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jnk inhibitor viii  (MedChemExpress)


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    MedChemExpress jnk inhibitor viii
    Jnk Inhibitor Viii, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/jnk+inhibitor+viii/JNK+Inhibitor+VIII/bio_rxiv__64898__2026__07__23__740258-151-37-40
    Average 94 stars, based on 7 article reviews
    jnk inhibitor viii - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

    other:

    Article Title: Emetine dihydrochloride inhibits invasiveness and motility of hepatocellular carcinoma cells by blocking the MAPK pathway and inducing destabilization of Twist1
    Article Snippet: JNK inhibitor VIII (JNK inhibitor, HY107598) and SB203580 (p38 inhibitor, HY-10256) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

    Article Title: TLR9 agonist suppresses choroidal neovascularization by restricting endothelial cell motility via ERK/c-Jun pathway.
    Article Snippet: Introduction: Choroidal neovascularization (CNV) is the feature of neovascular age-related macular degeneration (AMD).. It has been demonstrated that inflammation plays a key role in the development of CNV.. Here we aim to investigate how TLR9 agonist (CpG-ODN), one of the key regulators of inflammatory responses, suppresses CNV

    Control:

    Article Title: EBV latent membrane protein 1 augments γδ T cell cytotoxicity against nasopharyngeal carcinoma by induction of butyrophilin molecules
    Article Snippet: .. Inhibitors were used prior to P 4 treatment in NPC cells: JSH-23 (10 μM; Cat. No. HY-13982, MedChemExpress) against NF-κB, SB 203580 (50 nM; Cat. No. HY-10256, MedChemExpress) against p38, JNK inhibitor VIII (50 nM/ 160 nM; Cat. No. HY-10526, MedChemExpress) against JNK1 and JNK2 respectively, or DMSO control (Cat. No. D8418, Sigma). ..

    Article Title: EBV latent membrane protein 1 augments γδ T cell cytotoxicity against nasopharyngeal carcinoma by induction of butyrophilin molecules.
    Article Snippet: .. Inhibitors were used prior to P4 treatment in NPC cells: JSH-23 (10 μM; Cat. No. HY-13982, MedChemExpress) against NF-κB, SB 203580 (50 nM; Cat. No. HY-10256, MedChemExpress) against p38, JNK inhibitor VIII (50 nM/ 160 nM; Cat. No. HY-10526, MedChemExpress) against JNK1 and JNK2 respectively, or DMSO control (Cat. No. D8418, Sigma). ..

    Knock-Out:

    Article Title: A fast 2C-induction method reveals a barrier role of SP2 for totipotency
    Article Snippet: The mESCs containing MERVL-LTR-tdTomato reporter was a gift from Wang’s lab. All the mESCs were cultured in mESC medium (DMEM High-glucose (HyClone, SH30022.01) supplemented with 15% FBS (Lonsera, S711-001s), NEAA (Gibco,11140076), Glutamax (Gibco, 35050079), Sodium Pyruvate (Gibco, 11360070), 2-Mercaptoethanol (Sigma, M3148-100ML), Leukemia Inhibitory Factor (novoprotein, C690), MEK inhibitor PD0325901 (1 μM, DC CHEMICALS, DC1056), and GSK3 inhibitor CHIR99021 (3 μM, DC CHEMICALS, DC1023)) on 0.1% gelatin coated plates. .. For 2C cell induction, mESCs were switched to 2C medium containing DMEM High-glucose, FBS (Gibco, 10099141), KnockOut SR (Gibco, 10828028), B27 (Gibco, 17504044), NEAA, 2-Mercaptoethanol, 100 nM AM580 (Selleck, S2933), 1 μM BML277 (TargetMOL, T2033), 1 μM JNK inhibitor VIII (MCE, HY-107598-1mg), 100 μM VPA (TargetMol, T7064), 5 μM EPZ5676 (Selleck, S7062), 5 mM LiCl (Sigma, 793620-500G), and 50 μg/mL Vitamin C (Sigma, 49752) for 36 h. ..



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    Fig. 4 Knockdown of ITGB3 promotes osteogenic differentiation in osteosarcoma by activating the <t>JNK/c-JUN/RUNX2</t> pathway. ITGB3-knockdown (IT GB3-KD) and ITGB3-negative control (ITGB3-NC) HOS and U2OS cells were subjected to either 8 Gy of irradiation (IR) or non-IR treatment, and additional groups were established via the application of a JNK inhibitor (SP600125, <t>JNKi)</t> 4 h before the IR or non-IR treatment to perform rescue experiments. Protein samples were collected 24 h posttreatment for western blot analysis to explore the regulatory effect of ITGB3-KD on the JNK/c-JUN pathway (A, C, and E) and whether the JNK/c-JUN pathway directly regulated osteogenic differentiation (B, D, and F) in HOS and U2OS cells. *P<0.05, **P<0.01, ***P<0.001, ns = not significant
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    Fig. 4 Knockdown of ITGB3 promotes osteogenic differentiation in osteosarcoma by activating the <t>JNK/c-JUN/RUNX2</t> pathway. ITGB3-knockdown (IT GB3-KD) and ITGB3-negative control (ITGB3-NC) HOS and U2OS cells were subjected to either 8 Gy of irradiation (IR) or non-IR treatment, and additional groups were established via the application of a JNK inhibitor (SP600125, <t>JNKi)</t> 4 h before the IR or non-IR treatment to perform rescue experiments. Protein samples were collected 24 h posttreatment for western blot analysis to explore the regulatory effect of ITGB3-KD on the JNK/c-JUN pathway (A, C, and E) and whether the JNK/c-JUN pathway directly regulated osteogenic differentiation (B, D, and F) in HOS and U2OS cells. *P<0.05, **P<0.01, ***P<0.001, ns = not significant
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    Fig. 4 Knockdown of ITGB3 promotes osteogenic differentiation in osteosarcoma by activating the <t>JNK/c-JUN/RUNX2</t> pathway. ITGB3-knockdown (IT GB3-KD) and ITGB3-negative control (ITGB3-NC) HOS and U2OS cells were subjected to either 8 Gy of irradiation (IR) or non-IR treatment, and additional groups were established via the application of a JNK inhibitor (SP600125, <t>JNKi)</t> 4 h before the IR or non-IR treatment to perform rescue experiments. Protein samples were collected 24 h posttreatment for western blot analysis to explore the regulatory effect of ITGB3-KD on the JNK/c-JUN pathway (A, C, and E) and whether the JNK/c-JUN pathway directly regulated osteogenic differentiation (B, D, and F) in HOS and U2OS cells. *P<0.05, **P<0.01, ***P<0.001, ns = not significant
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    Fig. 4 Knockdown of ITGB3 promotes osteogenic differentiation in osteosarcoma by activating the <t>JNK/c-JUN/RUNX2</t> pathway. ITGB3-knockdown (IT GB3-KD) and ITGB3-negative control (ITGB3-NC) HOS and U2OS cells were subjected to either 8 Gy of irradiation (IR) or non-IR treatment, and additional groups were established via the application of a JNK inhibitor (SP600125, <t>JNKi)</t> 4 h before the IR or non-IR treatment to perform rescue experiments. Protein samples were collected 24 h posttreatment for western blot analysis to explore the regulatory effect of ITGB3-KD on the JNK/c-JUN pathway (A, C, and E) and whether the JNK/c-JUN pathway directly regulated osteogenic differentiation (B, D, and F) in HOS and U2OS cells. *P<0.05, **P<0.01, ***P<0.001, ns = not significant
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    Fig. 4 Knockdown of ITGB3 promotes osteogenic differentiation in osteosarcoma by activating the <t>JNK/c-JUN/RUNX2</t> pathway. ITGB3-knockdown (IT GB3-KD) and ITGB3-negative control (ITGB3-NC) HOS and U2OS cells were subjected to either 8 Gy of irradiation (IR) or non-IR treatment, and additional groups were established via the application of a JNK inhibitor (SP600125, <t>JNKi)</t> 4 h before the IR or non-IR treatment to perform rescue experiments. Protein samples were collected 24 h posttreatment for western blot analysis to explore the regulatory effect of ITGB3-KD on the JNK/c-JUN pathway (A, C, and E) and whether the JNK/c-JUN pathway directly regulated osteogenic differentiation (B, D, and F) in HOS and U2OS cells. *P<0.05, **P<0.01, ***P<0.001, ns = not significant
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    Fig. 4 Knockdown of ITGB3 promotes osteogenic differentiation in osteosarcoma by activating the JNK/c-JUN/RUNX2 pathway. ITGB3-knockdown (IT GB3-KD) and ITGB3-negative control (ITGB3-NC) HOS and U2OS cells were subjected to either 8 Gy of irradiation (IR) or non-IR treatment, and additional groups were established via the application of a JNK inhibitor (SP600125, JNKi) 4 h before the IR or non-IR treatment to perform rescue experiments. Protein samples were collected 24 h posttreatment for western blot analysis to explore the regulatory effect of ITGB3-KD on the JNK/c-JUN pathway (A, C, and E) and whether the JNK/c-JUN pathway directly regulated osteogenic differentiation (B, D, and F) in HOS and U2OS cells. *P<0.05, **P<0.01, ***P<0.001, ns = not significant

    Journal: Journal of experimental & clinical cancer research : CR

    Article Title: Enhancing radiosensitivity of osteosarcoma by ITGB3 knockdown: a mechanism linked to enhanced osteogenic differentiation status through JNK/c-JUN/RUNX2 pathway activation.

    doi: 10.1186/s13046-025-03417-4

    Figure Lengend Snippet: Fig. 4 Knockdown of ITGB3 promotes osteogenic differentiation in osteosarcoma by activating the JNK/c-JUN/RUNX2 pathway. ITGB3-knockdown (IT GB3-KD) and ITGB3-negative control (ITGB3-NC) HOS and U2OS cells were subjected to either 8 Gy of irradiation (IR) or non-IR treatment, and additional groups were established via the application of a JNK inhibitor (SP600125, JNKi) 4 h before the IR or non-IR treatment to perform rescue experiments. Protein samples were collected 24 h posttreatment for western blot analysis to explore the regulatory effect of ITGB3-KD on the JNK/c-JUN pathway (A, C, and E) and whether the JNK/c-JUN pathway directly regulated osteogenic differentiation (B, D, and F) in HOS and U2OS cells. *P<0.05, **P<0.01, ***P<0.001, ns = not significant

    Article Snippet: In the cell experiments, cells treated with the JNK inhibitor (JNKi) received SP600125 (Selleck, S1460) at a final concentration of 10 μM, which was introduced into the culture medium 4 h before the application of either irradiation (IR) or non-IR treatments.

    Techniques: Knockdown, Negative Control, Irradiation, Western Blot

    Fig. 5 Knockdown of ITGB3 radiosensitizes osteosarcoma cells by promoting apoptosis through activating the JNK/c-JUN pathway. ITGB3-knockdown (ITGB3-KD) and ITGB3-negative control (ITGB3-NC) HOS and U2OS cells were subjected to either 8 Gy of irradiation (IR) or non-IR treatment, and additional groups were established in which a JNK inhibitor (SP600125, JNKi) was applied 4 h before the IR or non-IR treatment to perform rescue experiments. The apoptosis rates in HOS (A) and U2OS (B) cells were determined 24 h posttreatment using flow cytometry (n = 3 per group). Protein samples were col lected 24 h posttreatment for western blot analysis to explore the regulatory effect of the JNK/c-JUN pathway on apoptosis (C, D) in HOS and U2OS cells. *P<0.05, **P<0.01, ***P<0.001, ns = not significant

    Journal: Journal of experimental & clinical cancer research : CR

    Article Title: Enhancing radiosensitivity of osteosarcoma by ITGB3 knockdown: a mechanism linked to enhanced osteogenic differentiation status through JNK/c-JUN/RUNX2 pathway activation.

    doi: 10.1186/s13046-025-03417-4

    Figure Lengend Snippet: Fig. 5 Knockdown of ITGB3 radiosensitizes osteosarcoma cells by promoting apoptosis through activating the JNK/c-JUN pathway. ITGB3-knockdown (ITGB3-KD) and ITGB3-negative control (ITGB3-NC) HOS and U2OS cells were subjected to either 8 Gy of irradiation (IR) or non-IR treatment, and additional groups were established in which a JNK inhibitor (SP600125, JNKi) was applied 4 h before the IR or non-IR treatment to perform rescue experiments. The apoptosis rates in HOS (A) and U2OS (B) cells were determined 24 h posttreatment using flow cytometry (n = 3 per group). Protein samples were col lected 24 h posttreatment for western blot analysis to explore the regulatory effect of the JNK/c-JUN pathway on apoptosis (C, D) in HOS and U2OS cells. *P<0.05, **P<0.01, ***P<0.001, ns = not significant

    Article Snippet: In the cell experiments, cells treated with the JNK inhibitor (JNKi) received SP600125 (Selleck, S1460) at a final concentration of 10 μM, which was introduced into the culture medium 4 h before the application of either irradiation (IR) or non-IR treatments.

    Techniques: Knockdown, Negative Control, Irradiation, Flow Cytometry, Western Blot

    Fig. 7 Knockdown of ITGB3 exerts a radiosensitizing effect in osteosarcoma mouse models. ITGB3-knockdown (ITGB3-KD) and ITGB3-negative control (ITGB3-NC) HOS cells were injected into the inguinal subcutaneous region of BALB/c nude mice to establish a subcutaneous tumor model. Additionally, groups of mice receiving intraperitoneal injections of the JNK inhibitor (SP600125, JNKi) were established, with injections administered 24 h before, 4 h before, and daily after 20 Gy of local irradiation (IR) or non-IR treatment. Six days after receiving IR or non-IR treatment, mice were euthanized. Subsequent ly, the subcutaneous tumors were photographed (A), and the growth curves of the tumors were plotted, with n = 6 per group (B). ITGB3 immunohisto chemical staining was performed on subcutaneous tumor specimens from each group, and images were captured at 200x magnification (C). Statistical analysis of ITGB3 expression levels was conducted using the integrated optical density (IOD) method, with n = 3 per group. Furthermore, ITGB3-KD and ITGB3-NC HOS cells were injected into the tibial bone marrow cavity to establish an orthotopic tibial tumor model in BALB/c nude mice. The first biolumi nescence measurement was conducted before 20 Gy of local IR or non-IR treatment. On the 6th day after treatment, bioluminescence measurement was repeated to calculate the ratio of bioluminescent flux increase in the tumor area of each mouse, reflecting tumor growth. Typical images are presented (D). Note: The bioluminescent flux scale has been standardized. *P<0.05, **P<0.01, ***P<0.001, ns = not significant

    Journal: Journal of experimental & clinical cancer research : CR

    Article Title: Enhancing radiosensitivity of osteosarcoma by ITGB3 knockdown: a mechanism linked to enhanced osteogenic differentiation status through JNK/c-JUN/RUNX2 pathway activation.

    doi: 10.1186/s13046-025-03417-4

    Figure Lengend Snippet: Fig. 7 Knockdown of ITGB3 exerts a radiosensitizing effect in osteosarcoma mouse models. ITGB3-knockdown (ITGB3-KD) and ITGB3-negative control (ITGB3-NC) HOS cells were injected into the inguinal subcutaneous region of BALB/c nude mice to establish a subcutaneous tumor model. Additionally, groups of mice receiving intraperitoneal injections of the JNK inhibitor (SP600125, JNKi) were established, with injections administered 24 h before, 4 h before, and daily after 20 Gy of local irradiation (IR) or non-IR treatment. Six days after receiving IR or non-IR treatment, mice were euthanized. Subsequent ly, the subcutaneous tumors were photographed (A), and the growth curves of the tumors were plotted, with n = 6 per group (B). ITGB3 immunohisto chemical staining was performed on subcutaneous tumor specimens from each group, and images were captured at 200x magnification (C). Statistical analysis of ITGB3 expression levels was conducted using the integrated optical density (IOD) method, with n = 3 per group. Furthermore, ITGB3-KD and ITGB3-NC HOS cells were injected into the tibial bone marrow cavity to establish an orthotopic tibial tumor model in BALB/c nude mice. The first biolumi nescence measurement was conducted before 20 Gy of local IR or non-IR treatment. On the 6th day after treatment, bioluminescence measurement was repeated to calculate the ratio of bioluminescent flux increase in the tumor area of each mouse, reflecting tumor growth. Typical images are presented (D). Note: The bioluminescent flux scale has been standardized. *P<0.05, **P<0.01, ***P<0.001, ns = not significant

    Article Snippet: In the cell experiments, cells treated with the JNK inhibitor (JNKi) received SP600125 (Selleck, S1460) at a final concentration of 10 μM, which was introduced into the culture medium 4 h before the application of either irradiation (IR) or non-IR treatments.

    Techniques: Knockdown, Negative Control, Injection, Irradiation, Staining, Expressing