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Bethyl anti wdr5
Anti Wdr5, supplied by Bethyl, used in various techniques. Bioz Stars score: 94/100, based on 97 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti wdr5/product/Bethyl
Average 94 stars, based on 97 article reviews

anti wdr5 - by Bioz Stars, 2026-06

94/100 stars

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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

a. Growth curve analysis of PATC53 cells carrying shRNAs targeting WDR5 (shWDR5), DPY30 (shDPY30) or control (shCTR) and treated with vehicle (off) or doxycycline (dox) to induce the gene silencing. b. Growth curve (left) and western blot (right) of control (sgCTR) or Dpy30 -KO (sgDPY30) KPC cells. c. Clonogenic assay of KPC cells, as described in b, is shown (left) and quantified (right). d-e. Volume (d) and weight (e) of tumors from control (sgCTR) or DPY30-KO (sgDPY30) PATC53 cells grown in NSG mice. f-g . Micrographs showing the histology and Ki67 labeling in tumors described in (d). Hematoxylin and eosin (H&E) (f) staining, Ki67 IHC staining (g, left) and quantification (g, right) are shown. h-j. Heatmap showing Spearman correlations between samples and biological replicates of ATACseq (h), and H3K27ac (i) or H3K4me3 (j) Chip-seq in shCTR, shDPY30 or shWDR5 PATC53 cells. Samples are clustered by Euclidean distance and single-linkage clustering. k. Scatter plot showing mean normalized signals of H3K4me3 from samples described in j. Regions that significantly (FDR < 0.05) gained or lost H3K4me3 peaks in shDPY30 or shWDR5 versus shCTR are depicted in pink and blue, respectively. Not significant peaks are indicated as gray dots. In (a-e, g), data are expressed as mean ± SD, and dots represent biological replicates. Statistical significance was calculated using one-way ANOVA and Tukey’s multiple comparison tests (a, d, e), or Student t test (b, c, g). In panels f-g, scale bar = 200 μm.

Journal: bioRxiv

Article Title: WRAD core perturbation impairs DNA replication fidelity promoting immunoediting in pancreatic cancer

doi: 10.1101/2024.10.21.619543

Figure Lengend Snippet: a. Growth curve analysis of PATC53 cells carrying shRNAs targeting WDR5 (shWDR5), DPY30 (shDPY30) or control (shCTR) and treated with vehicle (off) or doxycycline (dox) to induce the gene silencing. b. Growth curve (left) and western blot (right) of control (sgCTR) or Dpy30 -KO (sgDPY30) KPC cells. c. Clonogenic assay of KPC cells, as described in b, is shown (left) and quantified (right). d-e. Volume (d) and weight (e) of tumors from control (sgCTR) or DPY30-KO (sgDPY30) PATC53 cells grown in NSG mice. f-g . Micrographs showing the histology and Ki67 labeling in tumors described in (d). Hematoxylin and eosin (H&E) (f) staining, Ki67 IHC staining (g, left) and quantification (g, right) are shown. h-j. Heatmap showing Spearman correlations between samples and biological replicates of ATACseq (h), and H3K27ac (i) or H3K4me3 (j) Chip-seq in shCTR, shDPY30 or shWDR5 PATC53 cells. Samples are clustered by Euclidean distance and single-linkage clustering. k. Scatter plot showing mean normalized signals of H3K4me3 from samples described in j. Regions that significantly (FDR < 0.05) gained or lost H3K4me3 peaks in shDPY30 or shWDR5 versus shCTR are depicted in pink and blue, respectively. Not significant peaks are indicated as gray dots. In (a-e, g), data are expressed as mean ± SD, and dots represent biological replicates. Statistical significance was calculated using one-way ANOVA and Tukey’s multiple comparison tests (a, d, e), or Student t test (b, c, g). In panels f-g, scale bar = 200 μm.

Article Snippet: The primary antibodies used were anti-WDR5 (rabbit), anti-DPY30 (rabbit, Bethyl), anti-PCNA (rabbit) and anti-BrdU (mouse).

Techniques: Control, Western Blot, Clonogenic Assay, Labeling, Staining, Immunohistochemistry, ChIP-sequencing, Comparison

a. Schematic representation of DPY30 interactors involved in DNA repair, replisome, and proteosome signaling pathways in PATC53, PATC66, and KPC cells. b. Western blot analysis of the indicated proteins in 293T cells co-overexpressing HA-tagged human DPY30 and His-tagged human MCM complex subunits. Control IgG and input are shown. c. Proximity Ligation Assay (PLA) staining detecting DPY30 interaction with WDHD1, MCM6, Ash2L (positive control) or Luciferase (negative control). d. Western blot analysis of the indicated proteins in 293T cells co-overexpressing Flag-tagged human WDR5 and His-tagged human MCM complex subunits. Control IgG and input are shown. e. PLA staining detecting WDR5 interaction with WDHD1, MCM6, RbBP5 (positive control) or Luciferase (negative control). f. PLA staining detecting WDR5 interaction with WDHD1 and MCM6 in PATC53 control (shCTR) or silenced for WDR5 (shWDR5). g-h. Western blot analysis of the indicated proteins in PATC53 cells control (shCTR) or silenced for WDR5 (shWDR5, g) or DPY30 (shDPy30, h). Control IgG and input are shown, and H3 was used as a loading control. i-j. Western blot analyses of the indicated proteins in KPC cells control or overexpressing DPY30 wild type (WT) or mutant (L69D) isoforms (i), and in KPC cells control or overexpressing WDR5 wild type (WT) or mutant (L240K, V268E) isoforms (j). Control IgG and input are shown, and H3 was used as a loading control. In figure, scale bar = 5 μm.

Journal: bioRxiv

Article Title: WRAD core perturbation impairs DNA replication fidelity promoting immunoediting in pancreatic cancer

doi: 10.1101/2024.10.21.619543

Figure Lengend Snippet: a. Schematic representation of DPY30 interactors involved in DNA repair, replisome, and proteosome signaling pathways in PATC53, PATC66, and KPC cells. b. Western blot analysis of the indicated proteins in 293T cells co-overexpressing HA-tagged human DPY30 and His-tagged human MCM complex subunits. Control IgG and input are shown. c. Proximity Ligation Assay (PLA) staining detecting DPY30 interaction with WDHD1, MCM6, Ash2L (positive control) or Luciferase (negative control). d. Western blot analysis of the indicated proteins in 293T cells co-overexpressing Flag-tagged human WDR5 and His-tagged human MCM complex subunits. Control IgG and input are shown. e. PLA staining detecting WDR5 interaction with WDHD1, MCM6, RbBP5 (positive control) or Luciferase (negative control). f. PLA staining detecting WDR5 interaction with WDHD1 and MCM6 in PATC53 control (shCTR) or silenced for WDR5 (shWDR5). g-h. Western blot analysis of the indicated proteins in PATC53 cells control (shCTR) or silenced for WDR5 (shWDR5, g) or DPY30 (shDPy30, h). Control IgG and input are shown, and H3 was used as a loading control. i-j. Western blot analyses of the indicated proteins in KPC cells control or overexpressing DPY30 wild type (WT) or mutant (L69D) isoforms (i), and in KPC cells control or overexpressing WDR5 wild type (WT) or mutant (L240K, V268E) isoforms (j). Control IgG and input are shown, and H3 was used as a loading control. In figure, scale bar = 5 μm.

Article Snippet: The primary antibodies used were anti-WDR5 (rabbit), anti-DPY30 (rabbit, Bethyl), anti-PCNA (rabbit) and anti-BrdU (mouse).

Techniques: Protein-Protein interactions, Western Blot, Control, Proximity Ligation Assay, Staining, Positive Control, Luciferase, Negative Control, Mutagenesis

a. Western blot analysis of proteins bound to nascent DNA retrieved using iPOND or input control in KPC cells. Cells were treated as follows: control (negative control, no biotin in the click reaction), EdU pulse (EdU treatment for 2, 5 or 10 min), chase (EdU treatment for 10 min, followed by a 60 min thymidine chase). Histone H3 was used as a loading control. b. Modified PLA (SIRF) assay detecting the interaction between the incorporated BrdU (5 min pulse) and WDR5 (left) or DPY30 (right). BrdU:PCNA and BrdU:luciferase were used as positive and negative control, respectively. Scale bar = 5 μm. c. Western blot analysis of iPOND or input control in control (sgCTR) or Dpy30 -KO (sgDpy30) KPC cells. Cells were treated as described in a. Histone H3 was used as a loading control. d. Schematic illustration and confocal images of DNA fiber assay in sgCTR and sgDpy30 KPC cells. e. Violin plots reporting mean fork progression rate (left) and fork symmetry (right) in cells as in d. f. Confocal images of DNA fiber assay in sgCTR or sgDpy30 KPC cells. White arrows indicate a fiber with non-aberrant DNA replication, yellow arrows indicate overlapped CldU and IdU incorporation (DNA re-replication). g. Violin plots reporting the frequency of DNA re-replication (left) and the fiber re-replication ratio (right) in cells as in f. h. Trend curves showing the dual CldU:IdU incorporation (score) calculated from the density of ChIPseq reads of IdU and CldU IP in sgCTR and sgDpy30 KPC cells. h. Bar plot showing genome length of single (IdU or CldU) and double nucleotide (CldU+IdU) incorporation in sgCTR and sgDpy30. j. immunofluorescence images of sgCTR or sgDpy30 KPC cells stained for pS4-8 RPA (red), pS139 H2AX (γH2AX, green), and nuclei (blue). Right, graphs reporting the percentage of γH2AX-positive or pS4-8 RPA-positive sgCTR or sgDpy30 KPC cells. Each dot represents a different analyzed field, scale bar = 100 μm. k. Left, immunofluorescence images of mitotic KPC cells stained with DAPI (DNA, white). Yellow arrows indicate lagging chromosomes and chromosome bridges. Right, violin plot reporting the mean percentage of sgCTR or sgDpy30 KPC cells with aberrant mitotic outcomes in vitro . k. Left panel, images of metaphase spreads in sgCTR or sgDpy30 KPC cells stained with Giemsa (chromosome). Red arrow indicates chromosome fusion and fragmentation. Right panel, percentage of KPC cells with normal (gray) or aberrant (yellow) mitotic outcomes. In the figure, n indicates the number of analyzed events. Data are expressed as mean values ± SD. Statistical significance was calculated using the Mann-Whitney test (e, g), Student’s t test (j, k) or Fisher’s exact Chi square test (i, l).

Journal: bioRxiv

Article Title: WRAD core perturbation impairs DNA replication fidelity promoting immunoediting in pancreatic cancer

doi: 10.1101/2024.10.21.619543

Figure Lengend Snippet: a. Western blot analysis of proteins bound to nascent DNA retrieved using iPOND or input control in KPC cells. Cells were treated as follows: control (negative control, no biotin in the click reaction), EdU pulse (EdU treatment for 2, 5 or 10 min), chase (EdU treatment for 10 min, followed by a 60 min thymidine chase). Histone H3 was used as a loading control. b. Modified PLA (SIRF) assay detecting the interaction between the incorporated BrdU (5 min pulse) and WDR5 (left) or DPY30 (right). BrdU:PCNA and BrdU:luciferase were used as positive and negative control, respectively. Scale bar = 5 μm. c. Western blot analysis of iPOND or input control in control (sgCTR) or Dpy30 -KO (sgDpy30) KPC cells. Cells were treated as described in a. Histone H3 was used as a loading control. d. Schematic illustration and confocal images of DNA fiber assay in sgCTR and sgDpy30 KPC cells. e. Violin plots reporting mean fork progression rate (left) and fork symmetry (right) in cells as in d. f. Confocal images of DNA fiber assay in sgCTR or sgDpy30 KPC cells. White arrows indicate a fiber with non-aberrant DNA replication, yellow arrows indicate overlapped CldU and IdU incorporation (DNA re-replication). g. Violin plots reporting the frequency of DNA re-replication (left) and the fiber re-replication ratio (right) in cells as in f. h. Trend curves showing the dual CldU:IdU incorporation (score) calculated from the density of ChIPseq reads of IdU and CldU IP in sgCTR and sgDpy30 KPC cells. h. Bar plot showing genome length of single (IdU or CldU) and double nucleotide (CldU+IdU) incorporation in sgCTR and sgDpy30. j. immunofluorescence images of sgCTR or sgDpy30 KPC cells stained for pS4-8 RPA (red), pS139 H2AX (γH2AX, green), and nuclei (blue). Right, graphs reporting the percentage of γH2AX-positive or pS4-8 RPA-positive sgCTR or sgDpy30 KPC cells. Each dot represents a different analyzed field, scale bar = 100 μm. k. Left, immunofluorescence images of mitotic KPC cells stained with DAPI (DNA, white). Yellow arrows indicate lagging chromosomes and chromosome bridges. Right, violin plot reporting the mean percentage of sgCTR or sgDpy30 KPC cells with aberrant mitotic outcomes in vitro . k. Left panel, images of metaphase spreads in sgCTR or sgDpy30 KPC cells stained with Giemsa (chromosome). Red arrow indicates chromosome fusion and fragmentation. Right panel, percentage of KPC cells with normal (gray) or aberrant (yellow) mitotic outcomes. In the figure, n indicates the number of analyzed events. Data are expressed as mean values ± SD. Statistical significance was calculated using the Mann-Whitney test (e, g), Student’s t test (j, k) or Fisher’s exact Chi square test (i, l).

Article Snippet: The primary antibodies used were anti-WDR5 (rabbit), anti-DPY30 (rabbit, Bethyl), anti-PCNA (rabbit) and anti-BrdU (mouse).

Techniques: Western Blot, Control, Negative Control, Modification, Luciferase, Immunofluorescence, Staining, In Vitro, MANN-WHITNEY

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