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wdr5 (Cell Signaling Technology Inc)

Name: wdr5
Brand: Cell Signaling Technology Inc
Rating: 95 (119 reviews)

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Cell Signaling Technology Inc wdr5
Wdr5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 119 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/wdr5/product/Cell Signaling Technology Inc
Average 95 stars, based on 119 article reviews

wdr5 - by Bioz Stars, 2026-02

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( A ) MYC transcript levels in control and MEN1-KO cells as determined by RT-qPCR. ns p > 0.05, * p ≤ 0.05. ( B ) MYC transcript counts from RNA-seq of A673 control and MEN1-KO tumors. ( C ) Western blot of MYC and Vinculin levels in A673 and TC32 control and MEN1-KO cells ( D ) Western blot of MYC and Vinculin in tumors derived from A673 control and MEN1-KO cells. ( E ) Co-immunoprecipitations with an anti-Menin antibody were performed on A673, CHLA10 and U2OS nuclear extracts and immunoblotted for Menin, MYC, MLL2 and WDR5. ( F ) Co-immunoprecipitations with an anti-MYC antibody were performed on A673 and CHLA10 nuclear extracts and immunoblotted for MYC, Menin, MAX, MLL2 and WDR5.

Journal: bioRxiv

Article Title: Menin inhibition impairs metastatic colonization of Ewing sarcoma

doi: 10.1101/2025.11.10.687648

Figure Lengend Snippet: ( A ) MYC transcript levels in control and MEN1-KO cells as determined by RT-qPCR. ns p > 0.05, * p ≤ 0.05. ( B ) MYC transcript counts from RNA-seq of A673 control and MEN1-KO tumors. ( C ) Western blot of MYC and Vinculin levels in A673 and TC32 control and MEN1-KO cells ( D ) Western blot of MYC and Vinculin in tumors derived from A673 control and MEN1-KO cells. ( E ) Co-immunoprecipitations with an anti-Menin antibody were performed on A673, CHLA10 and U2OS nuclear extracts and immunoblotted for Menin, MYC, MLL2 and WDR5. ( F ) Co-immunoprecipitations with an anti-MYC antibody were performed on A673 and CHLA10 nuclear extracts and immunoblotted for MYC, Menin, MAX, MLL2 and WDR5.

Article Snippet: Membranes were blocked with Intercept (TBS) Blocking Buffer (LICORbio 927-60001) and probed for the primary antibodies GAPDH Rabbit mAb (Cell Signaling 2118), MAX Rabbit pAb (Cell Signaling 4739), Menin Goat pAb (Bethyl A300-106A), MLL1-C (C-terminal) Rabbit pAb (Bethyl A300-374A), MLL2-C (C-terminal) Rabbit mAb (Cell Signaling 63735), MYC Rabbit mAb (Cell Signaling 18583), Vinculin Rabbit mAb (Cell Signaling 13901) or WDR5 Rabbit pAb (Bethyl A302-430A) followed by the secondary antibody Goat anti-Rabbit 800CW (Licor 926-32211), Donkey anti-Rabbit 800CW (Licor 926-32213) or Donkey anti-Goat 680RD (Licor 926-68074).

Techniques: Control, Quantitative RT-PCR, RNA Sequencing, Western Blot, Derivative Assay

( A ) Incucyte proliferation assay plotting percent confluence for A673 and TC32 cells treated with 0.1% DMSO or 10 µM VTP50469 starting at time 0. Representative of n=3-4). ( B and C ) Invasion of cells from a sphere of A673 cells embedded in rat tail collagen and treated with 0.1% DMSO or 10 µM VTP50469 for 5 days. ( B ) Representative phase and phalloidin (red)/DAPI (blue) stained images are shown (scale bars=100 µm). ( C ) Plot of circularity quantified from replicate spheroids treated as in ( B ). ( D ) A673 and TC32 cells were treated with 0.1% DMSO or 10 µM VTP50469 for 72 hours and genes that were significantly downregulated in VTP50469-treated cells (padj<0.05) were overlapped with genes downregulated in MEN1-KO cells. The top 5 enriched Hallmark pathways for the overlapping downregulated genes in each cell line are shown along with the overlap/total genes for each pathway. The green arrows indicate pathways that were reactivated in A673 MEN1-KO tumors (see ). ( E ) MYC transcript levels in A673, CHLA10 and TC32 cells treated with 0.1% DMSO or 10 µM VTP50469 for 72 hours as determined by RT-qPCR (ns p > 0.05). ( F ) Western of MYC and Vinculin in cells treated with 0.1% DMSO or 10 µM VTP50469 for 72 hours. ( G ) Co-immunoprecipitations with an anti-Menin antibody were performed on nuclear extracts from A673 and CHLA10 cells treated with 0.1% DMSO or 10 µM VTP50469 for 72 hours and immunoblotted for Menin, MYC, MLL2 and WDR5.

Journal: bioRxiv

Article Title: Menin inhibition impairs metastatic colonization of Ewing sarcoma

doi: 10.1101/2025.11.10.687648

Figure Lengend Snippet: ( A ) Incucyte proliferation assay plotting percent confluence for A673 and TC32 cells treated with 0.1% DMSO or 10 µM VTP50469 starting at time 0. Representative of n=3-4). ( B and C ) Invasion of cells from a sphere of A673 cells embedded in rat tail collagen and treated with 0.1% DMSO or 10 µM VTP50469 for 5 days. ( B ) Representative phase and phalloidin (red)/DAPI (blue) stained images are shown (scale bars=100 µm). ( C ) Plot of circularity quantified from replicate spheroids treated as in ( B ). ( D ) A673 and TC32 cells were treated with 0.1% DMSO or 10 µM VTP50469 for 72 hours and genes that were significantly downregulated in VTP50469-treated cells (padj<0.05) were overlapped with genes downregulated in MEN1-KO cells. The top 5 enriched Hallmark pathways for the overlapping downregulated genes in each cell line are shown along with the overlap/total genes for each pathway. The green arrows indicate pathways that were reactivated in A673 MEN1-KO tumors (see ). ( E ) MYC transcript levels in A673, CHLA10 and TC32 cells treated with 0.1% DMSO or 10 µM VTP50469 for 72 hours as determined by RT-qPCR (ns p > 0.05). ( F ) Western of MYC and Vinculin in cells treated with 0.1% DMSO or 10 µM VTP50469 for 72 hours. ( G ) Co-immunoprecipitations with an anti-Menin antibody were performed on nuclear extracts from A673 and CHLA10 cells treated with 0.1% DMSO or 10 µM VTP50469 for 72 hours and immunoblotted for Menin, MYC, MLL2 and WDR5.

Techniques: Proliferation Assay, Staining, Quantitative RT-PCR, Western Blot

FIGURE 2 | Identification of methyltransferase mixed-lineage leukemia 1 (MLL1)/WD-40 repeat protein 5 (WDR5) and cellular senescence marker p16INK4a in human peritoneal mesothelial cells (HPMCs) from patients undergoing peritoneal dialysis (PD). (A) Representative western blotting analyses showing MLL1, WDR5, H3K4 trimethylation (H3K4me3), and p16INK4a expression in HPMCs from non-PD and PD patients. (B) Quantitative analysis of MLL1, WDR5, H3K4me3, and p16INK4a protein expression in HPMCs from non-PD and PD. Protein abundance for MLL1, WDR5, and p16INK4a was normalized to that of α-tubulin, and H3K4me3 protein abundance was normalized to that of histone H3 (H3). n = 5 per group. *p < 0.05, and **p < 0.01 by two-tailed Student's t test. (C) Correlation analysis between peritoneal function (D/P Cre) and p16INK4a expression in HPMCs from patients undergoing PD (n = 10) using Spearman's rank correlation test. ρ, Spearman correlation coefficient; ρ = 0.82, p = 0.003.

Journal: The FASEB Journal

Article Title: Targeting MLL1/WDR5‐Mediated Epigenetic Regulation Mitigates Peritoneal Fibrosis by Reducing p16^INK4a

doi: 10.1096/fj.202402382r

Figure Lengend Snippet: FIGURE 2 | Identification of methyltransferase mixed-lineage leukemia 1 (MLL1)/WD-40 repeat protein 5 (WDR5) and cellular senescence marker p16INK4a in human peritoneal mesothelial cells (HPMCs) from patients undergoing peritoneal dialysis (PD). (A) Representative western blotting analyses showing MLL1, WDR5, H3K4 trimethylation (H3K4me3), and p16INK4a expression in HPMCs from non-PD and PD patients. (B) Quantitative analysis of MLL1, WDR5, H3K4me3, and p16INK4a protein expression in HPMCs from non-PD and PD. Protein abundance for MLL1, WDR5, and p16INK4a was normalized to that of α-tubulin, and H3K4me3 protein abundance was normalized to that of histone H3 (H3). n = 5 per group. *p < 0.05, and **p < 0.01 by two-tailed Student's t test. (C) Correlation analysis between peritoneal function (D/P Cre) and p16INK4a expression in HPMCs from patients undergoing PD (n = 10) using Spearman's rank correlation test. ρ, Spearman correlation coefficient; ρ = 0.82, p = 0.003.

Article Snippet: The following antibodies were used: rabbit monoclonal anti- MLL1 antibody (1:1000, #14197, Cell Signaling Technology, Danvers, MA, USA, RRID:AB_2688010), rabbit monoclonal anti- WDR5 (1:1000, #13105, Cell Signaling Technology, RRID:AB_2620133), rabbit polyclonal antiH3K4me3 (1:2000, ab8580, Abcam, RRID:AB_306649), rabbit monoclonal anti- p16INK4a (1:2500, ab51243, Abcam, RRID:AB_2059963), rabbit monoclonal anti- p21WAF1/CIP1 (1:1000, ab109199, Abcam, RRID: AB_10861551), rabbit polyclonal anti- p53 (1:1000, #9282, Cell Signaling Technology, RRID: AB_331476), mouse monoclonal anti- α- SMA (1:5000, A2547, Sigma- Aldrich, St. Louis, MO, USA, RRID:AB_476701), rabbit polyclonal anti- collagen Iα1 (1:1000, NBP1- 30054, 15306860, 2025, 8, D ow nloaded from https://faseb.onlinelibrary.w iley.com /doi/10.1096/fj.202402382R , W iley O nline L ibrary on [22/05/2025].

Techniques: Marker, Western Blot, Expressing, Quantitative Proteomics, Two Tailed Test

FIGURE 3 | Effects of mixed-lineage leukemia 1 (MLL1)/ WD-40 repeat protein 5 (WDR5) complex inhibitors on H3K4 trimethylation (H3K4me3) and p16INK4a expression in mice with peritoneal fibrosis. (A) Representative hematoxylin–eosin staining of peritoneal tissues from control mice and methylglyoxal (MGO)-injected mice. Bars indicate the thickness of submesothelial compact zone (scale bar: 100 μm). (B) Representative immunohis- tochemical analyses showing the expression of MLL1 and WDR5 in peritoneal tissues from control mice and MGO-injected mice. The right panels show high-magnification images of the boxed regions (scale bar: 100 μm). (C) Quantitative analysis of MLL1- and WDR5-positive cells in peritoneal tissues. ***p < 0.001 by 2-tailed Student's t test. (D, F) Representative immunohistochemical analyses showing H3K4me3 and p16INK4a expression in peritoneal tissue from control mice, MGO-injected mice, and MGO-injected mice receiving (D) MM-102 and (F) OICR-9429. The right panels show high-magnification images of the boxed regions (scale bar: 100 μm). (E, G) Quantitative analysis of H3K4me3-positive cells and p16INK4a-positive cells in peritoneal tissues from control mice, MGO-injected mice, and MGO-injected mice receiving (E) MM-102 and (G) OICR-9429. n = 5 per group. **p < 0.01 and ***p < 0.001 by one-way analysis of variance (ANOVA) followed by Tukey's post hoc test. CTL, control.

Journal: The FASEB Journal

Article Title: Targeting MLL1/WDR5‐Mediated Epigenetic Regulation Mitigates Peritoneal Fibrosis by Reducing p16^INK4a

doi: 10.1096/fj.202402382r

Figure Lengend Snippet: FIGURE 3 | Effects of mixed-lineage leukemia 1 (MLL1)/ WD-40 repeat protein 5 (WDR5) complex inhibitors on H3K4 trimethylation (H3K4me3) and p16INK4a expression in mice with peritoneal fibrosis. (A) Representative hematoxylin–eosin staining of peritoneal tissues from control mice and methylglyoxal (MGO)-injected mice. Bars indicate the thickness of submesothelial compact zone (scale bar: 100 μm). (B) Representative immunohis- tochemical analyses showing the expression of MLL1 and WDR5 in peritoneal tissues from control mice and MGO-injected mice. The right panels show high-magnification images of the boxed regions (scale bar: 100 μm). (C) Quantitative analysis of MLL1- and WDR5-positive cells in peritoneal tissues. ***p < 0.001 by 2-tailed Student's t test. (D, F) Representative immunohistochemical analyses showing H3K4me3 and p16INK4a expression in peritoneal tissue from control mice, MGO-injected mice, and MGO-injected mice receiving (D) MM-102 and (F) OICR-9429. The right panels show high-magnification images of the boxed regions (scale bar: 100 μm). (E, G) Quantitative analysis of H3K4me3-positive cells and p16INK4a-positive cells in peritoneal tissues from control mice, MGO-injected mice, and MGO-injected mice receiving (E) MM-102 and (G) OICR-9429. n = 5 per group. **p < 0.01 and ***p < 0.001 by one-way analysis of variance (ANOVA) followed by Tukey's post hoc test. CTL, control.

Techniques: Expressing, Staining, Control, Injection, Immunohistochemical staining

FIGURE 4 | Effects of mixed-lineage leukemia 1 (MLL1)/ WD-40 repeat protein 5 (WDR5) complex inhibitors on chronic peritoneal injury following methylglyoxal (MGO) administration. (A, C) Representative hematoxylin–eosin staining and Masson's trichrome staining of peritoneal tissues from control mice, MGO-injected mice, and MGO-injected mice treated with (A) MM-102 and (C) OICR-9429. The right panels show high- magnification images of the boxed regions (scale bar: 200 μm). Bars indicate the thickness of the submesothelial compact zone. (B, D) Quantitative analysis of cell density and submesothelial compact zone thickness in peritoneal tissues from control mice, MGO-injected mice, and MGO-injected mice treated with (B) MM-102 and (D) OICR-9429. n = 5 per group. **p < 0.01 and ***p < 0.001 by one-way analysis of variance (ANOVA) followed by Tukey's post hoc test. CTL, control.

Journal: The FASEB Journal

Article Title: Targeting MLL1/WDR5‐Mediated Epigenetic Regulation Mitigates Peritoneal Fibrosis by Reducing p16^INK4a

doi: 10.1096/fj.202402382r

Figure Lengend Snippet: FIGURE 4 | Effects of mixed-lineage leukemia 1 (MLL1)/ WD-40 repeat protein 5 (WDR5) complex inhibitors on chronic peritoneal injury following methylglyoxal (MGO) administration. (A, C) Representative hematoxylin–eosin staining and Masson's trichrome staining of peritoneal tissues from control mice, MGO-injected mice, and MGO-injected mice treated with (A) MM-102 and (C) OICR-9429. The right panels show high- magnification images of the boxed regions (scale bar: 200 μm). Bars indicate the thickness of the submesothelial compact zone. (B, D) Quantitative analysis of cell density and submesothelial compact zone thickness in peritoneal tissues from control mice, MGO-injected mice, and MGO-injected mice treated with (B) MM-102 and (D) OICR-9429. n = 5 per group. **p < 0.01 and ***p < 0.001 by one-way analysis of variance (ANOVA) followed by Tukey's post hoc test. CTL, control.

Techniques: Staining, Control, Injection

FIGURE 5 | Effects of mixed-lineage leukemia 1 (MLL1)/ WD-40 repeat protein 5 (WDR5) complex inhibitors on methylglyoxal (MGO)-induced peritoneal fibrosis in mice. (A, D) mRNA abundance of Acta2 and Col1a1 in control mice, MGO-injected mice, and MGO-injected mice treated with (A) MM-102 and (D) OICR-9429. Gene expression was normalized to the internal control Gapdh. n = 5 per group. (B, E) Representative immunohis- tochemical analyses showing α-smooth muscle actin (SMA), fibroblast-specific protein (FSP)-1, and collagen I expression in peritoneal tissues from control mice, MGO-injected mice, and MGO-injected mice treated with (B) MM-102 and (E) OICR-9429. The right panels show high-magnification images of the boxed regions (scale bar: 100 μm). (C, F) Quantitative analysis of α-SMA-positive cells, FSP-1-positive cells, and collagen I-positive areas in peritoneal tissues from control mice, MGO-injected mice, and MGO-injected mice treated with (C) MM-102 and (E) OICR-9429. n = 5 per group. **p < 0.01, and ***p < 0.001 by one-way analysis of variance (ANOVA) followed by Tukey's post hoc test. CTL, control.

Journal: The FASEB Journal

Article Title: Targeting MLL1/WDR5‐Mediated Epigenetic Regulation Mitigates Peritoneal Fibrosis by Reducing p16^INK4a

doi: 10.1096/fj.202402382r

Figure Lengend Snippet: FIGURE 5 | Effects of mixed-lineage leukemia 1 (MLL1)/ WD-40 repeat protein 5 (WDR5) complex inhibitors on methylglyoxal (MGO)-induced peritoneal fibrosis in mice. (A, D) mRNA abundance of Acta2 and Col1a1 in control mice, MGO-injected mice, and MGO-injected mice treated with (A) MM-102 and (D) OICR-9429. Gene expression was normalized to the internal control Gapdh. n = 5 per group. (B, E) Representative immunohis- tochemical analyses showing α-smooth muscle actin (SMA), fibroblast-specific protein (FSP)-1, and collagen I expression in peritoneal tissues from control mice, MGO-injected mice, and MGO-injected mice treated with (B) MM-102 and (E) OICR-9429. The right panels show high-magnification images of the boxed regions (scale bar: 100 μm). (C, F) Quantitative analysis of α-SMA-positive cells, FSP-1-positive cells, and collagen I-positive areas in peritoneal tissues from control mice, MGO-injected mice, and MGO-injected mice treated with (C) MM-102 and (E) OICR-9429. n = 5 per group. **p < 0.01, and ***p < 0.001 by one-way analysis of variance (ANOVA) followed by Tukey's post hoc test. CTL, control.

Techniques: Control, Injection, Gene Expression, Expressing

FIGURE 6 | Effects of mixed-lineage leukemia 1 (MLL1)/ WD-40 repeat protein 5 (WDR5) complex inhibitors on peritoneal inflammation. (A, D) mRNA abundance of Il1b and Tnf in control mice, methylglyoxal (MGO)-injected mice, and MGO-injected mice treated with (A) MM-102 and (D) OICR-9429. Gene expression was normalized to the internal control Gapdh. n = 5 per group. (B, E) Representative immunohistochemical analyses showing interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α expression in peritoneal tissue from control mice, MGO-injected mice, and MGO-injected mice treated with (B) MM-102 and (E) OICR-9429. The right panels show high-magnification images of the boxed regions (scale bar: 100 μm). (C, F) Quantitative analysis of IL-1β-positive cells, IL-6-positive cells, and TNF-α-positive cells in peritoneal tissue from control mice, MGO- injected mice, and MGO-injected mice treated with (C) MM-102 and (F) OICR-9429. n = 5 per group. *p < 0.05, **p < 0.01, and ***p < 0.001 by one-way analysis of variance (ANOVA) followed by Tukey's post hoc test. CTL, control.

Journal: The FASEB Journal

Article Title: Targeting MLL1/WDR5‐Mediated Epigenetic Regulation Mitigates Peritoneal Fibrosis by Reducing p16^INK4a

doi: 10.1096/fj.202402382r

Figure Lengend Snippet: FIGURE 6 | Effects of mixed-lineage leukemia 1 (MLL1)/ WD-40 repeat protein 5 (WDR5) complex inhibitors on peritoneal inflammation. (A, D) mRNA abundance of Il1b and Tnf in control mice, methylglyoxal (MGO)-injected mice, and MGO-injected mice treated with (A) MM-102 and (D) OICR-9429. Gene expression was normalized to the internal control Gapdh. n = 5 per group. (B, E) Representative immunohistochemical analyses showing interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α expression in peritoneal tissue from control mice, MGO-injected mice, and MGO-injected mice treated with (B) MM-102 and (E) OICR-9429. The right panels show high-magnification images of the boxed regions (scale bar: 100 μm). (C, F) Quantitative analysis of IL-1β-positive cells, IL-6-positive cells, and TNF-α-positive cells in peritoneal tissue from control mice, MGO- injected mice, and MGO-injected mice treated with (C) MM-102 and (F) OICR-9429. n = 5 per group. *p < 0.05, **p < 0.01, and ***p < 0.001 by one-way analysis of variance (ANOVA) followed by Tukey's post hoc test. CTL, control.

Techniques: Control, Injection, Gene Expression, Immunohistochemical staining, Expressing

FIGURE 7 | Effects of mixed-lineage leukemia 1 (MLL1)/ WD-40 re- peat protein 5 (WDR5) complex inhibitors on functional impairment of the peritoneal membrane in mice with peritoneal fibrosis. (A, B) The dialysate/plasma ratio of urea nitrogen (D/P UN) and the peritoneal absorption of glucose from dialysate (D/D0 glucose) were assessed in control mice, methylglyoxal (MGO)-injected mice, and MGO-injected mice treated with (A) MM-102 and (B) OICR-9429 during a 10 min di- alysate dwell time (4.25% dialysis solution). n = 5 per group. **p < 0.01 and ***p < 0.001 by one-way analysis of variance (ANOVA) followed by Tukey's post hoc test. CTL, control.

Journal: The FASEB Journal

Article Title: Targeting MLL1/WDR5‐Mediated Epigenetic Regulation Mitigates Peritoneal Fibrosis by Reducing p16^INK4a

doi: 10.1096/fj.202402382r

Figure Lengend Snippet: FIGURE 7 | Effects of mixed-lineage leukemia 1 (MLL1)/ WD-40 re- peat protein 5 (WDR5) complex inhibitors on functional impairment of the peritoneal membrane in mice with peritoneal fibrosis. (A, B) The dialysate/plasma ratio of urea nitrogen (D/P UN) and the peritoneal absorption of glucose from dialysate (D/D0 glucose) were assessed in control mice, methylglyoxal (MGO)-injected mice, and MGO-injected mice treated with (A) MM-102 and (B) OICR-9429 during a 10 min di- alysate dwell time (4.25% dialysis solution). n = 5 per group. **p < 0.01 and ***p < 0.001 by one-way analysis of variance (ANOVA) followed by Tukey's post hoc test. CTL, control.

Techniques: Functional Assay, Membrane, Clinical Proteomics, Control, Injection

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