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primary antibodies against nik  (Proteintech)


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    Proteintech primary antibodies against nik
    SMP protected against CCl 4 -induced liver injury in mice by inhibiting <t>NIK/NF-κB.</t> 8-Week-old male C57BL/6J mice were divided into the following five groups: the control group (treated daily with saline and an intraperitoneal injection of olive oil on the 14th day), CCl 4 group (treated daily with saline and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day), SMP group (treated daily with SMP at 50, 100, or 200 mg/kg, and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day). (A) Immunofluorescence observation of macrophages in liver tissue (F4/80); (B) Immunofluorescence observation of neutrophils in liver tissue (Ly6G); (C) Immunofluorescence observation of CD8 T cells in liver tissue (CD8 + ); (D) Protein expression levels of NRF2 determined via Western blot; (E) Protein expression levels of TRAF3 determined via Western blot; (F) Protein expression levels of NIK, and <t>p52</t> determined via Western blot. All data are presented as the mean ± SD. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. For immunofluorescence and Western blot analyses, quantitative data were derived from independent biological samples from individual mice. n = 8, *P < 0.05, **P < 0.01, ***P < 0.001.
    Primary Antibodies Against Nik, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 25 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+map4k4/MAP4K4+Antibody/pmc13677544-150-1-6
    Average 93 stars, based on 25 article reviews
    primary antibodies against nik - by Bioz Stars, 2026-11
    93/100 stars

    Images

    1) Product Images from "Silybum marianum peptide-rich fraction alleviates acute liver injury by inhibiting TRAF3/NIK/NF-κB and is associated with changes in gut microbiota composition"

    Article Title: Silybum marianum peptide-rich fraction alleviates acute liver injury by inhibiting TRAF3/NIK/NF-κB and is associated with changes in gut microbiota composition

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2026.1915943

    SMP protected against CCl 4 -induced liver injury in mice by inhibiting NIK/NF-κB. 8-Week-old male C57BL/6J mice were divided into the following five groups: the control group (treated daily with saline and an intraperitoneal injection of olive oil on the 14th day), CCl 4 group (treated daily with saline and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day), SMP group (treated daily with SMP at 50, 100, or 200 mg/kg, and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day). (A) Immunofluorescence observation of macrophages in liver tissue (F4/80); (B) Immunofluorescence observation of neutrophils in liver tissue (Ly6G); (C) Immunofluorescence observation of CD8 T cells in liver tissue (CD8 + ); (D) Protein expression levels of NRF2 determined via Western blot; (E) Protein expression levels of TRAF3 determined via Western blot; (F) Protein expression levels of NIK, and p52 determined via Western blot. All data are presented as the mean ± SD. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. For immunofluorescence and Western blot analyses, quantitative data were derived from independent biological samples from individual mice. n = 8, *P < 0.05, **P < 0.01, ***P < 0.001.
    Figure Legend Snippet: SMP protected against CCl 4 -induced liver injury in mice by inhibiting NIK/NF-κB. 8-Week-old male C57BL/6J mice were divided into the following five groups: the control group (treated daily with saline and an intraperitoneal injection of olive oil on the 14th day), CCl 4 group (treated daily with saline and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day), SMP group (treated daily with SMP at 50, 100, or 200 mg/kg, and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day). (A) Immunofluorescence observation of macrophages in liver tissue (F4/80); (B) Immunofluorescence observation of neutrophils in liver tissue (Ly6G); (C) Immunofluorescence observation of CD8 T cells in liver tissue (CD8 + ); (D) Protein expression levels of NRF2 determined via Western blot; (E) Protein expression levels of TRAF3 determined via Western blot; (F) Protein expression levels of NIK, and p52 determined via Western blot. All data are presented as the mean ± SD. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. For immunofluorescence and Western blot analyses, quantitative data were derived from independent biological samples from individual mice. n = 8, *P < 0.05, **P < 0.01, ***P < 0.001.

    Techniques Used: Control, Saline, Injection, Immunofluorescence, Tissue, Expressing, Western Blot, Derivative Assay

    SMP alleviated cell damage by inhibiting NIK/NF-κB. After the appropriate SMP concentration (0, 0.01, 0.1, 1, 10, 20, 40, 80, or 160 μg/mL) was determined in normal Hepa1-6 cells, the effect of SMP on the expression of inflammation-induced marker genes was evaluated in Hepa1-6 cells overexpressing the NIK gene. Hepa1-6 cells were divided into the following five groups (n = 3): the oe-vector group (overexpressing vector and administered saline), the solvent group (overexpressing the NIK gene and administered solvent), and the SMP group (overexpressing the NIK gene and administered SMP at concentrations of 10, 20, or 40 μg/mL). (A) CCK8 assay was used to measure the viability of normal Hepa1-6 cells; (B) Protein expression levels of NRF2, NIK, and p52 determined via Western blot; (C) Relative dual luciferase activity indicating transcription activity; (D) mRNA expression levels of TNF-α, CCL2, and CCL5, as detected by qPCR; (E) Cytokine levels, including those of TNF-α, CCL2, and CCL5, were detected via ELISA; (F) The mRNA expression levels of CXCL5 and NOS2 were detected by qPCR. Data are presented as the mean ± SD from three independent experiments (n = 3), with three technical replicates per independent experiment. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. N = 3, *P < 0.05, **P < 0.01, ***P < 0.001. SMP, Silybum marianum peptides.
    Figure Legend Snippet: SMP alleviated cell damage by inhibiting NIK/NF-κB. After the appropriate SMP concentration (0, 0.01, 0.1, 1, 10, 20, 40, 80, or 160 μg/mL) was determined in normal Hepa1-6 cells, the effect of SMP on the expression of inflammation-induced marker genes was evaluated in Hepa1-6 cells overexpressing the NIK gene. Hepa1-6 cells were divided into the following five groups (n = 3): the oe-vector group (overexpressing vector and administered saline), the solvent group (overexpressing the NIK gene and administered solvent), and the SMP group (overexpressing the NIK gene and administered SMP at concentrations of 10, 20, or 40 μg/mL). (A) CCK8 assay was used to measure the viability of normal Hepa1-6 cells; (B) Protein expression levels of NRF2, NIK, and p52 determined via Western blot; (C) Relative dual luciferase activity indicating transcription activity; (D) mRNA expression levels of TNF-α, CCL2, and CCL5, as detected by qPCR; (E) Cytokine levels, including those of TNF-α, CCL2, and CCL5, were detected via ELISA; (F) The mRNA expression levels of CXCL5 and NOS2 were detected by qPCR. Data are presented as the mean ± SD from three independent experiments (n = 3), with three technical replicates per independent experiment. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. N = 3, *P < 0.05, **P < 0.01, ***P < 0.001. SMP, Silybum marianum peptides.

    Techniques Used: Concentration Assay, Expressing, Marker, Plasmid Preparation, Saline, Solvent, CCK-8 Assay, Western Blot, Luciferase, Activity Assay, Enzyme-linked Immunosorbent Assay

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    Incubation:

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    Negative Control:

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    Conjugation Assay:

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    Magnetic Beads:

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    Western Blot:

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    Immunohistochemistry:

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    Tissue:

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    Transcranial Magnetic Stimulation:

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    Analysis:

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    Comparative analysis of MAP4K4 inhibitors reveals differential effects on H9c2 cell viability in the presence of doxorubicin. (A) Effect of MAP4K4 Inhibitors on the viability of H9c2 Cells. (B) Schematic illustrating viability studies conducted on H9c2 cells treated with doxorubicin and MAP4K4 inhibitors. (C) Viability of H9c2 Cells Treated with Doxorubicin and DMX-5804. (D) Viability of H9c2 cells treated with doxorubicin and GNE-495, (E) Viability of H9c2 cells treated with doxorubicin and MAP4K4-IN3, (F) Viability of H9c2 cells treated with doxorubicin and PF-06260933. Statistical analysis was performed using two-way ANOVA to assess the effects of treatment and concentration, followed by Sidak’s multiple-comparisons post hoc test to compare groups at matched concentrations. Data are presented as mean ± stdev, **p<0.01, ***p<0.001, ****p<0.0001.

    Journal: bioRxiv

    Article Title: Phosphatidylserine-Based Liposomes Encapsulating DMX-5804 Protect Against Doxorubicin-Induced Cardiotoxicity

    doi: 10.64898/2026.02.12.705423

    Figure Lengend Snippet: Comparative analysis of MAP4K4 inhibitors reveals differential effects on H9c2 cell viability in the presence of doxorubicin. (A) Effect of MAP4K4 Inhibitors on the viability of H9c2 Cells. (B) Schematic illustrating viability studies conducted on H9c2 cells treated with doxorubicin and MAP4K4 inhibitors. (C) Viability of H9c2 Cells Treated with Doxorubicin and DMX-5804. (D) Viability of H9c2 cells treated with doxorubicin and GNE-495, (E) Viability of H9c2 cells treated with doxorubicin and MAP4K4-IN3, (F) Viability of H9c2 cells treated with doxorubicin and PF-06260933. Statistical analysis was performed using two-way ANOVA to assess the effects of treatment and concentration, followed by Sidak’s multiple-comparisons post hoc test to compare groups at matched concentrations. Data are presented as mean ± stdev, **p<0.01, ***p<0.001, ****p<0.0001.

    Article Snippet: The following primary antibodies were used: MAP4K4 (rabbit IgG, Proteintech catalog no. 55247-1-AP, 1:1000 dilution), phospho-MAP4K4 (Ser629) (rabbit IgG, Bioss, catalog no. BS-5491R, 1:2000 dilution), cJUN (rabbit IgG, catalog no. 1:1000 dilution), phospho-cJUN (Ser73) (rabbit IgG, Cell Signaling Technology catalog no. 3270, 1:1000), and beta-actin, HRP (rabbit IgG, Invitrogen, catalog no. PA1-183-HRP, 1:1000) dilution.

    Techniques: Concentration Assay

    Effects of DMX-5804 on doxorubicin-induced gene expression, drug uptake, and protein signaling in H9c2 cardiomyoblasts. (A) qPCR analysis of H9c2 cells treated with doxorubicin, DMX-5804, or both for 4 hours. (B) qPCR analysis of H9c2 cells treated with doxorubicin, DMX-5804, or both for 24 hours. RT-qPCR data are shown as mean ± SD from n = 3 independent biological replicates, each measured in duplicate technical replicates. (C) Uptake of 10 μM doxorubicin into H9c2 cells co-treated with 10 μM MAP4K4 inhibitors (DMX-5804, GNE-495, MAP4K4-IN3, and PF-06260933) after 24 hours. Data represent mean ± standard deviation from six technical replicates per condition from a single experiment; statistical comparisons were performed using one-way ANOVA. (D) Uptake of 10 μM doxorubicin into H9c2 cells co treated with increasing concentrations of DMX-5804 (5 μM, 10 μM, and 20 μM) after 24 hours. Data represent mean ± standard deviation from six technical replicates per condition from a single experiment; statistical comparisons were performed using one-way ANOVA followed by Dunnett’s multiple comparison’s post-test. (E) Western blot analysis of H9c2 cells treated with doxorubicin, DMX-5804, or both for 24 hours and 4 hours. Membranes were probed for β-actin as a loading control to verify equal protein loading across lanes. Blots shown are representative of at least three independent experiments.

    Journal: bioRxiv

    Article Title: Phosphatidylserine-Based Liposomes Encapsulating DMX-5804 Protect Against Doxorubicin-Induced Cardiotoxicity

    doi: 10.64898/2026.02.12.705423

    Figure Lengend Snippet: Effects of DMX-5804 on doxorubicin-induced gene expression, drug uptake, and protein signaling in H9c2 cardiomyoblasts. (A) qPCR analysis of H9c2 cells treated with doxorubicin, DMX-5804, or both for 4 hours. (B) qPCR analysis of H9c2 cells treated with doxorubicin, DMX-5804, or both for 24 hours. RT-qPCR data are shown as mean ± SD from n = 3 independent biological replicates, each measured in duplicate technical replicates. (C) Uptake of 10 μM doxorubicin into H9c2 cells co-treated with 10 μM MAP4K4 inhibitors (DMX-5804, GNE-495, MAP4K4-IN3, and PF-06260933) after 24 hours. Data represent mean ± standard deviation from six technical replicates per condition from a single experiment; statistical comparisons were performed using one-way ANOVA. (D) Uptake of 10 μM doxorubicin into H9c2 cells co treated with increasing concentrations of DMX-5804 (5 μM, 10 μM, and 20 μM) after 24 hours. Data represent mean ± standard deviation from six technical replicates per condition from a single experiment; statistical comparisons were performed using one-way ANOVA followed by Dunnett’s multiple comparison’s post-test. (E) Western blot analysis of H9c2 cells treated with doxorubicin, DMX-5804, or both for 24 hours and 4 hours. Membranes were probed for β-actin as a loading control to verify equal protein loading across lanes. Blots shown are representative of at least three independent experiments.

    Article Snippet: The following primary antibodies were used: MAP4K4 (rabbit IgG, Proteintech catalog no. 55247-1-AP, 1:1000 dilution), phospho-MAP4K4 (Ser629) (rabbit IgG, Bioss, catalog no. BS-5491R, 1:2000 dilution), cJUN (rabbit IgG, catalog no. 1:1000 dilution), phospho-cJUN (Ser73) (rabbit IgG, Cell Signaling Technology catalog no. 3270, 1:1000), and beta-actin, HRP (rabbit IgG, Invitrogen, catalog no. PA1-183-HRP, 1:1000) dilution.

    Techniques: Gene Expression, Quantitative RT-PCR, Standard Deviation, Western Blot, Control

    Effects of MAP4K4 inhibition on doxorubicin uptake, cell viability, and protein signaling in breast cancer cells. (A) Effect of MAP4K4 inhibitors on the cell viability of MDA-MB-231 cells. (B) Uptake of doxorubicin into MDA-MB-231 cells co-treated with MAP4K4 inhibitors after 24 hours. (C) Viability of MDA-MB-231 cells treated with doxorubicin and DMX-5804. (D) Viability of 4T1 cells treated with Doxorubicin and DMX-5804. (E) Western blot analysis of MDA-MB-231 cells treated with doxorubicin, DMX-5804, or both for 24 hours. Data are presented as mean ± stdev, n=4. Statistical analysis was performed using two-way ANOVA to assess the effects of treatment and concentration, followed by Sidak’s multiple-comparisons post hoc test to compare groups at matched concentrations. Data are presented as mean ± stdev, **p<0.01, ***p<0.001, ****p<0.0001.

    Journal: bioRxiv

    Article Title: Phosphatidylserine-Based Liposomes Encapsulating DMX-5804 Protect Against Doxorubicin-Induced Cardiotoxicity

    doi: 10.64898/2026.02.12.705423

    Figure Lengend Snippet: Effects of MAP4K4 inhibition on doxorubicin uptake, cell viability, and protein signaling in breast cancer cells. (A) Effect of MAP4K4 inhibitors on the cell viability of MDA-MB-231 cells. (B) Uptake of doxorubicin into MDA-MB-231 cells co-treated with MAP4K4 inhibitors after 24 hours. (C) Viability of MDA-MB-231 cells treated with doxorubicin and DMX-5804. (D) Viability of 4T1 cells treated with Doxorubicin and DMX-5804. (E) Western blot analysis of MDA-MB-231 cells treated with doxorubicin, DMX-5804, or both for 24 hours. Data are presented as mean ± stdev, n=4. Statistical analysis was performed using two-way ANOVA to assess the effects of treatment and concentration, followed by Sidak’s multiple-comparisons post hoc test to compare groups at matched concentrations. Data are presented as mean ± stdev, **p<0.01, ***p<0.001, ****p<0.0001.

    Article Snippet: The following primary antibodies were used: MAP4K4 (rabbit IgG, Proteintech catalog no. 55247-1-AP, 1:1000 dilution), phospho-MAP4K4 (Ser629) (rabbit IgG, Bioss, catalog no. BS-5491R, 1:2000 dilution), cJUN (rabbit IgG, catalog no. 1:1000 dilution), phospho-cJUN (Ser73) (rabbit IgG, Cell Signaling Technology catalog no. 3270, 1:1000), and beta-actin, HRP (rabbit IgG, Invitrogen, catalog no. PA1-183-HRP, 1:1000) dilution.

    Techniques: Inhibition, Western Blot, Concentration Assay

    SMP protected against CCl 4 -induced liver injury in mice by inhibiting NIK/NF-κB. 8-Week-old male C57BL/6J mice were divided into the following five groups: the control group (treated daily with saline and an intraperitoneal injection of olive oil on the 14th day), CCl 4 group (treated daily with saline and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day), SMP group (treated daily with SMP at 50, 100, or 200 mg/kg, and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day). (A) Immunofluorescence observation of macrophages in liver tissue (F4/80); (B) Immunofluorescence observation of neutrophils in liver tissue (Ly6G); (C) Immunofluorescence observation of CD8 T cells in liver tissue (CD8 + ); (D) Protein expression levels of NRF2 determined via Western blot; (E) Protein expression levels of TRAF3 determined via Western blot; (F) Protein expression levels of NIK, and p52 determined via Western blot. All data are presented as the mean ± SD. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. For immunofluorescence and Western blot analyses, quantitative data were derived from independent biological samples from individual mice. n = 8, *P < 0.05, **P < 0.01, ***P < 0.001.

    Journal: Frontiers in Pharmacology

    Article Title: Silybum marianum peptide-rich fraction alleviates acute liver injury by inhibiting TRAF3/NIK/NF-κB and is associated with changes in gut microbiota composition

    doi: 10.3389/fphar.2026.1915943

    Figure Lengend Snippet: SMP protected against CCl 4 -induced liver injury in mice by inhibiting NIK/NF-κB. 8-Week-old male C57BL/6J mice were divided into the following five groups: the control group (treated daily with saline and an intraperitoneal injection of olive oil on the 14th day), CCl 4 group (treated daily with saline and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day), SMP group (treated daily with SMP at 50, 100, or 200 mg/kg, and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day). (A) Immunofluorescence observation of macrophages in liver tissue (F4/80); (B) Immunofluorescence observation of neutrophils in liver tissue (Ly6G); (C) Immunofluorescence observation of CD8 T cells in liver tissue (CD8 + ); (D) Protein expression levels of NRF2 determined via Western blot; (E) Protein expression levels of TRAF3 determined via Western blot; (F) Protein expression levels of NIK, and p52 determined via Western blot. All data are presented as the mean ± SD. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. For immunofluorescence and Western blot analyses, quantitative data were derived from independent biological samples from individual mice. n = 8, *P < 0.05, **P < 0.01, ***P < 0.001.

    Article Snippet: Then, primary antibodies against NIK (#55247-1-AP, Proteintech), p52 (#15503-1-AP, Proteintech), NRF2 (#80593-1-RR, Proteintech), GAPDH (#60004-1-Ig, Proteintech), and TRAF3 (#SAB3500376-100UG, Sigma-Aldrich) were added at a dilution of 1:2000 and incubated ove,rnight at 4 °C.

    Techniques: Control, Saline, Injection, Immunofluorescence, Tissue, Expressing, Western Blot, Derivative Assay

    SMP alleviated cell damage by inhibiting NIK/NF-κB. After the appropriate SMP concentration (0, 0.01, 0.1, 1, 10, 20, 40, 80, or 160 μg/mL) was determined in normal Hepa1-6 cells, the effect of SMP on the expression of inflammation-induced marker genes was evaluated in Hepa1-6 cells overexpressing the NIK gene. Hepa1-6 cells were divided into the following five groups (n = 3): the oe-vector group (overexpressing vector and administered saline), the solvent group (overexpressing the NIK gene and administered solvent), and the SMP group (overexpressing the NIK gene and administered SMP at concentrations of 10, 20, or 40 μg/mL). (A) CCK8 assay was used to measure the viability of normal Hepa1-6 cells; (B) Protein expression levels of NRF2, NIK, and p52 determined via Western blot; (C) Relative dual luciferase activity indicating transcription activity; (D) mRNA expression levels of TNF-α, CCL2, and CCL5, as detected by qPCR; (E) Cytokine levels, including those of TNF-α, CCL2, and CCL5, were detected via ELISA; (F) The mRNA expression levels of CXCL5 and NOS2 were detected by qPCR. Data are presented as the mean ± SD from three independent experiments (n = 3), with three technical replicates per independent experiment. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. N = 3, *P < 0.05, **P < 0.01, ***P < 0.001. SMP, Silybum marianum peptides.

    Journal: Frontiers in Pharmacology

    Article Title: Silybum marianum peptide-rich fraction alleviates acute liver injury by inhibiting TRAF3/NIK/NF-κB and is associated with changes in gut microbiota composition

    doi: 10.3389/fphar.2026.1915943

    Figure Lengend Snippet: SMP alleviated cell damage by inhibiting NIK/NF-κB. After the appropriate SMP concentration (0, 0.01, 0.1, 1, 10, 20, 40, 80, or 160 μg/mL) was determined in normal Hepa1-6 cells, the effect of SMP on the expression of inflammation-induced marker genes was evaluated in Hepa1-6 cells overexpressing the NIK gene. Hepa1-6 cells were divided into the following five groups (n = 3): the oe-vector group (overexpressing vector and administered saline), the solvent group (overexpressing the NIK gene and administered solvent), and the SMP group (overexpressing the NIK gene and administered SMP at concentrations of 10, 20, or 40 μg/mL). (A) CCK8 assay was used to measure the viability of normal Hepa1-6 cells; (B) Protein expression levels of NRF2, NIK, and p52 determined via Western blot; (C) Relative dual luciferase activity indicating transcription activity; (D) mRNA expression levels of TNF-α, CCL2, and CCL5, as detected by qPCR; (E) Cytokine levels, including those of TNF-α, CCL2, and CCL5, were detected via ELISA; (F) The mRNA expression levels of CXCL5 and NOS2 were detected by qPCR. Data are presented as the mean ± SD from three independent experiments (n = 3), with three technical replicates per independent experiment. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. N = 3, *P < 0.05, **P < 0.01, ***P < 0.001. SMP, Silybum marianum peptides.

    Article Snippet: Then, primary antibodies against NIK (#55247-1-AP, Proteintech), p52 (#15503-1-AP, Proteintech), NRF2 (#80593-1-RR, Proteintech), GAPDH (#60004-1-Ig, Proteintech), and TRAF3 (#SAB3500376-100UG, Sigma-Aldrich) were added at a dilution of 1:2000 and incubated ove,rnight at 4 °C.

    Techniques: Concentration Assay, Expressing, Marker, Plasmid Preparation, Saline, Solvent, CCK-8 Assay, Western Blot, Luciferase, Activity Assay, Enzyme-linked Immunosorbent Assay

    Comparative analysis of MAP4K4 inhibitors reveals differential effects on H9c2 cell viability in the presence of doxorubicin. (A) Effect of MAP4K4 Inhibitors on the viability of H9c2 Cells. (B) Schematic illustrating viability studies conducted on H9c2 cells treated with doxorubicin and MAP4K4 inhibitors. (C) Viability of H9c2 Cells Treated with Doxorubicin and DMX-5804. (D) Viability of H9c2 cells treated with doxorubicin and GNE-495, (E) Viability of H9c2 cells treated with doxorubicin and MAP4K4-IN3, (F) Viability of H9c2 cells treated with doxorubicin and PF-06260933. Statistical analysis was performed using two-way ANOVA to assess the effects of treatment and concentration, followed by Sidak’s multiple-comparisons post hoc test to compare groups at matched concentrations. Data are presented as mean ± stdev, **p<0.01, ***p<0.001, ****p<0.0001.

    Journal: bioRxiv

    Article Title: Phosphatidylserine-Based Liposomes Encapsulating DMX-5804 Protect Against Doxorubicin-Induced Cardiotoxicity

    doi: 10.64898/2026.02.12.705423

    Figure Lengend Snippet: Comparative analysis of MAP4K4 inhibitors reveals differential effects on H9c2 cell viability in the presence of doxorubicin. (A) Effect of MAP4K4 Inhibitors on the viability of H9c2 Cells. (B) Schematic illustrating viability studies conducted on H9c2 cells treated with doxorubicin and MAP4K4 inhibitors. (C) Viability of H9c2 Cells Treated with Doxorubicin and DMX-5804. (D) Viability of H9c2 cells treated with doxorubicin and GNE-495, (E) Viability of H9c2 cells treated with doxorubicin and MAP4K4-IN3, (F) Viability of H9c2 cells treated with doxorubicin and PF-06260933. Statistical analysis was performed using two-way ANOVA to assess the effects of treatment and concentration, followed by Sidak’s multiple-comparisons post hoc test to compare groups at matched concentrations. Data are presented as mean ± stdev, **p<0.01, ***p<0.001, ****p<0.0001.

    Article Snippet: The following primary antibodies were used: MAP4K4 (rabbit IgG, Proteintech catalog no. 55247-1-AP, 1:1000 dilution), phospho-MAP4K4 (Ser629) (rabbit IgG, Bioss, catalog no. BS-5491R, 1:2000 dilution), cJUN (rabbit IgG, catalog no. 1:1000 dilution), phospho-cJUN (Ser73) (rabbit IgG, Cell Signaling Technology catalog no. 3270, 1:1000), and beta-actin, HRP (rabbit IgG, Invitrogen, catalog no. PA1-183-HRP, 1:1000) dilution.

    Techniques: Concentration Assay

    Effects of DMX-5804 on doxorubicin-induced gene expression, drug uptake, and protein signaling in H9c2 cardiomyoblasts. (A) qPCR analysis of H9c2 cells treated with doxorubicin, DMX-5804, or both for 4 hours. (B) qPCR analysis of H9c2 cells treated with doxorubicin, DMX-5804, or both for 24 hours. RT-qPCR data are shown as mean ± SD from n = 3 independent biological replicates, each measured in duplicate technical replicates. (C) Uptake of 10 μM doxorubicin into H9c2 cells co-treated with 10 μM MAP4K4 inhibitors (DMX-5804, GNE-495, MAP4K4-IN3, and PF-06260933) after 24 hours. Data represent mean ± standard deviation from six technical replicates per condition from a single experiment; statistical comparisons were performed using one-way ANOVA. (D) Uptake of 10 μM doxorubicin into H9c2 cells co treated with increasing concentrations of DMX-5804 (5 μM, 10 μM, and 20 μM) after 24 hours. Data represent mean ± standard deviation from six technical replicates per condition from a single experiment; statistical comparisons were performed using one-way ANOVA followed by Dunnett’s multiple comparison’s post-test. (E) Western blot analysis of H9c2 cells treated with doxorubicin, DMX-5804, or both for 24 hours and 4 hours. Membranes were probed for β-actin as a loading control to verify equal protein loading across lanes. Blots shown are representative of at least three independent experiments.

    Journal: bioRxiv

    Article Title: Phosphatidylserine-Based Liposomes Encapsulating DMX-5804 Protect Against Doxorubicin-Induced Cardiotoxicity

    doi: 10.64898/2026.02.12.705423

    Figure Lengend Snippet: Effects of DMX-5804 on doxorubicin-induced gene expression, drug uptake, and protein signaling in H9c2 cardiomyoblasts. (A) qPCR analysis of H9c2 cells treated with doxorubicin, DMX-5804, or both for 4 hours. (B) qPCR analysis of H9c2 cells treated with doxorubicin, DMX-5804, or both for 24 hours. RT-qPCR data are shown as mean ± SD from n = 3 independent biological replicates, each measured in duplicate technical replicates. (C) Uptake of 10 μM doxorubicin into H9c2 cells co-treated with 10 μM MAP4K4 inhibitors (DMX-5804, GNE-495, MAP4K4-IN3, and PF-06260933) after 24 hours. Data represent mean ± standard deviation from six technical replicates per condition from a single experiment; statistical comparisons were performed using one-way ANOVA. (D) Uptake of 10 μM doxorubicin into H9c2 cells co treated with increasing concentrations of DMX-5804 (5 μM, 10 μM, and 20 μM) after 24 hours. Data represent mean ± standard deviation from six technical replicates per condition from a single experiment; statistical comparisons were performed using one-way ANOVA followed by Dunnett’s multiple comparison’s post-test. (E) Western blot analysis of H9c2 cells treated with doxorubicin, DMX-5804, or both for 24 hours and 4 hours. Membranes were probed for β-actin as a loading control to verify equal protein loading across lanes. Blots shown are representative of at least three independent experiments.

    Article Snippet: The following primary antibodies were used: MAP4K4 (rabbit IgG, Proteintech catalog no. 55247-1-AP, 1:1000 dilution), phospho-MAP4K4 (Ser629) (rabbit IgG, Bioss, catalog no. BS-5491R, 1:2000 dilution), cJUN (rabbit IgG, catalog no. 1:1000 dilution), phospho-cJUN (Ser73) (rabbit IgG, Cell Signaling Technology catalog no. 3270, 1:1000), and beta-actin, HRP (rabbit IgG, Invitrogen, catalog no. PA1-183-HRP, 1:1000) dilution.

    Techniques: Gene Expression, Quantitative RT-PCR, Standard Deviation, Western Blot, Control

    Effects of MAP4K4 inhibition on doxorubicin uptake, cell viability, and protein signaling in breast cancer cells. (A) Effect of MAP4K4 inhibitors on the cell viability of MDA-MB-231 cells. (B) Uptake of doxorubicin into MDA-MB-231 cells co-treated with MAP4K4 inhibitors after 24 hours. (C) Viability of MDA-MB-231 cells treated with doxorubicin and DMX-5804. (D) Viability of 4T1 cells treated with Doxorubicin and DMX-5804. (E) Western blot analysis of MDA-MB-231 cells treated with doxorubicin, DMX-5804, or both for 24 hours. Data are presented as mean ± stdev, n=4. Statistical analysis was performed using two-way ANOVA to assess the effects of treatment and concentration, followed by Sidak’s multiple-comparisons post hoc test to compare groups at matched concentrations. Data are presented as mean ± stdev, **p<0.01, ***p<0.001, ****p<0.0001.

    Journal: bioRxiv

    Article Title: Phosphatidylserine-Based Liposomes Encapsulating DMX-5804 Protect Against Doxorubicin-Induced Cardiotoxicity

    doi: 10.64898/2026.02.12.705423

    Figure Lengend Snippet: Effects of MAP4K4 inhibition on doxorubicin uptake, cell viability, and protein signaling in breast cancer cells. (A) Effect of MAP4K4 inhibitors on the cell viability of MDA-MB-231 cells. (B) Uptake of doxorubicin into MDA-MB-231 cells co-treated with MAP4K4 inhibitors after 24 hours. (C) Viability of MDA-MB-231 cells treated with doxorubicin and DMX-5804. (D) Viability of 4T1 cells treated with Doxorubicin and DMX-5804. (E) Western blot analysis of MDA-MB-231 cells treated with doxorubicin, DMX-5804, or both for 24 hours. Data are presented as mean ± stdev, n=4. Statistical analysis was performed using two-way ANOVA to assess the effects of treatment and concentration, followed by Sidak’s multiple-comparisons post hoc test to compare groups at matched concentrations. Data are presented as mean ± stdev, **p<0.01, ***p<0.001, ****p<0.0001.

    Article Snippet: The following primary antibodies were used: MAP4K4 (rabbit IgG, Proteintech catalog no. 55247-1-AP, 1:1000 dilution), phospho-MAP4K4 (Ser629) (rabbit IgG, Bioss, catalog no. BS-5491R, 1:2000 dilution), cJUN (rabbit IgG, catalog no. 1:1000 dilution), phospho-cJUN (Ser73) (rabbit IgG, Cell Signaling Technology catalog no. 3270, 1:1000), and beta-actin, HRP (rabbit IgG, Invitrogen, catalog no. PA1-183-HRP, 1:1000) dilution.

    Techniques: Inhibition, Western Blot, Concentration Assay

    a. Protein interactions based on the analysis of the BioGRID and STRING databases. b. Immunohistochemical analysis of MAP4K4 expression in rat myocardial tissue exposed to sham, I/R and I/R-postC in rat myocardial tissue (scale bar = 25 µm). c. MAP4K4 expression in rat cardiomyocytes exposed to sham conditions, ischemia/reperfusion (I/R), or I/R + PostC. d. MAP4K4 expression in rat cardiomyocytes exposed to normoxia (N), hypoxia/reoxygenation (H/R), or H/R + PostC. e. MAP4K4 expression in cardiomyocytes transfected with si-RAP2C or si-NC and exposed to H/R or H/R + PostC. f. MAP4K4 expression in cardiomyocytes transduced with Ad-RAP2C or Ad-null and exposed to H/R or H/R + PostC. g. Co-immunoprecipitation assays using cardiomyocyte lysates and RAP2C antibody under normoxia, H/R, and H/R + PostC. MAP4K4 and RAP2C expression in input and immunoprecipitated samples was evaluated by western blotting. h. Colocalization of MAP4K4 and RAP2C by immunofluorescence double staining (scale bar = 5/10 μm). The degree of colocalization is shown in scatter plots and was calculated using Pearson’s correlation coefficient. Data are means and standard deviations of three biological replicates. p values were calculated by two-tailed Student’s t- test. one-way ANOVA with Tukey’s post hoc test was used for multiple group comparisons. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

    Journal: bioRxiv

    Article Title: The Cardioprotective Effect of Ischemic Postconditioning is Mediated by Inhibiting RAP2C-MAP4K4 Pathway

    doi: 10.1101/2024.12.04.626922

    Figure Lengend Snippet: a. Protein interactions based on the analysis of the BioGRID and STRING databases. b. Immunohistochemical analysis of MAP4K4 expression in rat myocardial tissue exposed to sham, I/R and I/R-postC in rat myocardial tissue (scale bar = 25 µm). c. MAP4K4 expression in rat cardiomyocytes exposed to sham conditions, ischemia/reperfusion (I/R), or I/R + PostC. d. MAP4K4 expression in rat cardiomyocytes exposed to normoxia (N), hypoxia/reoxygenation (H/R), or H/R + PostC. e. MAP4K4 expression in cardiomyocytes transfected with si-RAP2C or si-NC and exposed to H/R or H/R + PostC. f. MAP4K4 expression in cardiomyocytes transduced with Ad-RAP2C or Ad-null and exposed to H/R or H/R + PostC. g. Co-immunoprecipitation assays using cardiomyocyte lysates and RAP2C antibody under normoxia, H/R, and H/R + PostC. MAP4K4 and RAP2C expression in input and immunoprecipitated samples was evaluated by western blotting. h. Colocalization of MAP4K4 and RAP2C by immunofluorescence double staining (scale bar = 5/10 μm). The degree of colocalization is shown in scatter plots and was calculated using Pearson’s correlation coefficient. Data are means and standard deviations of three biological replicates. p values were calculated by two-tailed Student’s t- test. one-way ANOVA with Tukey’s post hoc test was used for multiple group comparisons. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

    Article Snippet: Myocardial tissue was fixed in 4% paraformaldehyde for 10 min and permeabilized in Triton X-100 1% for 20 min. Endogenous peroxidase activity was blocked using 5% BSA for 1 h. Tissues were incubated with primary antibodies against RAP2C (orb474405, Biorbyt, Cambridge, UK) and MAP4K4 (sc-100445, Santa Cruz) overnight at 4℃, followed by incubation with CoraLite594-conjugated goat anti-mouse antibody (SA00013-3, Proteintech) and CoraLite488-conjugated goat anti-rabbit antibody (SA00013-2, Proteintech) at room temperature for 1 h. Nuclei were stained with DAPI.

    Techniques: Immunohistochemical staining, Expressing, Transfection, Transduction, Immunoprecipitation, Western Blot, Immunofluorescence, Double Staining, Two Tailed Test

    a. Western blot analysis of the efficiency of siRNA-mediated silencing of MAP4K4 expression. b. p-ERK, p-JNK, and p-P38 expression in cardiomyocytes transfected with si-MAP4K4 or si-NC and exposed to normoxia (N), H/R, or H/R + PostC. c. Number of TUNEL-positive cells in different groups (×10) (scale bar = 200 µm). d. Flow cytometry analysis of total apoptosis rates in different groups. e. Western blot analysis of the expression of cleaved caspase-3 and −9 and the Bax/Bcl-2 ratio. Data are means and standard deviations of three biological replicates. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

    Journal: bioRxiv

    Article Title: The Cardioprotective Effect of Ischemic Postconditioning is Mediated by Inhibiting RAP2C-MAP4K4 Pathway

    doi: 10.1101/2024.12.04.626922

    Figure Lengend Snippet: a. Western blot analysis of the efficiency of siRNA-mediated silencing of MAP4K4 expression. b. p-ERK, p-JNK, and p-P38 expression in cardiomyocytes transfected with si-MAP4K4 or si-NC and exposed to normoxia (N), H/R, or H/R + PostC. c. Number of TUNEL-positive cells in different groups (×10) (scale bar = 200 µm). d. Flow cytometry analysis of total apoptosis rates in different groups. e. Western blot analysis of the expression of cleaved caspase-3 and −9 and the Bax/Bcl-2 ratio. Data are means and standard deviations of three biological replicates. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

    Article Snippet: Myocardial tissue was fixed in 4% paraformaldehyde for 10 min and permeabilized in Triton X-100 1% for 20 min. Endogenous peroxidase activity was blocked using 5% BSA for 1 h. Tissues were incubated with primary antibodies against RAP2C (orb474405, Biorbyt, Cambridge, UK) and MAP4K4 (sc-100445, Santa Cruz) overnight at 4℃, followed by incubation with CoraLite594-conjugated goat anti-mouse antibody (SA00013-3, Proteintech) and CoraLite488-conjugated goat anti-rabbit antibody (SA00013-2, Proteintech) at room temperature for 1 h. Nuclei were stained with DAPI.

    Techniques: Western Blot, Expressing, Transfection, TUNEL Assay, Flow Cytometry

    a. Western blot analysis of RAP2C and MAP4K4 expression in cells transfected with Ad-RAP2C or Ad-RAP2C + si-MAP4K4 and exposed to hypoxia/reoxygenation (H/R) and ischemic postconditioning (PostC). b. Protein expression of p-ERK, p-JNK, and p-P38 in different groups. c. Number of TUNEL-positive cells in different groups (×10) (scale bar = 100 µm). d. Flow cytometry analysis of the rate of apoptosis. e. Western blot analysis of the Bax/Bcl-2 ratio and the expression of cleaved caspase-3 and −9 in cardiomyocytes. Data are means and standard deviations of three biological replicates. p values were calculated by two-tailed Student’s t- test. one-way ANOVA with Tukey’s post hoc test was used for multiple group comparisons. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

    Journal: bioRxiv

    Article Title: The Cardioprotective Effect of Ischemic Postconditioning is Mediated by Inhibiting RAP2C-MAP4K4 Pathway

    doi: 10.1101/2024.12.04.626922

    Figure Lengend Snippet: a. Western blot analysis of RAP2C and MAP4K4 expression in cells transfected with Ad-RAP2C or Ad-RAP2C + si-MAP4K4 and exposed to hypoxia/reoxygenation (H/R) and ischemic postconditioning (PostC). b. Protein expression of p-ERK, p-JNK, and p-P38 in different groups. c. Number of TUNEL-positive cells in different groups (×10) (scale bar = 100 µm). d. Flow cytometry analysis of the rate of apoptosis. e. Western blot analysis of the Bax/Bcl-2 ratio and the expression of cleaved caspase-3 and −9 in cardiomyocytes. Data are means and standard deviations of three biological replicates. p values were calculated by two-tailed Student’s t- test. one-way ANOVA with Tukey’s post hoc test was used for multiple group comparisons. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

    Article Snippet: Myocardial tissue was fixed in 4% paraformaldehyde for 10 min and permeabilized in Triton X-100 1% for 20 min. Endogenous peroxidase activity was blocked using 5% BSA for 1 h. Tissues were incubated with primary antibodies against RAP2C (orb474405, Biorbyt, Cambridge, UK) and MAP4K4 (sc-100445, Santa Cruz) overnight at 4℃, followed by incubation with CoraLite594-conjugated goat anti-mouse antibody (SA00013-3, Proteintech) and CoraLite488-conjugated goat anti-rabbit antibody (SA00013-2, Proteintech) at room temperature for 1 h. Nuclei were stained with DAPI.

    Techniques: Western Blot, Expressing, Transfection, TUNEL Assay, Flow Cytometry, Two Tailed Test