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rabbit anti ddx6 antibody  (Novus Biologicals)


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    Novus Biologicals rabbit anti ddx6 antibody
    Rabbit Anti Ddx6 Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ddx6/DDX6+Antibody/us12565650-788-39-42
    Average 94 stars, based on 19 article reviews
    rabbit anti ddx6 antibody - by Bioz Stars, 2026-09
    94/100 stars

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    Related Articles

    Biomarker Discovery:

    Article Title: Translational repression by 4E-T is crucial to maintain the prophase-I arrest in vertebrate oocytes
    Article Snippet: DDX6 (Abcam ab174277), DDB1 (Abcam ab109027) and 4E-T (Thermo Fisher Scientific PA5-51680) antibody validation can be found on the company website and they were previously used in Cheng et al., Science 378, (2022). .. CPEB1 (Biozol MBS9213514), ppMAPK (Cell Signaling #9106), MAPK (Santa Cruz sc-154), Cdk1 (Santa Cruz sc-54), p150 (BD Transduction Laboratories 610473), DDX6 (Novus Biologicals NB200-191) antibody validation can be found on the company website and they were previously used in Heim et al., Development 149, (2022). ppCdk antibody was previously used e.g. in Bouftas et al., Dev Cell 57, (2022) and Heim et al., Development 149, (2022). eIF4E (Cell Signaling #9742); CSDE1 (Bethyl Laboratories A303-158A) and CNOT1 (Cell Signaling #30289) antibodies target highly conserved regions of the respective proteins and validation can be found on the company website. ..

    other:

    Article Title: Non-redundant roles for the human mRNA decapping cofactor paralogs DCP1a and DCP1b
    Article Snippet: The following antibodies were used: DCP1a (ab47811; Abcam), DCP1b (mAb #13233; Cell Signaling Technologies), EDC4 (ab72408; Abcam), DCP2 (ab28658; Abcam), EDC3 (mAb #14495; Cell Signaling Technologies), GAPDH (mAb #5174; Cell Signaling Technologies), DDX6 (NB200-192; Novus Biologicals), and p53 (sc-6243 X; Santa Cruz Biotechnology).

    Article Title: Non-redundant roles for the human mRNA decapping cofactor paralogs DCP1a and DCP1b
    Article Snippet: DCP1a (Abcam, Cambridge, UK, ab47811), DCP1b (Cell Signaling Technologies, Danvers, Massachusetts, USA, mAb #13233), EDC4 (Abcam, Cambridge, UK, ab72408), EDC3 (Cell Signaling Technologies, Danvers, Massachusetts, USA, mAb #14495), GAPDH (Cell Signaling Technologies, Danvers, Massachusetts, USA, mAb #5174), DDX6 (Novus Biologicals, Littleton, Colorado, NB200-192)

    Article Title: Non-redundant roles for the human mRNA decapping cofactor paralogs DCP1a and DCP1b.
    Article Snippet: The following antibodies were used: DCP1a (ab47811; Abcam), DCP1b (mAb #13233; Cell Signaling Technologies), EDC4 (ab72408; Abcam), DCP2 (ab28658; Abcam), EDC3 (mAb #14495; Cell Signaling Technologies), GAPDH (mAb #5174; Cell Signaling Technologies), DDX6 (NB200-192; Novus Biologicals), and p53 (sc-6243 X; Santa Cruz Biotechnology).

    Blocking Assay:

    Article Title: MYCN-induced nucleolar stress drives an early senescence-like transcriptional program in hTERT-immortalized RPE cells.
    Article Snippet: Subsequently, cells were permeabilized with 0.3% Triton X-100 (8 min) and washed (2 × 5 min), after which a blocking step was added with 50% FBS for 30 min and incubated with primary antibody diluted in 50% FBS for 60 min. After minimally 3 washing steps with PBS, plates were incubated with secondary antibody diluted in 50% FBS for 60 min, washed again, and counterstained with DAPI (5 μg/ml) for 20 min. Primary antibodies were directed against p21 (F-5) (SC-6246, Santa Cruz Biotechnology Inc., 1:100 dilution), p53 (7F5) (#2527 T, Cell Signalling Technology, 1:1600 dilution), Lamin B1 (ab16048, Abcam, 1:1000 dilution), Ki-67 (M7240) (M724029-2, Agilent, 1:400 dilution), γH2AX (phospho-S139) (ab2893, Abcam, 1:1000 dilution), RPA32/RPA2 (9H8) (ab2175, Abcam, 1:300 dilution), Fibrillarin (H-140) (SC-25397, Santa Cruz Biotechnology Inc., 1:50 dilution), DDX6 (200–192, Novus, 1:300 dilution) and c a Fibrillarin 24 h 48 h 72 h * * MYCN-ONMYCN-OFF FIBRILLARIN DAPI MERGED M Y C N -O F F M Y C N -O N b 5 10 15 0 10 20 30 N uc le ol ar A re a S in gl e N uc le ol us F ra ct io n MYCN-OFF MYCN-ON 24 h 48 h 72 h *n. s. n. s. n. s. d 10 20 30 40 24 h C el ls w ith 1 n uc le ol us ( % ) 10 20 30 40 48 h 10 20 30 40 72 h MYCN-OFF MYCN-ON G1 S G2 G1 S G2 G1 S G2 *n. s. * * ** ** n. s. *n. s. Fibrillarin/DAPI Figure 6. .. Subsequently, cells were permeabilized with 0.3% Triton X-100 (8 min) and washed (2 × 5 min), after which a blocking step was added with 50% FBS for 30 min and incubated with primary antibody diluted in 50% FBS for 60 min. After minimally 3 washing steps with PBS, plates were incubated with secondary antibody diluted in 50% FBS for 60 min, washed again, and counterstained with DAPI (5 μg/ml) for 20 min. Primary antibodies were directed against p21 (F-5) (SC-6246, Santa Cruz Biotechnology Inc., 1:100 dilution), p53 (7F5) (#2527 T, Cell Signalling Technology, 1:1600 dilution), Lamin B1 (ab16048, Abcam, 1:1000 dilution), Ki-67 (M7240) (M724029-2, Agilent, 1:400 dilution), γH2AX (phospho-S139) (ab2893, Abcam, 1:1000 dilution), RPA32/RPA2 (9H8) (ab2175, Abcam, 1:300 dilution), Fibrillarin (H-140) (SC-25397, Santa Cruz Biotechnology Inc., 1:50 dilution), DDX6 (200–192, Novus, 1:300 dilution) and c a Fibrillarin 24 h 48 h 72 h * * MYCN-ONMYCN-OFF FIBRILLARIN DAPI MERGED M Y C N -O F F M Y C N -O N b 5 10 15 0 10 20 30 N uc le ol ar A re a S in gl e N uc le ol us F ra ct io n MYCN-OFF MYCN-ON 24 h 48 h 72 h *n. s. n. s. n. s. d 10 20 30 40 24 h C el ls w ith 1 n uc le ol us ( % ) 10 20 30 40 48 h 10 20 30 40 72 h MYCN-OFF MYCN-ON G1 S G2 G1 S G2 G1 S G2 *n. s. * * ** ** n. s. *n. s. Fibrillarin/DAPI Figure 6. .. Images were visualised and annotated in Fiji (v.2.0.0-rc69/1.52p; http:// imagej. net/). (b) Area of fibrillarin foci (left) and percentage of nuclei with 1 nucleolus (right) in MYCN ON versus OFF, as measured by immunofluorescence staining and quantitative image analysis. (c) DAPI-based cell cycle staging of cells with 1 single nucleolus. (d) Representative images of DAPI stained MYCN-ON and OFF cells show increase in nucleolar size and enhanced cytoplasmic granularity 72 h p.i.

    Incubation:

    Article Title: MYCN-induced nucleolar stress drives an early senescence-like transcriptional program in hTERT-immortalized RPE cells.
    Article Snippet: Subsequently, cells were permeabilized with 0.3% Triton X-100 (8 min) and washed (2 × 5 min), after which a blocking step was added with 50% FBS for 30 min and incubated with primary antibody diluted in 50% FBS for 60 min. After minimally 3 washing steps with PBS, plates were incubated with secondary antibody diluted in 50% FBS for 60 min, washed again, and counterstained with DAPI (5 μg/ml) for 20 min. Primary antibodies were directed against p21 (F-5) (SC-6246, Santa Cruz Biotechnology Inc., 1:100 dilution), p53 (7F5) (#2527 T, Cell Signalling Technology, 1:1600 dilution), Lamin B1 (ab16048, Abcam, 1:1000 dilution), Ki-67 (M7240) (M724029-2, Agilent, 1:400 dilution), γH2AX (phospho-S139) (ab2893, Abcam, 1:1000 dilution), RPA32/RPA2 (9H8) (ab2175, Abcam, 1:300 dilution), Fibrillarin (H-140) (SC-25397, Santa Cruz Biotechnology Inc., 1:50 dilution), DDX6 (200–192, Novus, 1:300 dilution) and c a Fibrillarin 24 h 48 h 72 h * * MYCN-ONMYCN-OFF FIBRILLARIN DAPI MERGED M Y C N -O F F M Y C N -O N b 5 10 15 0 10 20 30 N uc le ol ar A re a S in gl e N uc le ol us F ra ct io n MYCN-OFF MYCN-ON 24 h 48 h 72 h *n. s. n. s. n. s. d 10 20 30 40 24 h C el ls w ith 1 n uc le ol us ( % ) 10 20 30 40 48 h 10 20 30 40 72 h MYCN-OFF MYCN-ON G1 S G2 G1 S G2 G1 S G2 *n. s. * * ** ** n. s. *n. s. Fibrillarin/DAPI Figure 6. .. Subsequently, cells were permeabilized with 0.3% Triton X-100 (8 min) and washed (2 × 5 min), after which a blocking step was added with 50% FBS for 30 min and incubated with primary antibody diluted in 50% FBS for 60 min. After minimally 3 washing steps with PBS, plates were incubated with secondary antibody diluted in 50% FBS for 60 min, washed again, and counterstained with DAPI (5 μg/ml) for 20 min. Primary antibodies were directed against p21 (F-5) (SC-6246, Santa Cruz Biotechnology Inc., 1:100 dilution), p53 (7F5) (#2527 T, Cell Signalling Technology, 1:1600 dilution), Lamin B1 (ab16048, Abcam, 1:1000 dilution), Ki-67 (M7240) (M724029-2, Agilent, 1:400 dilution), γH2AX (phospho-S139) (ab2893, Abcam, 1:1000 dilution), RPA32/RPA2 (9H8) (ab2175, Abcam, 1:300 dilution), Fibrillarin (H-140) (SC-25397, Santa Cruz Biotechnology Inc., 1:50 dilution), DDX6 (200–192, Novus, 1:300 dilution) and c a Fibrillarin 24 h 48 h 72 h * * MYCN-ONMYCN-OFF FIBRILLARIN DAPI MERGED M Y C N -O F F M Y C N -O N b 5 10 15 0 10 20 30 N uc le ol ar A re a S in gl e N uc le ol us F ra ct io n MYCN-OFF MYCN-ON 24 h 48 h 72 h *n. s. n. s. n. s. d 10 20 30 40 24 h C el ls w ith 1 n uc le ol us ( % ) 10 20 30 40 48 h 10 20 30 40 72 h MYCN-OFF MYCN-ON G1 S G2 G1 S G2 G1 S G2 *n. s. * * ** ** n. s. *n. s. Fibrillarin/DAPI Figure 6. .. Images were visualised and annotated in Fiji (v.2.0.0-rc69/1.52p; http:// imagej. net/). (b) Area of fibrillarin foci (left) and percentage of nuclei with 1 nucleolus (right) in MYCN ON versus OFF, as measured by immunofluorescence staining and quantitative image analysis. (c) DAPI-based cell cycle staging of cells with 1 single nucleolus. (d) Representative images of DAPI stained MYCN-ON and OFF cells show increase in nucleolar size and enhanced cytoplasmic granularity 72 h p.i.

    Article Title: Combinatorial microRNA activity is essential for the transition of pluripotent cells from proliferation into dormancy.
    Article Snippet: After washing once in PBS-T (PBS with 0.2% Tween-20), cells were blocked with blocking buffer (PBS-T, 2% BSA, and 5% goat serum; Jackson Immunoresearch/Dianova 017-000-121) for 1 h at RT. .. Cells were then stained with the primary antibodies PML 1:200 (Novus NB100-59787), SRSF2 1:2000 (Sigma-Aldrich S4045), and DDX6 1:400 (Novus NB200-192) overnight at 4°C; and washed for 3 × 10 min with wash buffer (PBS-T, 2% BSA); incubated with secondary antibodies (antimouse Alexa Fluor 488 [Thermo Fisher Scientific A32766] or antirabbit Alexa Fluor 568 [Thermo Fisher Scientific A10042], 1:700) for 1 h at RT, followed by 3 ×10-min washes with wash buffer. .. The coverslips were then mounted with Vectashield with DAPI (VectorLabs H-2000) and sealed with nail polish.

    Staining:

    Article Title: Combinatorial microRNA activity is essential for the transition of pluripotent cells from proliferation into dormancy.
    Article Snippet: After washing once in PBS-T (PBS with 0.2% Tween-20), cells were blocked with blocking buffer (PBS-T, 2% BSA, and 5% goat serum; Jackson Immunoresearch/Dianova 017-000-121) for 1 h at RT. .. Cells were then stained with the primary antibodies PML 1:200 (Novus NB100-59787), SRSF2 1:2000 (Sigma-Aldrich S4045), and DDX6 1:400 (Novus NB200-192) overnight at 4°C; and washed for 3 × 10 min with wash buffer (PBS-T, 2% BSA); incubated with secondary antibodies (antimouse Alexa Fluor 488 [Thermo Fisher Scientific A32766] or antirabbit Alexa Fluor 568 [Thermo Fisher Scientific A10042], 1:700) for 1 h at RT, followed by 3 ×10-min washes with wash buffer. .. The coverslips were then mounted with Vectashield with DAPI (VectorLabs H-2000) and sealed with nail polish.



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    Image Search Results


    Overview of PB-scope: an unsupervised deep learning-based framework for large-scale phenotypic screening on P-bodies (A) HCT116 cells stably expressing DDX6-GFP were plated in 96-well plates, treated with 280 compounds at 10 μM concentrations, and subjected to high-content imaging using the CQ1 confocal quantitative imaging system. (B) The analyzed images consist of four channels: (1) bright-field image for cellular morphology, (2) mitochondrial network, (3) processing body, and (4) nucleus. Merged composite demonstrates spatial relationships between these subcellular compartments. Scale bar, 10 μm. (C) Mitochondrial channels were processed through Cellpose 3.0 to generate a curated dataset containing over 400,000 high-quality single-cell images. (D) A contrastive clustering framework was implemented for unsupervised feature extraction, followed by UMAP dimensionality reduction to identify compounds with analogous mechanism-of-action (MOA) profiles through cluster localization analysis. (E) Quantitative analysis of P-body formation followed by drug treatment. (F) Mechanistic evaluation of lead compounds via imaging analysis.

    Journal: iScience

    Article Title: Contrastive learning of dynamic processing body formation reveals undefined mechanisms of approved compounds

    doi: 10.1016/j.isci.2026.114866

    Figure Lengend Snippet: Overview of PB-scope: an unsupervised deep learning-based framework for large-scale phenotypic screening on P-bodies (A) HCT116 cells stably expressing DDX6-GFP were plated in 96-well plates, treated with 280 compounds at 10 μM concentrations, and subjected to high-content imaging using the CQ1 confocal quantitative imaging system. (B) The analyzed images consist of four channels: (1) bright-field image for cellular morphology, (2) mitochondrial network, (3) processing body, and (4) nucleus. Merged composite demonstrates spatial relationships between these subcellular compartments. Scale bar, 10 μm. (C) Mitochondrial channels were processed through Cellpose 3.0 to generate a curated dataset containing over 400,000 high-quality single-cell images. (D) A contrastive clustering framework was implemented for unsupervised feature extraction, followed by UMAP dimensionality reduction to identify compounds with analogous mechanism-of-action (MOA) profiles through cluster localization analysis. (E) Quantitative analysis of P-body formation followed by drug treatment. (F) Mechanistic evaluation of lead compounds via imaging analysis.

    Article Snippet: As primary antibodies, we used DDX6 rabbit polyclonal antibody (Proteintech, 14632-1-AP) and EDC4 mouse monoclonal antibody (Santa Cruz Biotechnology, sc-376382).

    Techniques: Stable Transfection, Expressing, Imaging, Single Cell, Extraction

    Quantification and mechanisms of action analysis of selected drugs (A) A simulation model of intracellular P-body was constructed to generate synthetic P-body distributions with ground truth annotations. (B) A YOLO-v7 architecture trained on synthetic datasets was implemented for automated identification and quantitative analysis of P-body formation. (C) Example of P-body detection, achieving >95% agreement with manual annotations . (D) P-body numbers per cell in the time course under different drug treatment groups. (E) DDX6-GFP intensity (a.u.) per cell under different drug treatment groups. Error bars represent the STD of three independent analyses for (D) and (E). (F) Quantitative analysis of P-body numbers at 6 h post-treatment across different drug groups. (G) Quantitative analysis of DDX6-GFP intensity (a.u.) at 6 h post-treatment across different drug groups. The p -values were determined using the two-tailed Mann-Whitney U test for (F) and (G). The statistical significance compared with DMSO was indicated as ∗∗∗ p < 0.001; ∗ p < 0.05; ns, no significant difference. Data points that lay outside the 15%–85% range were deemed outliers and excluded from the statistical analysis. (H and I) Mechanism of action (MOA) profiling for drugs in Groups 1 and 3.

    Journal: iScience

    Article Title: Contrastive learning of dynamic processing body formation reveals undefined mechanisms of approved compounds

    doi: 10.1016/j.isci.2026.114866

    Figure Lengend Snippet: Quantification and mechanisms of action analysis of selected drugs (A) A simulation model of intracellular P-body was constructed to generate synthetic P-body distributions with ground truth annotations. (B) A YOLO-v7 architecture trained on synthetic datasets was implemented for automated identification and quantitative analysis of P-body formation. (C) Example of P-body detection, achieving >95% agreement with manual annotations . (D) P-body numbers per cell in the time course under different drug treatment groups. (E) DDX6-GFP intensity (a.u.) per cell under different drug treatment groups. Error bars represent the STD of three independent analyses for (D) and (E). (F) Quantitative analysis of P-body numbers at 6 h post-treatment across different drug groups. (G) Quantitative analysis of DDX6-GFP intensity (a.u.) at 6 h post-treatment across different drug groups. The p -values were determined using the two-tailed Mann-Whitney U test for (F) and (G). The statistical significance compared with DMSO was indicated as ∗∗∗ p < 0.001; ∗ p < 0.05; ns, no significant difference. Data points that lay outside the 15%–85% range were deemed outliers and excluded from the statistical analysis. (H and I) Mechanism of action (MOA) profiling for drugs in Groups 1 and 3.

    Article Snippet: As primary antibodies, we used DDX6 rabbit polyclonal antibody (Proteintech, 14632-1-AP) and EDC4 mouse monoclonal antibody (Santa Cruz Biotechnology, sc-376382).

    Techniques: Construct, Two Tailed Test, MANN-WHITNEY

    Perturbation of JAK leads to enhanced P-bodies (A) HCT116 cells were knocked down using JAK1 and JAK2 siRNA, and immunostained for P-body components DDX6 (magenta) and EDC4 (green). The nuclei were visualized with DAPI (blue). Scale bar, 10 μm. (B) Quantification of P-body number per cell across three experimental groups. Statistical significance determined by an unpaired t test was indicated as ∗∗∗ p < 0.001. (C) Model of JAK-STAT signaling pathway-mediated P-body regulation. JAK is activated when cytokines or growth factors bind to their respective receptors, leading to receptor dimerization, JAK and STAT phosphorylation, and subsequent transcriptional regulation. Inhibition of the pathway by knockdown of JAK1/2 leads induction of P-body formation. (D) Summary of JAK inhibitors identified in this work that modulate P-body formation.

    Journal: iScience

    Article Title: Contrastive learning of dynamic processing body formation reveals undefined mechanisms of approved compounds

    doi: 10.1016/j.isci.2026.114866

    Figure Lengend Snippet: Perturbation of JAK leads to enhanced P-bodies (A) HCT116 cells were knocked down using JAK1 and JAK2 siRNA, and immunostained for P-body components DDX6 (magenta) and EDC4 (green). The nuclei were visualized with DAPI (blue). Scale bar, 10 μm. (B) Quantification of P-body number per cell across three experimental groups. Statistical significance determined by an unpaired t test was indicated as ∗∗∗ p < 0.001. (C) Model of JAK-STAT signaling pathway-mediated P-body regulation. JAK is activated when cytokines or growth factors bind to their respective receptors, leading to receptor dimerization, JAK and STAT phosphorylation, and subsequent transcriptional regulation. Inhibition of the pathway by knockdown of JAK1/2 leads induction of P-body formation. (D) Summary of JAK inhibitors identified in this work that modulate P-body formation.

    Article Snippet: As primary antibodies, we used DDX6 rabbit polyclonal antibody (Proteintech, 14632-1-AP) and EDC4 mouse monoclonal antibody (Santa Cruz Biotechnology, sc-376382).

    Techniques: Phospho-proteomics, Inhibition, Knockdown