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rabbit polyclonal anti ezh2  (Proteintech)


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    Structured Review

    Proteintech rabbit polyclonal anti ezh2
    Rabbit Polyclonal Anti Ezh2, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 175 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+ezh2/EZH2+Antibody/10__3390_slash_v18040409-65-6-9
    Average 96 stars, based on 175 article reviews
    rabbit polyclonal anti ezh2 - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    Incubation:

    Article Title: Microglial PCGF1 alleviates neuroinflammation associated depressive behavior in adolescent mice
    Article Snippet: .. Membranes were incubated with the following 68 antibodies: mouse anti-β-actin (HC201, Transs), mouse anti-PCGF1 (sc-515371, Santa 69 Cruz Biotechnology), rabbit anti-MMP10 (ab261733, abcam), rabbit anti-H3K4me3 70 (#9751, CELL SIGNALING TECHNOLOGY), rabbit anti-H2AK119ub (#8240, 71 CELL SIGNALING TECHNOLOGY), rabbit anti-H3K27me3 (#9733, CELL 72 SIGNALING TECHNOLOGY), rabbit anti-H3K9me3 (#13969, CELL SIGNALING 73 TECHNOLOGY), rabbit anti-H3K9/K14ac (#9677, CELL SIGNALING 74 TECHNOLOGY), rabbit anti-H3K18ac (#9675P, CELL SIGNALING 75 TECHNOLOGY), rabbit anti-H3 (#4499, CELL SIGNALING TECHNOLOGY), 76 rabbit anti-p65 (#8242S, CELL SIGNALING TECHNOLOGY), rabbit anti-p-p65 77 (#3033T, CELL SIGNALING TECHNOLOGY), rabbit anti-p44/42 MAPK(Erk1/2) 78 (#4695, CELL SIGNALING TECHNOLOGY), rabbit anti-p-p44/4IN2 MAPK(Erk1/2) 79 (#4370, CELL SIGNALING TECHNOLOGY), rabbit anti-JNK (#9252, CELL 80 SIGNALING TECHNOLOGY), rabbit anti-p-JNK (#4668, CELL SIGNALING 81 TECHNOLOGY), rabbit anti-p38 (#8690, CELL SIGNALING TECHNOLOGY), 82 rabbit anti-p-p38 (#4511, CELL SIGNALING TECHNOLOGY), rabbit anti-RING1B 83 (16031-1-AP, proteintech), rabbit anti-EZH2 (21800-1-AP, proteintech). ..

    Article Title: MAT2A is essential for zygotic genome activation by maintaining of histone methylation in porcine embryos.
    Article Snippet: Methionine adenosyltransferase 2A (MAT2A) is an essential enzyme in the methionine cycle that generates Sadenosylmethionine (SAM) by reacting with methionine and ATP.. SAM acts as a methyl donors for histone and DNA methylation, which plays key roles in zygotic genome activation (ZGA).. However, the effects of MAT2A on porcine ZGA remain unclear.

    Article Title: Analysis of histone modifications in key cellular subpopulations in the context of azoospermia using spermatogenic single-cell RNA-seq data
    Article Snippet: .. Samples were incubated overnight at 4°C with the following primary antibodies diluted in phosphate-buffered saline: rabbit anti-EZH2 (Proteintech, 21,800-1- AP, 1:500), mouse anti-IL-6 (Proteintech, 66146-1-Ig, 1:500), and rabbit anti-HDAC2 antibody (2540S,1:500). ..

    Saline:

    Article Title: Analysis of histone modifications in key cellular subpopulations in the context of azoospermia using spermatogenic single-cell RNA-seq data
    Article Snippet: .. Samples were incubated overnight at 4°C with the following primary antibodies diluted in phosphate-buffered saline: rabbit anti-EZH2 (Proteintech, 21,800-1- AP, 1:500), mouse anti-IL-6 (Proteintech, 66146-1-Ig, 1:500), and rabbit anti-HDAC2 antibody (2540S,1:500). ..

    Western Blot:

    Article Title: Mettl3/Eed/Ythdc1 regulatory axis controls endometrial receptivity and function
    Article Snippet: Rabbit anti-EED, Abclonal, Cat# A5371; RRID: AB_2766181, 1:1000 for IB. .. Rabbit anti-EZH2, ProteinTech, Cat# 21800-1-AP; RRID: AB_10858790, 1:1000 for WB,1:500 for IF,4μg for IP. .. Rabbit anti-SUZ12 Abclonal, Cat# A7786;RRID: AB_2863561, 1:1000 for WB, 1:500 for IF, 4μg for IP.

    Article Title: Inhibition of Nrf2 degradation alleviates age-related osteoporosis induced by 1,25-Dihydroxyvitamin D deficiency.
    Article Snippet: Previous studies have shown that 1,25(OH)2D plays an anti-osteoporosis role by an anti-aging mechanism.. Oxidative stress is a key mediator of aging and bone loss; however, whether 1,25(OH)2D can exert its antiosteoporosis effect by inhibiting oxidative stress is unclear.. In this study, osteoporosis and the bone aging phenotype induced by 1,25(OH)2D deficiency in male mice were significantly rescued in vivo upon the supplementation of oltipraz, an inhibitor of Nrf2 degradation.

    Article Title: NEAT1 Promotes the Perineural Invasion of Pancreatic Cancer via the E2F1/GDNF Axis.
    Article Snippet: 11 Pancreatic cancer is characterized by an insidious onset and high degree of 12 malignancy, with a 5-year survival rate of less than 11%.. Perineural invasion (PNI) is 13 one of the pathological features of pancreatic cancer and provides a pathway for 14 distant tumor metastasis, which leads to a poor prognosis.. Although NEAT1 promotes 15 the progression of pancreatic cancer, its impact on PNI has not been studied.



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    Anti-transcription activity of γPNA1 with HDACi in lymphoma cells Relative fold change of c-Myc levels in U2932 cells measured by real-time PCR on day 2 after treatment with (A) γPNA1 and (B) ScR-γPNA2 in combination with romidepsin, entinostat, vorinostat, panobinostat, and belinostat. Results are presented as mean ± SEM and two-way ANOVA was used to determine the statistically significant difference between groups. Western blot analysis representing the change in c-MYC protein on day 2 after treatment with γPNA1 and ScR-γPNA2 in combination with (C) romidepsin, (D) entinostat, (E) vorinostat, (F) panobinostat, and (G) belinostat. ∗∗(C–F) Cyclophilin B was used as an endogenous control, and the same blots are presented in C–S3G. c-MYC, <t>EZH2,</t> and cyclophilin B were probed from the same blot. Results are presented as mean ± SEM, and the p value between groups was determined using one-way ANOVA.
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    Cell Signaling Technology Inc anti ezh2
    Anti-transcription activity of γPNA1 with HDACi in lymphoma cells Relative fold change of c-Myc levels in U2932 cells measured by real-time PCR on day 2 after treatment with (A) γPNA1 and (B) ScR-γPNA2 in combination with romidepsin, entinostat, vorinostat, panobinostat, and belinostat. Results are presented as mean ± SEM and two-way ANOVA was used to determine the statistically significant difference between groups. Western blot analysis representing the change in c-MYC protein on day 2 after treatment with γPNA1 and ScR-γPNA2 in combination with (C) romidepsin, (D) entinostat, (E) vorinostat, (F) panobinostat, and (G) belinostat. ∗∗(C–F) Cyclophilin B was used as an endogenous control, and the same blots are presented in C–S3G. c-MYC, <t>EZH2,</t> and cyclophilin B were probed from the same blot. Results are presented as mean ± SEM, and the p value between groups was determined using one-way ANOVA.
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    Image Search Results


    Anti-transcription activity of γPNA1 with HDACi in lymphoma cells Relative fold change of c-Myc levels in U2932 cells measured by real-time PCR on day 2 after treatment with (A) γPNA1 and (B) ScR-γPNA2 in combination with romidepsin, entinostat, vorinostat, panobinostat, and belinostat. Results are presented as mean ± SEM and two-way ANOVA was used to determine the statistically significant difference between groups. Western blot analysis representing the change in c-MYC protein on day 2 after treatment with γPNA1 and ScR-γPNA2 in combination with (C) romidepsin, (D) entinostat, (E) vorinostat, (F) panobinostat, and (G) belinostat. ∗∗(C–F) Cyclophilin B was used as an endogenous control, and the same blots are presented in C–S3G. c-MYC, EZH2, and cyclophilin B were probed from the same blot. Results are presented as mean ± SEM, and the p value between groups was determined using one-way ANOVA.

    Journal: Molecular Therapy. Nucleic Acids

    Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

    doi: 10.1016/j.omtn.2025.102804

    Figure Lengend Snippet: Anti-transcription activity of γPNA1 with HDACi in lymphoma cells Relative fold change of c-Myc levels in U2932 cells measured by real-time PCR on day 2 after treatment with (A) γPNA1 and (B) ScR-γPNA2 in combination with romidepsin, entinostat, vorinostat, panobinostat, and belinostat. Results are presented as mean ± SEM and two-way ANOVA was used to determine the statistically significant difference between groups. Western blot analysis representing the change in c-MYC protein on day 2 after treatment with γPNA1 and ScR-γPNA2 in combination with (C) romidepsin, (D) entinostat, (E) vorinostat, (F) panobinostat, and (G) belinostat. ∗∗(C–F) Cyclophilin B was used as an endogenous control, and the same blots are presented in C–S3G. c-MYC, EZH2, and cyclophilin B were probed from the same blot. Results are presented as mean ± SEM, and the p value between groups was determined using one-way ANOVA.

    Article Snippet: Primary antibodies for c-MYC (Cell Signaling Technology, #5605) and EZH2 (Cell Signaling Technology, #5246) were applied using a rabbit monoclonal antibody diluted in 3% BSA at 4°C overnight.

    Techniques: Activity Assay, Real-time Polymerase Chain Reaction, Western Blot, Control

    MYC/MAX inhibitors in combination with anti-transcription γPNA1 Cell viability of (A) U2932 and (B) Raji cells treated with increasing doses of MYC/MAX inhibitors (Myci975, EN4, 10058-F4, and sAJM589) alone and in combination with γPNA1 and ScR-γPNA2 (8 μM) for 72 h. Results are presented as mean ± SEM. The IC 50 (95% CI) values of MYC/MAX inhibitors alone and combination treatment of MYC/MAX with γPNA1 in (C) U2932 and (D) Raji cells. (E) Cell viability of γPNA1-treated U2932 and Raji cells at 8 μM concentration. Western blot analysis representing the change in c-MYC protein 72 h after treatment with γPNA1 and ScR-γPNA2 in combination with (F) Myci975, (G) EN4, (H) 10058-F4, and (I) sAJM589. ∗∗(F–I) Cyclophilin B was used as an endogenous control, and the same blots are presented in A–S7D. c-MYC, EZH2, and cyclophilin B were probed from the same blot. Results are presented as mean ± SEM, p value for one-way ANOVA.

    Journal: Molecular Therapy. Nucleic Acids

    Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

    doi: 10.1016/j.omtn.2025.102804

    Figure Lengend Snippet: MYC/MAX inhibitors in combination with anti-transcription γPNA1 Cell viability of (A) U2932 and (B) Raji cells treated with increasing doses of MYC/MAX inhibitors (Myci975, EN4, 10058-F4, and sAJM589) alone and in combination with γPNA1 and ScR-γPNA2 (8 μM) for 72 h. Results are presented as mean ± SEM. The IC 50 (95% CI) values of MYC/MAX inhibitors alone and combination treatment of MYC/MAX with γPNA1 in (C) U2932 and (D) Raji cells. (E) Cell viability of γPNA1-treated U2932 and Raji cells at 8 μM concentration. Western blot analysis representing the change in c-MYC protein 72 h after treatment with γPNA1 and ScR-γPNA2 in combination with (F) Myci975, (G) EN4, (H) 10058-F4, and (I) sAJM589. ∗∗(F–I) Cyclophilin B was used as an endogenous control, and the same blots are presented in A–S7D. c-MYC, EZH2, and cyclophilin B were probed from the same blot. Results are presented as mean ± SEM, p value for one-way ANOVA.

    Article Snippet: Primary antibodies for c-MYC (Cell Signaling Technology, #5605) and EZH2 (Cell Signaling Technology, #5246) were applied using a rabbit monoclonal antibody diluted in 3% BSA at 4°C overnight.

    Techniques: Concentration Assay, Western Blot, Control