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anti mybl2 antibody (Proteintech)

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Proteintech anti mybl2 antibody
Anti Mybl2 Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 33 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+mybl2/B-Myb+Antibody/pm41866755-130-7-10
Average 93 stars, based on 33 article reviews

anti mybl2 antibody - by Bioz Stars, 2026-09

93/100 stars

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Expressing:

Article Title: 7,7”-dimethoxyagastisflavone induced MYCN/MYBL2-dependent apoptosis and metabolism reprogramming in Sonic Hedgehog medulloblastoma
Article Snippet: .. To assess MYCN and MYBL2 expression levels, we used anti-MYCN (Proteintech, Cat#10159-2-AP, RRID: AB_2266881) and anti-MYBL2 (Proteintech, Cat#18896-1-AP, RRID: AB_10644283) antibodies, respectively. ..

Immunohistochemistry:

Article Title: WEE1 inhibitor exerts synergistic effect with KRAS G12C inhibitor via MYBL2-RRM2 axis in KRAS G12C -mutant lung cancer
Article Snippet: .. For IHC staining, Ki67, MYBL2, RRM2, and γH2AX protein levels in the tumor samples harvested from mice were assessed by IHC using anti-Ki67 (1:1600 dilution, ABclonal), anti-MYBL2 (1:1000 dilution, Proteintech), anti-RRM2 (1:1200 dilution, ABclonal), and anti-γH2AX (1:800 dilution, ABclonal). .. For IHC staining in human LUAD tissue, MYBL2 and RRM2 protein levels in the tumor and normal lung samples were assessed by IHC using anti-MYBL2 (1:400 dilution, Proteintech) and anti-RRM2 (1:400 dilution, ABclonal).

Article Title: WEE1 inhibitor exerts synergistic effect with KRAS G12C inhibitor via MYBL2-RRM2 axis in KRAS G12C -mutant lung cancer
Article Snippet: For IHC staining, Ki67, MYBL2, RRM2, and γH2AX protein levels in the tumor samples harvested from mice were assessed by IHC using anti-Ki67 (1:1600 dilution, ABclonal), anti-MYBL2 (1:1000 dilution, Proteintech), anti-RRM2 (1:1200 dilution, ABclonal), and anti-γH2AX (1:800 dilution, ABclonal). .. For IHC staining in human LUAD tissue, MYBL2 and RRM2 protein levels in the tumor and normal lung samples were assessed by IHC using anti-MYBL2 (1:400 dilution, Proteintech) and anti-RRM2 (1:400 dilution, ABclonal). ..

Article Title: WEE1 inhibitor exerts synergistic effect with KRAS G12C inhibitor via MYBL2-RRM2 axis in KRAS G12C -mutant lung cancer.
Article Snippet: For IHC staining, Ki67, MYBL2, RRM2, and γH2AX protein levels in the tumor Cell Death and Disease (2025) 16:661 samples harvested from mice were assessed by IHC using anti-Ki67 (1:1600 dilution, ABclonal), anti-MYBL2 (1:1000 dilution, Proteintech), anti-RRM2 (1:1200 dilution, ABclonal), and anti-γH2AX (1:800 dilution, ABclonal). .. For IHC staining in human LUAD tissue, MYBL2 and RRM2 protein levels in the tumor and normal lung samples were assessed by IHC using anti-MYBL2 (1:400 dilution, Proteintech) and anti-RRM2 (1:400 dilution, ABclonal). ..

Article Title: WEE1 inhibitor exerts synergistic effect with KRAS G12C inhibitor via MYBL2-RRM2 axis in KRAS G12C -mutant lung cancer.
Article Snippet: .. For IHC staining, Ki67, MYBL2, RRM2, and γH2AX protein levels in the tumor Cell Death and Disease (2025) 16:661 samples harvested from mice were assessed by IHC using anti-Ki67 (1:1600 dilution, ABclonal), anti-MYBL2 (1:1000 dilution, Proteintech), anti-RRM2 (1:1200 dilution, ABclonal), and anti-γH2AX (1:800 dilution, ABclonal). .. For IHC staining in human LUAD tissue, MYBL2 and RRM2 protein levels in the tumor and normal lung samples were assessed by IHC using anti-MYBL2 (1:400 dilution, Proteintech) and anti-RRM2 (1:400 dilution, ABclonal).

Staining:

Western Blot:

Article Title: Up-regulation of RAN by MYBL2 maintains osteosarcoma cancer stem-like cells population during heterogeneous tumor generation.
Article Snippet: Intratumor heterogeneity is one of the major features of cancers, leading to aggressive disease and treatment failure.. Cancer stem-like cells (CSCs) are believed to give rise to the heterogeneous cell types within tumors.. Hence, understanding the regulatory mechanism underlying the recurrence process of heterogeneous tumor by CSCs could facilitate the development of CSC-targeted therapies.

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The expression of MYCN and MYBL2 was elevated in SHH MB patients and correlates with a poor prognosis. ( A ) MYCN and MYBL2 expression levels in SHH MB tumors and normal brains (NBs) were analyzed from the TVGH/TMUH cohort. Data are represented as mean ± SD ( n = 3 for the NB group, n = 24 for the SHH group). Statistical analyses were performed using the Student’s t -test. ( B ) Correlation of MYCN and MYBL2 gene expression. ( C ) Ratio of MYCN and MYBL2 expression in SHH MB patients. ( D ) Overall survival of SHH MB patients with high or low levels of MYCN and MYBL2

Journal: Journal of Translational Medicine

Article Title: 7,7”-dimethoxyagastisflavone induced MYCN/MYBL2-dependent apoptosis and metabolism reprogramming in Sonic Hedgehog medulloblastoma

doi: 10.1186/s12967-026-07809-8

Figure Lengend Snippet: The expression of MYCN and MYBL2 was elevated in SHH MB patients and correlates with a poor prognosis. ( A ) MYCN and MYBL2 expression levels in SHH MB tumors and normal brains (NBs) were analyzed from the TVGH/TMUH cohort. Data are represented as mean ± SD ( n = 3 for the NB group, n = 24 for the SHH group). Statistical analyses were performed using the Student’s t -test. ( B ) Correlation of MYCN and MYBL2 gene expression. ( C ) Ratio of MYCN and MYBL2 expression in SHH MB patients. ( D ) Overall survival of SHH MB patients with high or low levels of MYCN and MYBL2

Article Snippet: The expression of MYCN and MYBL2 in tumors was determined by staining with anti-mouse MYCN (1:500, Proteintech, Cat#10159-2-AP, RRID: AB_2266881) and anti-mouse MYBL2 (1:500, Proteintech, Cat#18896-1-AP, RRID: AB_10644283) antibodies.

Techniques: Expressing, Gene Expression

DMGF induced apoptotic cell death and cell cycle arrest through inhibiting MYCN and MYBL2 expression. ( A ) Inhibitory effects of DMGF on cell proliferation. MB cells were treated with various concentrations of DMGF for 48 h. Cell viability was measured by MTT assay. Results are shown as mean ± SD ( n = 6). ( B , C ) DMGF increased active caspase-3 activity and TUNEL signals. Paclitaxel (30 ng/mL) was used as a positive control. Ctrl: control (untreated) cells. P: Paclitaxel 30 ng/mL. D1 and D2: DMGF 1 and 2 µg/mL. *, P < 0.05; **, P < 0.01; ***, P < 0.001, compared to the control group using one-way ANOVA followed by Dunnett’s multiple comparison test. ( D ) The top 10 differentially down-regulated hallmark pathways in Daoy-MYCN cells after DMGF treatment. ( E ) The genes that overlap with the genes in the hallmark gene sets of MYC target v1, MYC target v2, and G2M checkpoint in Daoy-MYCN cells after DMGF treatment. ( F ) DMGF suppressed MYCN and MYBL2 expression in MB cells. MB cells were treated with DMGF for 48 h; MYCN and MYBL2 were detected by western blot. ( G ) Cell cycle distribution of DMGF-treated MB cells. After treatment for 24 h with DMGF (0 and 2 µg/mL), a propidium iodide staining assay was performed on MB cells. Cell cycle distribution was detected by flow cytometry. All data are represented as mean ± S.D. *, P < 0.05; **, P < 0.01; ***, P < 0.001, compared to the control group using one-way ANOVA followed by Dunnett’s multiple comparison test. ( H ) Effect of DMGF on expression of cell cycle checkpoint proteins, such as cyclins, CDKs, p21 and p27. All cell cycle checkpoint proteins were analyzed by Western blot. β-actin was used as a loading control

Journal: Journal of Translational Medicine

Article Title: 7,7”-dimethoxyagastisflavone induced MYCN/MYBL2-dependent apoptosis and metabolism reprogramming in Sonic Hedgehog medulloblastoma

doi: 10.1186/s12967-026-07809-8

Figure Lengend Snippet: DMGF induced apoptotic cell death and cell cycle arrest through inhibiting MYCN and MYBL2 expression. ( A ) Inhibitory effects of DMGF on cell proliferation. MB cells were treated with various concentrations of DMGF for 48 h. Cell viability was measured by MTT assay. Results are shown as mean ± SD ( n = 6). ( B , C ) DMGF increased active caspase-3 activity and TUNEL signals. Paclitaxel (30 ng/mL) was used as a positive control. Ctrl: control (untreated) cells. P: Paclitaxel 30 ng/mL. D1 and D2: DMGF 1 and 2 µg/mL. *, P < 0.05; **, P < 0.01; ***, P < 0.001, compared to the control group using one-way ANOVA followed by Dunnett’s multiple comparison test. ( D ) The top 10 differentially down-regulated hallmark pathways in Daoy-MYCN cells after DMGF treatment. ( E ) The genes that overlap with the genes in the hallmark gene sets of MYC target v1, MYC target v2, and G2M checkpoint in Daoy-MYCN cells after DMGF treatment. ( F ) DMGF suppressed MYCN and MYBL2 expression in MB cells. MB cells were treated with DMGF for 48 h; MYCN and MYBL2 were detected by western blot. ( G ) Cell cycle distribution of DMGF-treated MB cells. After treatment for 24 h with DMGF (0 and 2 µg/mL), a propidium iodide staining assay was performed on MB cells. Cell cycle distribution was detected by flow cytometry. All data are represented as mean ± S.D. *, P < 0.05; **, P < 0.01; ***, P < 0.001, compared to the control group using one-way ANOVA followed by Dunnett’s multiple comparison test. ( H ) Effect of DMGF on expression of cell cycle checkpoint proteins, such as cyclins, CDKs, p21 and p27. All cell cycle checkpoint proteins were analyzed by Western blot. β-actin was used as a loading control

Techniques: Expressing, MTT Assay, Activity Assay, TUNEL Assay, Positive Control, Control, Comparison, Western Blot, Staining, Flow Cytometry

Therapeutic effects of DMGF alone or in combination with cisplatin on tumor growth in orthotopic MYCN-overexpressing MB mice. SCID mice were inoculated with Daoy-MYCN cells in the left cerebral hemisphere and then intravenously treated with 10 mg/kg DMGF and/or 3 mg/kg cisplatin ( n = 7 for each treatment group and n = 8 for the control group). ( A ) IVIS image of tumor volumes in DMGF and/or cisplatin treated mice. Tumor cells in the C7, C8, and Cis3 mice metastasized to the lung. ( B ) Record of body weights in DMGF and/or cisplatin treated mice. Data are presented as mean ± SD. **, P < 0.01, compared to the untreated group using two-way ANOVA followed by Dunnett’s multiple comparison test. ( C ) Tumor metastasis in DMGF and/or cisplatin treated mice are summarized. Pink: tumor within brain. Blue: tumor metastasized to spine and outside the CNS. ( D ) Record of tumor volumes in DMGF and/or cisplatin-treated mice. Mouse tumor volumes on day 33 were shown ( n = 3–6). Statistical analyses were performed using two-way ANOVA followed by Dunnett’s multiple comparison test. ( E ) Survival curve of DMGF and/or cisplatin treated mice. Statistical analyses were performed using one-way ANOVA with log-rank test for survival curves. ( F ) MYCN, MYBL2 and active caspase-3 expression in tumors from DMGF/cisplatin-treated orthotopic Daoy-MYCN tumor mice. ( G ) M1 and M2 macrophages and their cytokines in tumor from DMGF and/or cisplatin-treated mice

Journal: Journal of Translational Medicine

Article Title: 7,7”-dimethoxyagastisflavone induced MYCN/MYBL2-dependent apoptosis and metabolism reprogramming in Sonic Hedgehog medulloblastoma

doi: 10.1186/s12967-026-07809-8

Figure Lengend Snippet: Therapeutic effects of DMGF alone or in combination with cisplatin on tumor growth in orthotopic MYCN-overexpressing MB mice. SCID mice were inoculated with Daoy-MYCN cells in the left cerebral hemisphere and then intravenously treated with 10 mg/kg DMGF and/or 3 mg/kg cisplatin ( n = 7 for each treatment group and n = 8 for the control group). ( A ) IVIS image of tumor volumes in DMGF and/or cisplatin treated mice. Tumor cells in the C7, C8, and Cis3 mice metastasized to the lung. ( B ) Record of body weights in DMGF and/or cisplatin treated mice. Data are presented as mean ± SD. **, P < 0.01, compared to the untreated group using two-way ANOVA followed by Dunnett’s multiple comparison test. ( C ) Tumor metastasis in DMGF and/or cisplatin treated mice are summarized. Pink: tumor within brain. Blue: tumor metastasized to spine and outside the CNS. ( D ) Record of tumor volumes in DMGF and/or cisplatin-treated mice. Mouse tumor volumes on day 33 were shown ( n = 3–6). Statistical analyses were performed using two-way ANOVA followed by Dunnett’s multiple comparison test. ( E ) Survival curve of DMGF and/or cisplatin treated mice. Statistical analyses were performed using one-way ANOVA with log-rank test for survival curves. ( F ) MYCN, MYBL2 and active caspase-3 expression in tumors from DMGF/cisplatin-treated orthotopic Daoy-MYCN tumor mice. ( G ) M1 and M2 macrophages and their cytokines in tumor from DMGF and/or cisplatin-treated mice

Techniques: Control, Comparison, Expressing

Brain-wide distribution of MYCN and MYBL2 expression in orthotopic xenograft mice. ( A-C ) Image profiles of the MYCN expression of Daoy-MYCN tumors in orthotopic xenograft mice that did not receive DMGF treatment and ( D-E ) in the DMGF-treated mice. ( A ) IVIS images of Daoy-MYCN tumors were detected on days 3 and 17 in the control mice. ( B ) MYCN expression in different horizontal sections of Daoy-MYCN tumors in the control mice. MYCN is highly expressed in the brain, including the cerebral cortex, hippocampal formations, midbrain, and cerebellum. ( C ) MYCN expression in the spinal cord in orthotopic xenograft mice that did not receive DMGF treatment. ( D ) IVIS images of Daoy-MYCN tumors were detected on days 3 and 17 in the DMGF-treated mice. ( E ) MYCN expression was low in horizontal sections of Daoy-MYCN tumors from mice treated with DMGF. ( F-H ) Image profiles of the MYBL2 expression of Daoy-MYCN tumors in orthotopic xenograft mice that did not receive DMGF treatment and ( I-J ) in the DMGF-treated mice. ( F ) IVIS images of Daoy-MYCN tumors were detected on days 3 and 17 in the control mice. ( G ) MYBL2 expression in different horizontal sections of Daoy-MYCN tumors in the control mice. MYBL2 is highly expressed in the brain, including the cerebral cortex, midbrain, and cerebellum. ( H ) MYBL2 expression in the spinal cord in orthotopic xenograft mice that did not receive DMGF treatment. ( I ) IVIS images of Daoy-MYCN tumors detected at days 3 and 17 in the DMGF-treated mice. ( J ) MYBL2 expression was low in horizontal sections of Daoy-MYCN tumors from mice treated with DMGF. Red: tumor cells with MYCN or MYBL2 expression. 1 and 2 mean Zoom in position 1 and 2 in each section

Journal: Journal of Translational Medicine

Article Title: 7,7”-dimethoxyagastisflavone induced MYCN/MYBL2-dependent apoptosis and metabolism reprogramming in Sonic Hedgehog medulloblastoma

doi: 10.1186/s12967-026-07809-8

Figure Lengend Snippet: Brain-wide distribution of MYCN and MYBL2 expression in orthotopic xenograft mice. ( A-C ) Image profiles of the MYCN expression of Daoy-MYCN tumors in orthotopic xenograft mice that did not receive DMGF treatment and ( D-E ) in the DMGF-treated mice. ( A ) IVIS images of Daoy-MYCN tumors were detected on days 3 and 17 in the control mice. ( B ) MYCN expression in different horizontal sections of Daoy-MYCN tumors in the control mice. MYCN is highly expressed in the brain, including the cerebral cortex, hippocampal formations, midbrain, and cerebellum. ( C ) MYCN expression in the spinal cord in orthotopic xenograft mice that did not receive DMGF treatment. ( D ) IVIS images of Daoy-MYCN tumors were detected on days 3 and 17 in the DMGF-treated mice. ( E ) MYCN expression was low in horizontal sections of Daoy-MYCN tumors from mice treated with DMGF. ( F-H ) Image profiles of the MYBL2 expression of Daoy-MYCN tumors in orthotopic xenograft mice that did not receive DMGF treatment and ( I-J ) in the DMGF-treated mice. ( F ) IVIS images of Daoy-MYCN tumors were detected on days 3 and 17 in the control mice. ( G ) MYBL2 expression in different horizontal sections of Daoy-MYCN tumors in the control mice. MYBL2 is highly expressed in the brain, including the cerebral cortex, midbrain, and cerebellum. ( H ) MYBL2 expression in the spinal cord in orthotopic xenograft mice that did not receive DMGF treatment. ( I ) IVIS images of Daoy-MYCN tumors detected at days 3 and 17 in the DMGF-treated mice. ( J ) MYBL2 expression was low in horizontal sections of Daoy-MYCN tumors from mice treated with DMGF. Red: tumor cells with MYCN or MYBL2 expression. 1 and 2 mean Zoom in position 1 and 2 in each section

Techniques: Expressing, Control

DMGF effectively induced cell death by inhibiting the expression of MYCN and MYBL2 in primary SHH MB cells. ( A ) Expression of MYCN and MYBL2 in primary cells generated from SHH MB patients in the TVGH/TMUH cohort. ( B , C ) Effects of DMGF on cytotoxicity and anti-migration in primary SHH MB cells. ( D ) DMGF suppressed MYCN and MYBL2 expression in primary SHH MB cells. ***, P < 0.001; ****, P < 0.0001, compared to the untreated group using one-way ANOVA followed by Dunnett’s multiple comparison test. All data are represented as mean ± SD from three independent experiments, each performed in triplicate ( n = 3)

Journal: Journal of Translational Medicine

Article Title: 7,7”-dimethoxyagastisflavone induced MYCN/MYBL2-dependent apoptosis and metabolism reprogramming in Sonic Hedgehog medulloblastoma

doi: 10.1186/s12967-026-07809-8

Figure Lengend Snippet: DMGF effectively induced cell death by inhibiting the expression of MYCN and MYBL2 in primary SHH MB cells. ( A ) Expression of MYCN and MYBL2 in primary cells generated from SHH MB patients in the TVGH/TMUH cohort. ( B , C ) Effects of DMGF on cytotoxicity and anti-migration in primary SHH MB cells. ( D ) DMGF suppressed MYCN and MYBL2 expression in primary SHH MB cells. ***, P < 0.001; ****, P < 0.0001, compared to the untreated group using one-way ANOVA followed by Dunnett’s multiple comparison test. All data are represented as mean ± SD from three independent experiments, each performed in triplicate ( n = 3)

Techniques: Expressing, Generated, Migration, Comparison

DMGF inhibited MYCN and MYBL2 by interacting activin receptor type IIB (ActRIIB). ( A ) The distinct classes of potential targets of DMGF. The protein targets were predicted by the Way2Drug webtool ( https://www.way2drug.com/passtargets/ ). ( B , C ) ActRIIB expression in MB patient’s tumors and MB cell lines was confirmed. ( D ) Docking of DMGF (pink) into the kinase domain of ActRIIB (AF- Q13705 -F1-v4). DMGF was located at the hinge loop (blue) containing the ATP binding site and interacted with Thr265, Ala266, Asp275, and Lys325. ( E ) DMGF was located at the activation loop (green) and interacted with Arg200, Thr274, Lys323, Ser324, Lys325, Asp339, and Tyr364. ( F-G ) Protein expression of Smad1/5/8 and PI3K/AKT/mTOR pathways

Journal: Journal of Translational Medicine

Article Title: 7,7”-dimethoxyagastisflavone induced MYCN/MYBL2-dependent apoptosis and metabolism reprogramming in Sonic Hedgehog medulloblastoma

doi: 10.1186/s12967-026-07809-8

Figure Lengend Snippet: DMGF inhibited MYCN and MYBL2 by interacting activin receptor type IIB (ActRIIB). ( A ) The distinct classes of potential targets of DMGF. The protein targets were predicted by the Way2Drug webtool ( https://www.way2drug.com/passtargets/ ). ( B , C ) ActRIIB expression in MB patient’s tumors and MB cell lines was confirmed. ( D ) Docking of DMGF (pink) into the kinase domain of ActRIIB (AF- Q13705 -F1-v4). DMGF was located at the hinge loop (blue) containing the ATP binding site and interacted with Thr265, Ala266, Asp275, and Lys325. ( E ) DMGF was located at the activation loop (green) and interacted with Arg200, Thr274, Lys323, Ser324, Lys325, Asp339, and Tyr364. ( F-G ) Protein expression of Smad1/5/8 and PI3K/AKT/mTOR pathways

Techniques: Expressing, Binding Assay, Activation Assay

The proposed mechanism of DMGF-induced inhibition of MYCN and MYBL2 contributes to cell death, anti-metastasis, and metabolic alteration in SHH MB cells, and affects macrophage polarization

Journal: Journal of Translational Medicine

Article Title: 7,7”-dimethoxyagastisflavone induced MYCN/MYBL2-dependent apoptosis and metabolism reprogramming in Sonic Hedgehog medulloblastoma

doi: 10.1186/s12967-026-07809-8

Figure Lengend Snippet: The proposed mechanism of DMGF-induced inhibition of MYCN and MYBL2 contributes to cell death, anti-metastasis, and metabolic alteration in SHH MB cells, and affects macrophage polarization

Techniques: Inhibition

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