , Abcam , Cat. #: ab192439 , IF (1:500). .. Antibody , Anti-ATF-6 (rabbit monoclonal) , Cell Signaling Technology , Cat. #: 65,880 , WB (1:1000). .. Antibody , Anti-Phospho-eIF2α (rabbit monoclonal) , Cell Signaling Technology , Cat. #: 3398 , WB (1:1000).

Article Title: Ssu72 phosphatase is essential for thermogenic adaptation by regulating cytosolic translation.
Article Snippet: These membranes were washed for 30min with TBS-T, subsequently incubated with horseradish peroxidase (HRP)-conjugated secondary antibodies in 5% skimmilk for 2 h at RT, and thenwashed for one hourwith TBS-T. Blotted proteins were detected using ECL solution (AbFrontier) and exposed on Medical X-ray film blue (AGFA). .. Nature Communications | (2023) 14:1097 12 The following primary antibodies were used (at the indicated dilutions): anti-Ssu72 (Cell signaling Technology (CST), #12816, 1:2000), anti-PP1α (CST, #2582, 1:750), anti-CDC25B (Thermo Fisher Scientific, #PA5-17759, 1:1000), anti-PTEN (CST, #9188, 1:1000), antiPP2A-B56-α (Santa Cruz Biotechnology (SCBT), #sc-271311, 1:1000), anti-β-actin (Sigma-Aldrich, #A2066, 1:3000), anti-UCP1 (SCBT, #sc6529, 1:750), anti-GAPDH (CST, #2118, 1:3000), anti-PGC1α (SCBT, #sc13067, 1:750), anti-HSP90 (SCBT, #sc-13119, 1:1000), anti-phosphoeIF2α (Ser51) (CST, #3398, 1:1000), anti-eIF2α (CST, #5324, 1:2000), anti-ATF4 (SCBT, #sc-390063, 1:1000), anti-CHOP (CST, #2895, 1:750), anti-phospho-PERK (Thr980) (Thermo Fisher Scientific, #MA5-15033, 1:1000), anti-phospho-IRE1α (Ser724) (Thermo Fisher Scientific, #PA116927, 1:1000), anti-ATF-6 (CST, #65880, 1:1000), anti-Myc-Tag (CST, #2276, 1:1500), anti-HA-Tag (SCBT, #sc-7392, 1:1000), anti-HA-Tag (CST, #3724, 1:2000), anti-β-actin (CST, #3700, 1:3000), anti-GST (SCBT, #sc-138, 1:2000), anti-puromycin (DSHB, #PMY-2A4, 1:200), anti-AMPKα (CST, #5831, 1:2000), anti-PKA C alpha (GeneTex, #GTX104934, 1:1000), anti-ClpP (SCBT, #sc-271284, 1:1000), anti-total OXPHOS Rodent WB Antibody Cocktail (Abcam, #ab110413, 1:500), anti-COX IV (CST, #4850, 1:1000), anti-MT-ND1 (Abcam, #ab181848, 1:1000). .. The following secondary antibodies were used (at the indicated dilutions): anti-Rabbit IgG(H + L)-HRP (GenDEPOT, #SA002-500, 1:7000), anti-Mouse IgG(H + L)-HRP (GenDEPOT, #SA001-500, 1:7000), anti-Goat IgG(H+ L)-HRP (GenDEPOT, #SA007-500, 1:7000).

Article Title: Ssu72 phosphatase is essential for thermogenic adaptation by regulating cytosolic translation
Article Snippet: These membranes were washed for 30 min with TBS-T, subsequently incubated with horseradish peroxidase (HRP)-conjugated secondary antibodies in 5% skim milk for 2 h at RT, and then washed for one hour with TBS-T. Blotted proteins were detected using ECL solution (AbFrontier) and exposed on Medical X-ray film blue (AGFA). .. The following primary antibodies were used (at the indicated dilutions): anti-Ssu72 (Cell signaling Technology (CST), #12816, 1:2000), anti-PP1α (CST, #2582, 1:750), anti-CDC25B (Thermo Fisher Scientific, #PA5-17759, 1:1000), anti-PTEN (CST, #9188, 1:1000), anti-PP2A-B56-α (Santa Cruz Biotechnology (SCBT), #sc-271311, 1:1000), anti-β-actin (Sigma-Aldrich, #A2066, 1:3000), anti-UCP1 (SCBT, #sc-6529, 1:750), anti-GAPDH (CST, #2118, 1:3000), anti-PGC1α (SCBT, #sc-13067, 1:750), anti-HSP90 (SCBT, #sc-13119, 1:1000), anti-phospho-eIF2α (Ser51) (CST, #3398, 1:1000), anti-eIF2α (CST, #5324, 1:2000), anti-ATF4 (SCBT, #sc-390063, 1:1000), anti-CHOP (CST, #2895, 1:750), anti-phospho-PERK (Thr980) (Thermo Fisher Scientific, #MA5-15033, 1:1000), anti-phospho-IRE1α (Ser724) (Thermo Fisher Scientific, #PA1-16927, 1:1000), anti-ATF-6 (CST, #65880, 1:1000), anti-Myc-Tag (CST, #2276, 1:1500), anti-HA-Tag (SCBT, #sc-7392, 1:1000), anti-HA-Tag (CST, #3724, 1:2000), anti-β-actin (CST, #3700, 1:3000), anti-GST (SCBT, #sc-138, 1:2000), anti-puromycin (DSHB, #PMY-2A4, 1:200), anti-AMPKα (CST, #5831, 1:2000), anti-PKA C alpha (GeneTex, #GTX104934, 1:1000), anti-ClpP (SCBT, #sc-271284, 1:1000), anti-total OXPHOS Rodent WB Antibody Cocktail (Abcam, #ab110413, 1:500), anti-COX IV (CST, #4850, 1:1000), anti-MT-ND1 (Abcam, #ab181848, 1:1000). .. The following secondary antibodies were used (at the indicated dilutions): anti-Rabbit IgG(H + L)-HRP (GenDEPOT, #SA002-500, 1:7000), anti-Mouse IgG(H + L)-HRP (GenDEPOT, #SA001-500, 1:7000), anti-Goat IgG(H + L)-HRP (GenDEPOT, #SA007-500, 1:7000).

Immunofluorescence:

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Qu-Me NPs attenuates MCAO-induced injury. (A,B) Open-field test performed 24 h post-MCAO shows improved locomotor activity in Qu- and Qu-Me NPs-treated mice compared with the MCAO and Me groups ( n = 6). (C,D) Y-maze test demonstrates ameliorated cognitive function in the Qu- and Qu-Me NPs-treated mice compared with the MCAO and Me groups ( n = 6). (E) Modified neurological severity scores (mNSS) for each group (Sham, MCAO, Me, Qu, and Qu-Me NPs) evaluated at 24 h post-MCAO ( n = 6). (F–J) Western blot analysis illustrates reduced expression of ER stress markers (ATF-6, CHOP) and pro-inflammatory cytokines (IL-1β, IL-6) in the Qu and Qu-Me NP groups compared with MCAO ( n = 3). Results are presented as averages ±SD * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant. Analysis was performed using one-way ANOVA followed by Dunnett multiple-comparisons test for mean differences.

Journal: ACS Biomaterials Science & Engineering

Article Title: Self-Assembled Quercetin–Mecobalamin Nanoparticles Mitigate Ischemic Stroke Injury via Enhanced Neuroprotection and Microglial Modulation

doi: 10.1021/acsbiomaterials.5c01855

Figure Lengend Snippet: Qu-Me NPs attenuates MCAO-induced injury. (A,B) Open-field test performed 24 h post-MCAO shows improved locomotor activity in Qu- and Qu-Me NPs-treated mice compared with the MCAO and Me groups ( n = 6). (C,D) Y-maze test demonstrates ameliorated cognitive function in the Qu- and Qu-Me NPs-treated mice compared with the MCAO and Me groups ( n = 6). (E) Modified neurological severity scores (mNSS) for each group (Sham, MCAO, Me, Qu, and Qu-Me NPs) evaluated at 24 h post-MCAO ( n = 6). (F–J) Western blot analysis illustrates reduced expression of ER stress markers (ATF-6, CHOP) and pro-inflammatory cytokines (IL-1β, IL-6) in the Qu and Qu-Me NP groups compared with MCAO ( n = 3). Results are presented as averages ±SD * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant. Analysis was performed using one-way ANOVA followed by Dunnett multiple-comparisons test for mean differences.

Article Snippet: Proteins were separated by SDS-PAGE, transferred to PVDF membranes, and incubated overnight with specific primary antibodies against β-actin (1/5000, ab170325, Abcam), ATF-6 (1:1000, A0202, ABclonal), CHOP (1:1000, A21902 , ABclonal), IL-1β (1/1000, 16806-1-AP, Proteintech), IL-6, pannexin1 (1/1000, ab124969, Abcam), and DDIT4 (1:1000, ab191871, Abcam).

Techniques: Activity Assay, Modification, Western Blot, Expressing

USP19 promotes cytoplasmic mislocalization of TDP-43 and enhances ER stress. ( A ) Representative images of TDP-43-tomato (red), USP19 (green), and DAPI (blue) in HeLa cells transfected with TDP-43 and control siRNA or USP19 siRNA ± proteasome inhibition with MG132 treatment (10 μM, 4 h). ( B ) Quantification of TDP-43-tomato in the cytoplasm vs. nucleus with MG132 treatment (one-sample t test, * P < 0.05; n = 3 independent experiments with 10 to 32 cells/condition averaged per experiment). ( C ) Representative images of TDP-43-tomato (red), USP19 (green), and DAPI (blue) in HeLa cells transfected with TDP-43 and USP19 variants or GFP control. ( D ) Quantification of TDP-43-tomato in the cytoplasm vs. nucleus (one-way ANOVA, F(2, 6) = 22.73, P = 0.0016; post hoc Dunnett, ** P < 0.005, n = 3 independent experiments with 13 to 33 cells/condition averaged per experiment). ( E ) Representative images of endogenous USP19–TDP-43 PLA puncta (green) and DAPI (blue) in HeLa cells transfected with control or USP19 siRNA. Negative controls with only 1 primary antibody or 1 secondary antibody probe ( Bottom ). ( F ) Representative images of endogenous USP19–TDP-43 PLA puncta (red) and DAPI (blue) in HeLa cells treated ± ER stressor tunicamycin (2 μM) for 24 h. Negative controls with only 1 primary antibody or 1 secondary antibody probe ( Bottom ). ( G ) Quantification of USP19–TDP-43 PLA intensity ± tunicamycin treatment (2 μM, 24 h) (one-sample t test, *** P < 0.001, n = 3 independent experiments with 29 to 36 cells/condition averaged per experiment). ( H ) Schematic of unfolded protein response (UPR) triggered by ER stressors, such as misfolded proteins, illustrating the activation of IRE1α-XBP1, PERK-ATF4, and ATF6 pathways, leading to CHOP induction. ( I ) Representative blots of ER stress-induced UPR markers from tet-induced HeLa-GFP-TDP-43 cells transfected with control or USP19 siRNA and treated ± tunicamycin (2 μM; 0, 8, 24 h). ( J – M ) Quantification of CHOP, cleaved ATF6 (cl-ATF6), ATF4, and IRE1α (two-way ANOVA; CHOP: F(1, 18) = 24.49, P = 0.0001; cl-ATF6: F(1, 18) = 41.93, P < 0.0001; ATF-4: F(1, 18) = 4.343, P = 0.0517; IRE1α: F(1, 18) = 2.80, P = 0.1571; post hoc Sidak, * P < 0.05, ** P < 0.005, *** P < 0.001, ns: not significant; n = 4 independent experiments with 2 to 3 replicates averaged per experiment).

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: Ubiquitin-specific peptidase-19 links TDP-43 aggregation to ER stress

doi: 10.1073/pnas.2514355123

Figure Lengend Snippet: USP19 promotes cytoplasmic mislocalization of TDP-43 and enhances ER stress. ( A ) Representative images of TDP-43-tomato (red), USP19 (green), and DAPI (blue) in HeLa cells transfected with TDP-43 and control siRNA or USP19 siRNA ± proteasome inhibition with MG132 treatment (10 μM, 4 h). ( B ) Quantification of TDP-43-tomato in the cytoplasm vs. nucleus with MG132 treatment (one-sample t test, * P < 0.05; n = 3 independent experiments with 10 to 32 cells/condition averaged per experiment). ( C ) Representative images of TDP-43-tomato (red), USP19 (green), and DAPI (blue) in HeLa cells transfected with TDP-43 and USP19 variants or GFP control. ( D ) Quantification of TDP-43-tomato in the cytoplasm vs. nucleus (one-way ANOVA, F(2, 6) = 22.73, P = 0.0016; post hoc Dunnett, ** P < 0.005, n = 3 independent experiments with 13 to 33 cells/condition averaged per experiment). ( E ) Representative images of endogenous USP19–TDP-43 PLA puncta (green) and DAPI (blue) in HeLa cells transfected with control or USP19 siRNA. Negative controls with only 1 primary antibody or 1 secondary antibody probe ( Bottom ). ( F ) Representative images of endogenous USP19–TDP-43 PLA puncta (red) and DAPI (blue) in HeLa cells treated ± ER stressor tunicamycin (2 μM) for 24 h. Negative controls with only 1 primary antibody or 1 secondary antibody probe ( Bottom ). ( G ) Quantification of USP19–TDP-43 PLA intensity ± tunicamycin treatment (2 μM, 24 h) (one-sample t test, *** P < 0.001, n = 3 independent experiments with 29 to 36 cells/condition averaged per experiment). ( H ) Schematic of unfolded protein response (UPR) triggered by ER stressors, such as misfolded proteins, illustrating the activation of IRE1α-XBP1, PERK-ATF4, and ATF6 pathways, leading to CHOP induction. ( I ) Representative blots of ER stress-induced UPR markers from tet-induced HeLa-GFP-TDP-43 cells transfected with control or USP19 siRNA and treated ± tunicamycin (2 μM; 0, 8, 24 h). ( J – M ) Quantification of CHOP, cleaved ATF6 (cl-ATF6), ATF4, and IRE1α (two-way ANOVA; CHOP: F(1, 18) = 24.49, P = 0.0001; cl-ATF6: F(1, 18) = 41.93, P < 0.0001; ATF-4: F(1, 18) = 4.343, P = 0.0517; IRE1α: F(1, 18) = 2.80, P = 0.1571; post hoc Sidak, * P < 0.05, ** P < 0.005, *** P < 0.001, ns: not significant; n = 4 independent experiments with 2 to 3 replicates averaged per experiment).

Article Snippet: Primary antibodies used in Western blotting: Ubiquitin-K48 (Abcam Cat# ab140601), Ubiquitin-K63 (Abcam, Cat# ab179434), Myc (Cell signaling, #2276s), Flag (MA5-48063), Actin (Santa Cruz, sc-47778), TDP-43 (Cell signaling, #3448), Tubulin (Cell signaling, #2146); USP19 (Abcam, #93159), NUP98 (cell signaling, #2598s), ATF4 (Cell signaling, #11815s), ATF6 (Cell signaling, #65880S), CHOP (Cell signaling, #2895s), IRE1α (Cell signaling, #3294s), HA (Cell signaling, 2367s).

Techniques: Transfection, Control, Inhibition, Activation Assay

(A ) Gene set enrichment analysis (GSEA) plot showing significant enrichment of the Hallmark Unfolded Protein Response (UPR) gene signature in EV-treated splenic DCs compared to Controls. The normalized enrichment score (NES = 5.12) and adjusted p-value (Padj < 0.05) are displayed. Representative of two independent experiments. (B) Western blot analysis of phosphorylated IRE1α (p-IRE1α) and total IRE1α in splenic DCs treated with EVs or tunicamycin (Tun) as a positive control. Representative of four independent experiments. (C) Western blot analysis of spliced XBP1 (XBP1s) protein expression in BMDCs. Top , Cells were treated with PBS (Ctrl), tumor-derived EVs (20 µg/ml; 24h), or Tunicamycin (Tun; 10µM; 4h) as a positive control. Bottom , Analysis of XBP1s levels in BMDCs treated with EVs in the presence or absence of the IRE1α inhibitor, 4µ8c. β-actin serves as the cytoplasmic loading control. Representative of four independent experiments. (D) Normalized mRNA expression of XBP1s and its target genes ( Sec61a, Dnajb9 ) in splenic DCs treated with PBS (Ctrl) or tumor EVs (20 µg/ml; 24h) (n=3-5). (E) Heatmap of relative gene expression (Z-score) for XBP1s target genes ( Icam1, Dnajb2, Clip2, Sec61a2, Dnajb9 ) in EV-uptaking (Exogreen + ) versus bystander (Exogreen - ) LNDCs isolated in vivo . Representative of two independent experiments. (F) Normalized mRNA expression of XBP1s and its target genes ( Sec61a, Dnajb9 ) in tumor-infiltrating DCs, comparing EV-uptaking (Emerald Green + ) versus bystander (Emerald Green - ) DC subsets (n=4-5). Data is aggregated from two independent experiments. All data is reported as mean ± SEM. * p <0.05, ** p <0.01 by two-way ANOVA (D) and unpaired Student’s t-test (F). EVs , extracellular vesicles; XBP1s , spliced X-box binding protein 1; Tun , tunicamycin (ER stress inducer); BMDCs , bone marrow-derived dendritic cells; LNDCs , lymph node dendritic cells; Ctrl , control.

Journal: bioRxiv

Article Title: Tumor-derived Extracellular Vesicles Induce ER Stress to Drive Tolerogenic Dendritic Cell Development in the Tumor Microenvironment

doi: 10.64898/2026.02.10.705213

Figure Lengend Snippet: (A ) Gene set enrichment analysis (GSEA) plot showing significant enrichment of the Hallmark Unfolded Protein Response (UPR) gene signature in EV-treated splenic DCs compared to Controls. The normalized enrichment score (NES = 5.12) and adjusted p-value (Padj < 0.05) are displayed. Representative of two independent experiments. (B) Western blot analysis of phosphorylated IRE1α (p-IRE1α) and total IRE1α in splenic DCs treated with EVs or tunicamycin (Tun) as a positive control. Representative of four independent experiments. (C) Western blot analysis of spliced XBP1 (XBP1s) protein expression in BMDCs. Top , Cells were treated with PBS (Ctrl), tumor-derived EVs (20 µg/ml; 24h), or Tunicamycin (Tun; 10µM; 4h) as a positive control. Bottom , Analysis of XBP1s levels in BMDCs treated with EVs in the presence or absence of the IRE1α inhibitor, 4µ8c. β-actin serves as the cytoplasmic loading control. Representative of four independent experiments. (D) Normalized mRNA expression of XBP1s and its target genes ( Sec61a, Dnajb9 ) in splenic DCs treated with PBS (Ctrl) or tumor EVs (20 µg/ml; 24h) (n=3-5). (E) Heatmap of relative gene expression (Z-score) for XBP1s target genes ( Icam1, Dnajb2, Clip2, Sec61a2, Dnajb9 ) in EV-uptaking (Exogreen + ) versus bystander (Exogreen - ) LNDCs isolated in vivo . Representative of two independent experiments. (F) Normalized mRNA expression of XBP1s and its target genes ( Sec61a, Dnajb9 ) in tumor-infiltrating DCs, comparing EV-uptaking (Emerald Green + ) versus bystander (Emerald Green - ) DC subsets (n=4-5). Data is aggregated from two independent experiments. All data is reported as mean ± SEM. * p <0.05, ** p <0.01 by two-way ANOVA (D) and unpaired Student’s t-test (F). EVs , extracellular vesicles; XBP1s , spliced X-box binding protein 1; Tun , tunicamycin (ER stress inducer); BMDCs , bone marrow-derived dendritic cells; LNDCs , lymph node dendritic cells; Ctrl , control.

Article Snippet: Primary antibodies included: Rab27a (Cell Signaling Technology [CST], Cat# 69295S), SREBP2 (Novus Biologicals, Cat# NB100-74543), ATF4 (CST, Cat# 11815S), ATF6 (CST, Cat# 65880S), IRE1α (CST, Cat# 3294S), SREBP1 (clone 2A4; Santa Cruz Biotechnology, Cat# sc-13551), Lamin B1 (clone B-10; Santa Cruz, Cat# sc-374015), XBP-1s (CST, Cat# 40435), PPARα (Thermo Fisher Scientific, Cat# PA1-822A), PPARγ (Santa Cruz, Cat# sc-7273), PPARβ (Santa Cruz, Cat# sc-74517) and Histone H3 (Santa Cruz, Cat# sc-517576).

Techniques: Western Blot, Positive Control, Expressing, Derivative Assay, Control, Gene Expression, Isolation, In Vivo, Binding Assay

(A) Flow cytometry analysis of neutral lipid accumulation in splenic DCs treated with PBS (Ctrl), tumor EVs (20 µg/ml; 24h), or tumor EVs (20 µg/ml; 24h) in the presence of the IRE1 α inhibitor 4μ8c. Left , Representative histograms of BODIPY 493/503 fluorescence. Right , quantification of the normalized mean fluorescence intensity (MFI) (n=3). Representative of three independent experiments. (B) GSEA plot from the scRNAseq data in , showing enrichment of the

Journal: bioRxiv

Article Title: Tumor-derived Extracellular Vesicles Induce ER Stress to Drive Tolerogenic Dendritic Cell Development in the Tumor Microenvironment

doi: 10.64898/2026.02.10.705213

Figure Lengend Snippet: (A) Flow cytometry analysis of neutral lipid accumulation in splenic DCs treated with PBS (Ctrl), tumor EVs (20 µg/ml; 24h), or tumor EVs (20 µg/ml; 24h) in the presence of the IRE1 α inhibitor 4μ8c. Left , Representative histograms of BODIPY 493/503 fluorescence. Right , quantification of the normalized mean fluorescence intensity (MFI) (n=3). Representative of three independent experiments. (B) GSEA plot from the scRNAseq data in , showing enrichment of the "Regulation of Lipid Metabolism by PPARα" gene set in EV-treated DCs compared to controls. Adjusted p-value (Padj < 0.05) is displayed. Representative of two independent experiments. (C) Western blot analysis of nuclear PPAR-α levels in BMDCs treated with or without EVs (20 µg/ml; 24h). Histone H3 is shown as a nuclear loading control. Representative of three independent experiments. (D) Immunoblot analysis of nuclear PPAR-α protein expression in BMDCs following treatment with PBS (Ctrl), tumor EVs (20 µg/ml; 24h), or EVs in the presence of the IRE1α inhibitor 4μ8c. Lamin B1 serves as the nuclear loading control. Representative of three independent experiments. (E) Quantification of PPAR-α DNA-binding activity in nuclear extracts from BMDCs treated with EVs (20 µg/ml; 24h), 4μ8c, or both (n=4-7). Representative of three independent experiments. (F) Flow cytometry quantification of neutral lipid content (BODIPY 493/503) in DCs treated with EVs (20 µg/ml; 24h) with or without the PPAR-α inhibitor TPST-1120. Representative of three independent experiments. (G) Flow cytometric analysis of fatty acid β-oxidation (FAO) activity in splenic DCs treated with PBS (Ctrl) or EVs (20 µg/ml; 24h) using FAO-Blue (n=5). (H) Normalized mRNA expression of Cpt1a , a key rate-limiting enzyme in FAO and a known PPAR-α target gene, in tumor-infiltrating DCs from the model in , comparing EV-uptaking (Emerald Green + ) versus bystander (Emerald Green - ) DC subsets (n=6). Representative of two independent experiments. (I) Heatmap of relative gene expression (Z-score) for triglyceride lipolysis ( Pnpla2 , Lipe , Mgll ) and fatty acid transport genes ( Fabp5 , Fabp4 ) in EV-uptaking (Exogreen + ) versus bystander (Exogreen - ) LNDCs isolated in vivo . Representative of two independent experiments. (J) Flow cytometric analysis of fatty acid uptake by splenic DCs treated with PBS (Ctrl) or EVs (20 µg/ml; 24h) using TF2-C12. Right , representative histogram. Representative of three independent experiments. All data is reported as mean ± SEM. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001 based on a one-way ANOVA (A,E,F) and an unpaired Student’s t-test (G,H,J). FAO , fatty acid oxidation; GSEA , gene set enrichment analysis; MFI , mean fluorescence intensity; PPARα , peroxisome proliferator-activated receptor alpha; BMDCs , bone marrow-derived dendritic cells; Ctrl , control ; EVs , extracellular vesicles; IRE1α, inositol-requiring enzyme 1 alpha.

Techniques: Flow Cytometry, Fluorescence, Western Blot, Control, Expressing, Binding Assay, Activity Assay, Gene Expression, Isolation, In Vivo, Derivative Assay

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anti atf6 d4z8v rabbit monoclonal antibody (Cell Signaling Technology Inc)

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