wee1 antibody (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc
wee1 antibody
Wee1 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/wee1/pmc13045254-251-0-2
Average 86 stars, based on 1 article reviews
Wee1 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/wee1/pmc13045254-251-0-2
Average 86 stars, based on 1 article reviews
wee1 antibody - by Bioz Stars,
2026-10
86/100 stars
Images
1) Product Images from "Dual Targeting of DNA and EGFR by ZYH005 Induces DNA Damage and Mitotic Catastrophe in Glioblastoma"
Article Title: Dual Targeting of DNA and EGFR by ZYH005 Induces DNA Damage and Mitotic Catastrophe in Glioblastoma
Journal: MedComm
doi: 10.1002/mco2.70717
Figure Legend Snippet: Z5 induces G2/M arrest and mitotic catastrophe in GBM cells. (A) Cell cycle distribution in GBM cell lines was analyzed by flow cytometry after 24 h of Z5 treatment. n = 3. (B) Representative flow cytometric analysis of PHH3+ and DNA contents > 4n cells. (C) Cell cycle profiles of NC and si‐EGFR GBM cells were assessed by flow cytometry after 24 h Z5 treatment. (D) Expression of WEE1, p‐WEE1, PHH3, CDC2, and p‐CDC2 was analyzed by immunoblotting after 48 h treatment with increasing concentrations of Z5. (E) IF staining was performed with anti‐tubulin (red) and anti‐PHH3 (green) antibodies in U87‐MG and U251‐MG cells treated with DMSO or Z5.
Techniques Used: Flow Cytometry, Expressing, Western Blot, Staining
Figure Legend Snippet: Z5 disrupts the nuclear EGFR–WEE1 axis. (A) Correlation between EGFR and WEE1 expression in GBM patients. (B) SPR analysis of the interaction between the kinase domains of EGFR and WEE1. (C) Co‐IP was performed to assess EGFR–WEE1 interaction in U87‐MG cells after 15 min Z5 treatment. (D) Western blot analysis of WEE1, p‐WEE1, p‐CDC2, EGFR, and p‐EGFR in HEK293T cells transfected with empty vector, WT‐EGFR, or E762V‐EGFR. (E) Subcellular localization of EGFR and WEE1 in the cytoplasm and nucleus was analyzed in U87‐MG cells after 15 min Z5 treatment. (F‐G) IF staining of EGFR and WEE1 in NC and siKPNA2‐1400 U87‐MG cells. (H) Growth curves of NC and siKPNA2‐1400 U87 cells after 48 h Z5 treatment. n = 3. (I) Antiproliferative effect of Z5 was assessed by EdU staining in NC and siKPNA2‐1400 U87‐MG cells. (J) Cell cycle distribution was analyzed by flow cytometry in NC and siKPNA2‐1400 U87‐MG cells after 24 h Z5 treatment.
Techniques Used: Expressing, Co-Immunoprecipitation Assay, Western Blot, Transfection, Plasmid Preparation, Staining, Flow Cytometry
Figure Legend Snippet: Z5 suppresses GSCs tumorigenesis and inhibits EGFR‐related signaling in vivo. (A) Representative tumor sphere formation assay in T3359 cells treated with different concentrations of Z5 for 48 h. Scale bar = 400 µm. (B) Quantitative analysis of tumor sphere fragmentation from (A). The data are presented as the mean ± SD, n = 3, compared with the “0” group. (C) Expression of γ‐H2AX, WEE1, p‐WEE1, PHH3, CDC2, p‐CDC2, EGFR, p‐EGFR, ERK, p‐ERK, mTOR, and p‐mTOR in T3359 cells with DMSO or Z5 treatment. (D) H&E staining of intracranial xenografts to assess tumor formation. (E) Survival analysis of mice orthotopically implanted with GSCs. The data are presented as the mean ± SD, n = 4, compared with the NT group. (F) Immunohistochemical analysis of EGFR and WEE1 expression in orthotopic tumor tissues. (G) Quantification of EGFR and WEE1 levels by average optical density from five fields per mouse. The data are presented as the mean ± SD, n = 15, compared with the NT group. (H) Schematic diagram illustrating the mechanism of Z5.
Techniques Used: In Vivo, Tube Formation Assay, Expressing, Staining, Immunohistochemical staining
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Article Snippet: Cells were lysed with Triton-X lysis buffer (50 mM Tris-HCl pH 7.5, 10 % glycerol, 150 mM NaCl, 1 mM EDTA, 1 % Triton-x-100, 50 mM NaF) supplemented with protease and phosphatase inhibitor cocktails (#B14001 and #B15001, Selleckchem). .. Protein in the lysates was quantified using Pierce 660 nm Protein Assay reagent and Nanodrop (Thermo Fisher Scientific), then mixed with 4X Laemmli sample buffer (#1610747, Bio-Rad Laboratories, California, USA) and β-mercaptoethanol, separated in SDS-PAGE with 4-20% gradient gels (Bio-Rad Laboratories), and transferred to 0.45 μm nitrocellulose membranes, followed by incubation with the following primary antibodies (all used 1:1,000 dilution, if not stated otherwise): β-tubulin (#2146, Cell Signaling Technology (CST), Danvers, MA, USA), β-actin (#4967, CST), caveolin 1 (#3267, CST), FoxO3a (#99199, CST), c-MYC (#13987, CST), AKT (#2920, CST), AKT- AR TI CL E IN P RE SS pSer473 (#4060, CST), E-cadherin (#14472S, CST), E-cadherin (#3195, CST), ERK1/2 (#4696, CST), ERK1/2-pThr202/Tyr204 (#9101, CST), GAPDH (#G8795, Sigma-Aldrich, Burlington, MA, USA or #AHP1628, Bio-Rad Laboratories), NF-kB p65 (#6956, CST), NF-kB p65-pSer536 (#3033, CST), STAT3 (#9139, CST), STAT3-pTyr705 (#9145, CST), STAT1 (#65917, CST), STAT1-pTyr701 (#88845, CST), PTK7 (#25618, CST), ROR1 (#16540, CST, 1:500), EGFR (#4267, CST), Article Title: ROR1-PI3K/AKT signaling drives adaptive resistance to cell cycle blockade in TP53 mutated ovarian cancer Article Snippet: Cells were lysed with Triton-X lysis buffer (50 mM Tris-HCl pH 7.5, 10% glycerol, 150 mM NaCl, 1 mM EDTA, 1% Triton-x-100, 50 mM NaF) supplemented with protease and phosphatase inhibitor cocktails (# B14001 and # B15001 , Selleckchem). .. 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Article Snippet: Cells were lysed with Triton-X lysis buffer (50 mM Tris-HCl pH 7.5, 10 % glycerol, 150 mM NaCl, 1 mM EDTA, 1 % Triton-x-100, 50 mM NaF) supplemented with protease and phosphatase inhibitor cocktails (#B14001 and #B15001, Selleckchem). .. 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Protein in the lysates was quantified using Pierce 660 nm Protein Assay reagent and Nanodrop (Thermo Fisher Scientific), then mixed with 4X Laemmli sample buffer (#1610747, Bio-Rad Laboratories, California, USA) and β-mercaptoethanol, separated in SDS-PAGE with 4-20% gradient gels (Bio-Rad Laboratories), and transferred to 0.45 μm nitrocellulose membranes, followed by incubation with the following primary antibodies (all used 1:1,000 dilution, if not stated otherwise): β-tubulin (#2146, Cell Signaling Technology (CST), Danvers, MA, USA), β-actin (#4967, CST), caveolin 1 (#3267, CST), FoxO3a (#99199, CST), c-MYC (#13987, CST), AKT (#2920, CST), AKT-pSer473 (#4060, CST), E-cadherin (#14472S, CST), E-cadherin (#3195, CST), ERK1/2 (#4696, CST), ERK1/2-pThr202/Tyr204 (#9101, CST), GAPDH (#G8795, Sigma-Aldrich, Burlington, MA, USA or #AHP1628, Bio-Rad Laboratories), NF-kB p65 (#6956, CST), NF-kB p65-pSer536 (#3033, CST), STAT3 (#9139, CST), STAT3-pTyr705 (#9145, CST), STAT1 (#65917, CST), STAT1-pTyr701 (#88845, CST), PTK7 (#25618, CST), ROR1 (#16540, CST, 1:500), EGFR (#4267, CST), |
