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Bio-Techne corporation nalp4 antibody
Nalp4 Antibody, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 94/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/nalp4 antibody/product/Bio-Techne corporation
Average 94 stars, based on 6 article reviews

nalp4 antibody - by Bioz Stars, 2026-05

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a Volcano plot showing the suppression of NLRP4 led to a greater susceptibility to olaparib in pancreatic cancer cell lines. b Immunoblot of NLRP4 in control and NLRP4-knockdown BxPC-3 and Capan-1 cells. BxPC-3 and Capan-1 cells were stably transfected with shNC, shNLRP4-1 and shNLRP4-2, and then MTS assays ( c , d ) and colony formation assays ( e , f ) were performed. *** p < 0.001. ** p < 0.01. The analysis of significant differences was performed with Student’s t test. g – j Control and NLRP4-knockdown BxPC-3 and Capan-1 cells were injected into the left flank of nude mice. Tumor volumes were measured every 3 days. Tumors were harvested on day 21, photographed and weighed. Tumor weights are shown in ( h ), BxPC-3 tumor volumes are shown in ( i ), and Capan-1 tumor volumes are shown in ( j ). Data are shown as the mean ± SD ( n = 5). *** p < 0.001. The analysis of significant differences was performed with Student’s t test. *** p < 0.001. ** p < 0.01. k , l Flow cytometry analysis of annexin V/7-ADD staining in the indicated cell lines. Data are presented as the mean ± SD from three independent experiments. The analysis of significant differences was performed with Student’s t test.

Journal: Cell Death & Disease

Article Title: NLRP4 renders pancreatic cancer resistant to olaparib through promotion of the DNA damage response and ROS-induced autophagy

doi: 10.1038/s41419-024-06984-0

Figure Lengend Snippet: a Volcano plot showing the suppression of NLRP4 led to a greater susceptibility to olaparib in pancreatic cancer cell lines. b Immunoblot of NLRP4 in control and NLRP4-knockdown BxPC-3 and Capan-1 cells. BxPC-3 and Capan-1 cells were stably transfected with shNC, shNLRP4-1 and shNLRP4-2, and then MTS assays ( c , d ) and colony formation assays ( e , f ) were performed. *** p < 0.001. ** p < 0.01. The analysis of significant differences was performed with Student’s t test. g – j Control and NLRP4-knockdown BxPC-3 and Capan-1 cells were injected into the left flank of nude mice. Tumor volumes were measured every 3 days. Tumors were harvested on day 21, photographed and weighed. Tumor weights are shown in ( h ), BxPC-3 tumor volumes are shown in ( i ), and Capan-1 tumor volumes are shown in ( j ). Data are shown as the mean ± SD ( n = 5). *** p < 0.001. The analysis of significant differences was performed with Student’s t test. *** p < 0.001. ** p < 0.01. k , l Flow cytometry analysis of annexin V/7-ADD staining in the indicated cell lines. Data are presented as the mean ± SD from three independent experiments. The analysis of significant differences was performed with Student’s t test.

Article Snippet: Antibodies against the following proteins were used: LC3I/II (14600-1-AP, Proteintech), GAPDH (60004-1-Ig, Proteintech), p62 (207305, Abcam), H3 (1791, Abcam), NOXO1 (97788, Abcam), NLRP4 (NB100-56156, Novus), γ-H2AX (80312, Cell Signaling Technology), Sirt7 (12994-1-AP, Proteintech), and β-actin (20536-1-AP, Proteintech).

Techniques: Western Blot, Control, Knockdown, Stable Transfection, Transfection, Injection, Flow Cytometry, Staining

a , b MTS assays were performed to calculate the IC50 of olaparib in the indicated cells. c , d The indicated cells were treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). MTS assays were performed to investigate the effect of NLRP4 on olaparib resistance. The analysis of significant differences was performed with one-way ANOVA. *** p < 0.001. e The indicated cells were treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). Colony formation assays were performed to investigate the effect of NLRP4 on olaparib resistance. The analysis of significant differences was performed with Student’s t test. *** p < 0.001. ** p < 0.01. f , g Flow cytometry results for annexin V/7-ADD staining in the indicated cell lines after exposure to DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). The analysis of significant differences was performed with Student’s t test. *** p < 0.001. h Control or NLRP4-knockdown Capan-1 cells were treated with DMSO or olaparib (500 nM) for RNA sequencing and were subjected to GO pathway enrichment analysis. i Co-IP experiments were conducted in NLRP4 OE cells, followed by LC‒MS/MS analysis. j Control or NLRP4-knockdown BxPC-3 and Capan-1 cells were treated with the indicated dose of olaparib for 48 h. Western blotting was performed with the indicated antibodies.

Journal: Cell Death & Disease

Article Title: NLRP4 renders pancreatic cancer resistant to olaparib through promotion of the DNA damage response and ROS-induced autophagy

doi: 10.1038/s41419-024-06984-0

Figure Lengend Snippet: a , b MTS assays were performed to calculate the IC50 of olaparib in the indicated cells. c , d The indicated cells were treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). MTS assays were performed to investigate the effect of NLRP4 on olaparib resistance. The analysis of significant differences was performed with one-way ANOVA. *** p < 0.001. e The indicated cells were treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). Colony formation assays were performed to investigate the effect of NLRP4 on olaparib resistance. The analysis of significant differences was performed with Student’s t test. *** p < 0.001. ** p < 0.01. f , g Flow cytometry results for annexin V/7-ADD staining in the indicated cell lines after exposure to DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). The analysis of significant differences was performed with Student’s t test. *** p < 0.001. h Control or NLRP4-knockdown Capan-1 cells were treated with DMSO or olaparib (500 nM) for RNA sequencing and were subjected to GO pathway enrichment analysis. i Co-IP experiments were conducted in NLRP4 OE cells, followed by LC‒MS/MS analysis. j Control or NLRP4-knockdown BxPC-3 and Capan-1 cells were treated with the indicated dose of olaparib for 48 h. Western blotting was performed with the indicated antibodies.

Techniques: Flow Cytometry, Staining, Control, Knockdown, RNA Sequencing, Co-Immunoprecipitation Assay, Western Blot

a – c Representative immunofluorescence micrographs and quantification of γ-H2AX foci in the indicated cells with or without olaparib treatment (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). The analysis of significant differences was performed with Student’s t test. ** p < 0.01, * p < 0.05. Scale bar, 5 μm. d Control or NLRP4-knockdown BxPC-3 and Capan-1 cells were treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h. Western blotting was performed with the indicated antibodies. e – g Representative comet assay micrographs and quantification of tail moments in the indicated cells with or without olaparib treatment (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). The analysis of significant differences was performed with Student’s t test. ** p < 0.01, * p < 0.05. h Representative immunofluorescence micrographs showing BRCA1 and Rad51 IRIF in the indicated cell lines at 6 h after olaparib treatment (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). Scale bar, 5 μm. i Changes in DNA repair genes in control and NLRP4-knockdown Capan-1 cells after olaparib treatment (500 nM olaparib for Capan-1 cells).

Journal: Cell Death & Disease

Article Title: NLRP4 renders pancreatic cancer resistant to olaparib through promotion of the DNA damage response and ROS-induced autophagy

doi: 10.1038/s41419-024-06984-0

Figure Lengend Snippet: a – c Representative immunofluorescence micrographs and quantification of γ-H2AX foci in the indicated cells with or without olaparib treatment (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). The analysis of significant differences was performed with Student’s t test. ** p < 0.01, * p < 0.05. Scale bar, 5 μm. d Control or NLRP4-knockdown BxPC-3 and Capan-1 cells were treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h. Western blotting was performed with the indicated antibodies. e – g Representative comet assay micrographs and quantification of tail moments in the indicated cells with or without olaparib treatment (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). The analysis of significant differences was performed with Student’s t test. ** p < 0.01, * p < 0.05. h Representative immunofluorescence micrographs showing BRCA1 and Rad51 IRIF in the indicated cell lines at 6 h after olaparib treatment (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). Scale bar, 5 μm. i Changes in DNA repair genes in control and NLRP4-knockdown Capan-1 cells after olaparib treatment (500 nM olaparib for Capan-1 cells).

Techniques: Immunofluorescence, Control, Knockdown, Western Blot, Single Cell Gel Electrophoresis

a – c Control or NLRP4-knockdown BxPC-3 and Capan-1 cells were treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h. Western blotting analysis and quantification were performed. The analysis of significant differences was performed with Student's t test.** p < 0.01. d – f Effect of NLRP4 on the levels of autophagic flux. The mRFP-GFP-LC3 plasmid was transfected into the indicated cells for 24 h, and then the cells were treated with olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h. Representative images were obtained by laser scanning confocal microscopy. The average fluorescence intensity of autophagic lysosomes (yellow dots in the merged images) and autophagic lysosomes (red in the merged images) in individual cells was quantified. Scale bar, 5 μm. The analysis of significant differences was performed with Student's t test. *** p < 0.001. g – i TEM-based ultrastructure analysis (autophagosomes) in the indicated cells. The analysis of significant differences was performed with Student’s t test. *** p < 0.001.

Journal: Cell Death & Disease

Article Title: NLRP4 renders pancreatic cancer resistant to olaparib through promotion of the DNA damage response and ROS-induced autophagy

doi: 10.1038/s41419-024-06984-0

Figure Lengend Snippet: a – c Control or NLRP4-knockdown BxPC-3 and Capan-1 cells were treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h. Western blotting analysis and quantification were performed. The analysis of significant differences was performed with Student's t test.** p < 0.01. d – f Effect of NLRP4 on the levels of autophagic flux. The mRFP-GFP-LC3 plasmid was transfected into the indicated cells for 24 h, and then the cells were treated with olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h. Representative images were obtained by laser scanning confocal microscopy. The average fluorescence intensity of autophagic lysosomes (yellow dots in the merged images) and autophagic lysosomes (red in the merged images) in individual cells was quantified. Scale bar, 5 μm. The analysis of significant differences was performed with Student's t test. *** p < 0.001. g – i TEM-based ultrastructure analysis (autophagosomes) in the indicated cells. The analysis of significant differences was performed with Student’s t test. *** p < 0.001.

Techniques: Control, Knockdown, Western Blot, Plasmid Preparation, Transfection, Confocal Microscopy, Fluorescence

a Cells treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h were incubated with an ROS indicator. Representative images were obtained. b , c Cells treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h were incubated with an ROS indicator, and fluorescence intensity was assessed with flow cytometry. The analysis of significant differences was performed with Student’s t test. *** p < 0.001. d , e Cells treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h were incubated with JC-1 working solution, and fluorescence intensity was assessed with flow cytometry. The analysis of significant differences was performed with Student’s t test. *** p < 0.001. f – h Cells treated with olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) plus DMSO or MitoQ for 48 h were incubated with MitoSOX. Representative images were obtained, and the fluorescence intensity was assessed with flow cytometry. The analysis of significant differences was performed with Student’s t test. *** p < 0.001. i Changes in ROS-related genes in control and NLRP4-knockdown Capan-1 cells after olaparib treatment (500 nM olaparib for Capan-1 cells). Scale bar, 5 μm. j Western blotting analysis was performed for the indicated antibodies.

Journal: Cell Death & Disease

Article Title: NLRP4 renders pancreatic cancer resistant to olaparib through promotion of the DNA damage response and ROS-induced autophagy

doi: 10.1038/s41419-024-06984-0

Figure Lengend Snippet: a Cells treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h were incubated with an ROS indicator. Representative images were obtained. b , c Cells treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h were incubated with an ROS indicator, and fluorescence intensity was assessed with flow cytometry. The analysis of significant differences was performed with Student’s t test. *** p < 0.001. d , e Cells treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h were incubated with JC-1 working solution, and fluorescence intensity was assessed with flow cytometry. The analysis of significant differences was performed with Student’s t test. *** p < 0.001. f – h Cells treated with olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) plus DMSO or MitoQ for 48 h were incubated with MitoSOX. Representative images were obtained, and the fluorescence intensity was assessed with flow cytometry. The analysis of significant differences was performed with Student’s t test. *** p < 0.001. i Changes in ROS-related genes in control and NLRP4-knockdown Capan-1 cells after olaparib treatment (500 nM olaparib for Capan-1 cells). Scale bar, 5 μm. j Western blotting analysis was performed for the indicated antibodies.

Techniques: Incubation, Fluorescence, Flow Cytometry, Control, Knockdown, Western Blot

a Silver staining of NLRP4-interacting proteins. b Molecular dynamics simulation-derived model structure of NLRP4 bound to Sirt7. c Cell lysates were immunoprecipitated with the indicated antibodies. d , e Western blot analysis was performed using the indicated antibodies. f – l ChIP-qPCR assay to assess H3K18ac status at the NOXO1 genomic region. The analysis of significant differences was performed with Student's t test. ** p < 0.01, *** p < 0.001. m qPCR analysis of NOXO1 expression. n Proposed model depicting the role of NLRP4-induced ROS.

Journal: Cell Death & Disease

Article Title: NLRP4 renders pancreatic cancer resistant to olaparib through promotion of the DNA damage response and ROS-induced autophagy

doi: 10.1038/s41419-024-06984-0

Figure Lengend Snippet: a Silver staining of NLRP4-interacting proteins. b Molecular dynamics simulation-derived model structure of NLRP4 bound to Sirt7. c Cell lysates were immunoprecipitated with the indicated antibodies. d , e Western blot analysis was performed using the indicated antibodies. f – l ChIP-qPCR assay to assess H3K18ac status at the NOXO1 genomic region. The analysis of significant differences was performed with Student's t test. ** p < 0.01, *** p < 0.001. m qPCR analysis of NOXO1 expression. n Proposed model depicting the role of NLRP4-induced ROS.

Techniques: Silver Staining, Derivative Assay, Immunoprecipitation, Western Blot, ChIP-qPCR, Expressing

a Representative immunofluorescence micrographs of γ-H2AX foci in the indicated cells with or without olaparib treatment (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). b TEM-based ultrastructure analysis (autophagosomes) in the indicated cells. c Cells were treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h. Western blotting analysis was performed for the indicated antibodies. d , e Cells treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h were incubated with an ROS indicator, and fluorescence intensity was assessed with flow cytometry. The analysis of significant differences was performed with one-way ANOVA. *** p < 0.001. f , g The indicated cells were treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). MTS assays were performed to investigate the effect of NLRP4 on olaparib resistance. The analysis of significant differences was performed with one-way ANOVA. *** p < 0.001. h Flow cytometry results for annexin V/7-ADD staining in the indicated cell lines after exposure to DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). The analysis of significant differences was performed with Student’s t test. *** p < 0.001. i Schematic model showing that NLRP4 renders pancreatic cancer resistant to PARPi through the promotion of the DNA damage response and ROS-induced autophagy.

Journal: Cell Death & Disease

Article Title: NLRP4 renders pancreatic cancer resistant to olaparib through promotion of the DNA damage response and ROS-induced autophagy

doi: 10.1038/s41419-024-06984-0

Figure Lengend Snippet: a Representative immunofluorescence micrographs of γ-H2AX foci in the indicated cells with or without olaparib treatment (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). b TEM-based ultrastructure analysis (autophagosomes) in the indicated cells. c Cells were treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h. Western blotting analysis was performed for the indicated antibodies. d , e Cells treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells) for 48 h were incubated with an ROS indicator, and fluorescence intensity was assessed with flow cytometry. The analysis of significant differences was performed with one-way ANOVA. *** p < 0.001. f , g The indicated cells were treated with DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). MTS assays were performed to investigate the effect of NLRP4 on olaparib resistance. The analysis of significant differences was performed with one-way ANOVA. *** p < 0.001. h Flow cytometry results for annexin V/7-ADD staining in the indicated cell lines after exposure to DMSO or olaparib (5 μM olaparib for BxPC-3 cells and 500 nM olaparib for Capan-1 cells). The analysis of significant differences was performed with Student’s t test. *** p < 0.001. i Schematic model showing that NLRP4 renders pancreatic cancer resistant to PARPi through the promotion of the DNA damage response and ROS-induced autophagy.

Techniques: Immunofluorescence, Western Blot, Incubation, Fluorescence, Flow Cytometry, Staining

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