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Targeting TRAF3IP2 alters protein levels of NAD salvage pathway markers in glioblastoma. Protein levels of TRAF3IP2 and NAMPT in U87, U118, and KNS cell lines ( A ). Protein levels of SIRT1, total <t>p53,</t> Acetyl-p53[K382] (a-p53), and Phosphorylated-p53[S392] (p-p53) in U87, U118, and KNS cell lines ( B ). Imagej analysis of band intensity in western blots, relative to β-actin (TRAF3IP2KD vs. SCR) ( C ). Immunohistochemical analysis of the tumor tissues demonstrating that U87 TRAF3IP2KD -derived tumors had reduced TRAF3IP2 and NAMPT expression, compared to SCR control tumor tissues (Size bar = 50 µM) ( D ). Relative fluorometric intensity of ROS in U87 TRAF3IP2KD , compared to U87 SCR showed that silencing TRA3IP2 increases ROS levels ( E ). Protein expression of LKB1, p-LKB1, AMPK, p-AMPK in transduced U87, U118, and KNS glioblastoma cell lines (F). Triplicate experiments, (* P < 0.05)
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Geranyl acetate (GA) mitigates para-phenylenediamine (PPD)-induced DNA damage response (DDR) signaling in HaCaT cells: A – D, HaCaT cells were seeded in 100 mm dishes (2 × 10 5 cells/dish) and incubated for 24 hours, followed by treatment with GA (0 - 500 μM), in the presence or absence of PPD (250 μM) for 48 hours. Protein expression levels of the DDR-related proteins, including ataxia telangiectasia and Rad3 related protein (ATR), p-ATR, <t>p53,</t> p-p53, p38, p-p38, c-Jun N-terminal kinases (JNK), p-JNK, extracellular signal-regulated kinases (ERK), and p-ERK, were analyzed by Western blotting. The β-Actin was used as a loading control. Protein band intensities were quantified using ImageJ software (version 1.53t). Data are presented as mean ± standard deviation (SD, n = 3). Statistical significance was determined by one-way analysis of variance (ANOVA) followed by Tukey’s post-hoc test (## P < 0.01 and ### P < 0.001 compared with the solvent-treated vehicle control group. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the PPD-treated negative control group).
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Geranyl acetate (GA) mitigates para-phenylenediamine (PPD)-induced DNA damage response (DDR) signaling in HaCaT cells: A – D, HaCaT cells were seeded in 100 mm dishes (2 × 10 5 cells/dish) and incubated for 24 hours, followed by treatment with GA (0 - 500 μM), in the presence or absence of PPD (250 μM) for 48 hours. Protein expression levels of the DDR-related proteins, including ataxia telangiectasia and Rad3 related protein (ATR), p-ATR, <t>p53,</t> p-p53, p38, p-p38, c-Jun N-terminal kinases (JNK), p-JNK, extracellular signal-regulated kinases (ERK), and p-ERK, were analyzed by Western blotting. The β-Actin was used as a loading control. Protein band intensities were quantified using ImageJ software (version 1.53t). Data are presented as mean ± standard deviation (SD, n = 3). Statistical significance was determined by one-way analysis of variance (ANOVA) followed by Tukey’s post-hoc test (## P < 0.01 and ### P < 0.001 compared with the solvent-treated vehicle control group. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the PPD-treated negative control group).
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Geranyl acetate (GA) mitigates para-phenylenediamine (PPD)-induced DNA damage response (DDR) signaling in HaCaT cells: A – D, HaCaT cells were seeded in 100 mm dishes (2 × 10 5 cells/dish) and incubated for 24 hours, followed by treatment with GA (0 - 500 μM), in the presence or absence of PPD (250 μM) for 48 hours. Protein expression levels of the DDR-related proteins, including ataxia telangiectasia and Rad3 related protein (ATR), p-ATR, <t>p53,</t> p-p53, p38, p-p38, c-Jun N-terminal kinases (JNK), p-JNK, extracellular signal-regulated kinases (ERK), and p-ERK, were analyzed by Western blotting. The β-Actin was used as a loading control. Protein band intensities were quantified using ImageJ software (version 1.53t). Data are presented as mean ± standard deviation (SD, n = 3). Statistical significance was determined by one-way analysis of variance (ANOVA) followed by Tukey’s post-hoc test (## P < 0.01 and ### P < 0.001 compared with the solvent-treated vehicle control group. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the PPD-treated negative control group).
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Geranyl acetate (GA) mitigates para-phenylenediamine (PPD)-induced DNA damage response (DDR) signaling in HaCaT cells: A – D, HaCaT cells were seeded in 100 mm dishes (2 × 10 5 cells/dish) and incubated for 24 hours, followed by treatment with GA (0 - 500 μM), in the presence or absence of PPD (250 μM) for 48 hours. Protein expression levels of the DDR-related proteins, including ataxia telangiectasia and Rad3 related protein (ATR), p-ATR, <t>p53,</t> p-p53, p38, p-p38, c-Jun N-terminal kinases (JNK), p-JNK, extracellular signal-regulated kinases (ERK), and p-ERK, were analyzed by Western blotting. The β-Actin was used as a loading control. Protein band intensities were quantified using ImageJ software (version 1.53t). Data are presented as mean ± standard deviation (SD, n = 3). Statistical significance was determined by one-way analysis of variance (ANOVA) followed by Tukey’s post-hoc test (## P < 0.01 and ### P < 0.001 compared with the solvent-treated vehicle control group. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the PPD-treated negative control group).
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Geranyl acetate (GA) mitigates para-phenylenediamine (PPD)-induced DNA damage response (DDR) signaling in HaCaT cells: A – D, HaCaT cells were seeded in 100 mm dishes (2 × 10 5 cells/dish) and incubated for 24 hours, followed by treatment with GA (0 - 500 μM), in the presence or absence of PPD (250 μM) for 48 hours. Protein expression levels of the DDR-related proteins, including ataxia telangiectasia and Rad3 related protein (ATR), p-ATR, <t>p53,</t> p-p53, p38, p-p38, c-Jun N-terminal kinases (JNK), p-JNK, extracellular signal-regulated kinases (ERK), and p-ERK, were analyzed by Western blotting. The β-Actin was used as a loading control. Protein band intensities were quantified using ImageJ software (version 1.53t). Data are presented as mean ± standard deviation (SD, n = 3). Statistical significance was determined by one-way analysis of variance (ANOVA) followed by Tukey’s post-hoc test (## P < 0.01 and ### P < 0.001 compared with the solvent-treated vehicle control group. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the PPD-treated negative control group).
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Geranyl acetate (GA) mitigates para-phenylenediamine (PPD)-induced DNA damage response (DDR) signaling in HaCaT cells: A – D, HaCaT cells were seeded in 100 mm dishes (2 × 10 5 cells/dish) and incubated for 24 hours, followed by treatment with GA (0 - 500 μM), in the presence or absence of PPD (250 μM) for 48 hours. Protein expression levels of the DDR-related proteins, including ataxia telangiectasia and Rad3 related protein (ATR), p-ATR, <t>p53,</t> p-p53, p38, p-p38, c-Jun N-terminal kinases (JNK), p-JNK, extracellular signal-regulated kinases (ERK), and p-ERK, were analyzed by Western blotting. The β-Actin was used as a loading control. Protein band intensities were quantified using ImageJ software (version 1.53t). Data are presented as mean ± standard deviation (SD, n = 3). Statistical significance was determined by one-way analysis of variance (ANOVA) followed by Tukey’s post-hoc test (## P < 0.01 and ### P < 0.001 compared with the solvent-treated vehicle control group. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the PPD-treated negative control group).
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Geranyl acetate (GA) mitigates para-phenylenediamine (PPD)-induced DNA damage response (DDR) signaling in HaCaT cells: A – D, HaCaT cells were seeded in 100 mm dishes (2 × 10 5 cells/dish) and incubated for 24 hours, followed by treatment with GA (0 - 500 μM), in the presence or absence of PPD (250 μM) for 48 hours. Protein expression levels of the DDR-related proteins, including ataxia telangiectasia and Rad3 related protein (ATR), p-ATR, <t>p53,</t> p-p53, p38, p-p38, c-Jun N-terminal kinases (JNK), p-JNK, extracellular signal-regulated kinases (ERK), and p-ERK, were analyzed by Western blotting. The β-Actin was used as a loading control. Protein band intensities were quantified using ImageJ software (version 1.53t). Data are presented as mean ± standard deviation (SD, n = 3). Statistical significance was determined by one-way analysis of variance (ANOVA) followed by Tukey’s post-hoc test (## P < 0.01 and ### P < 0.001 compared with the solvent-treated vehicle control group. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the PPD-treated negative control group).
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Image Search Results


Targeting TRAF3IP2 alters protein levels of NAD salvage pathway markers in glioblastoma. Protein levels of TRAF3IP2 and NAMPT in U87, U118, and KNS cell lines ( A ). Protein levels of SIRT1, total p53, Acetyl-p53[K382] (a-p53), and Phosphorylated-p53[S392] (p-p53) in U87, U118, and KNS cell lines ( B ). Imagej analysis of band intensity in western blots, relative to β-actin (TRAF3IP2KD vs. SCR) ( C ). Immunohistochemical analysis of the tumor tissues demonstrating that U87 TRAF3IP2KD -derived tumors had reduced TRAF3IP2 and NAMPT expression, compared to SCR control tumor tissues (Size bar = 50 µM) ( D ). Relative fluorometric intensity of ROS in U87 TRAF3IP2KD , compared to U87 SCR showed that silencing TRA3IP2 increases ROS levels ( E ). Protein expression of LKB1, p-LKB1, AMPK, p-AMPK in transduced U87, U118, and KNS glioblastoma cell lines (F). Triplicate experiments, (* P < 0.05)

Journal: Journal of Neuroimmune Pharmacology

Article Title: Inhibition of TRAF3IP2 Modulates NAMPT and NAD Metabolism in Glioblastoma

doi: 10.1007/s11481-025-10252-z

Figure Lengend Snippet: Targeting TRAF3IP2 alters protein levels of NAD salvage pathway markers in glioblastoma. Protein levels of TRAF3IP2 and NAMPT in U87, U118, and KNS cell lines ( A ). Protein levels of SIRT1, total p53, Acetyl-p53[K382] (a-p53), and Phosphorylated-p53[S392] (p-p53) in U87, U118, and KNS cell lines ( B ). Imagej analysis of band intensity in western blots, relative to β-actin (TRAF3IP2KD vs. SCR) ( C ). Immunohistochemical analysis of the tumor tissues demonstrating that U87 TRAF3IP2KD -derived tumors had reduced TRAF3IP2 and NAMPT expression, compared to SCR control tumor tissues (Size bar = 50 µM) ( D ). Relative fluorometric intensity of ROS in U87 TRAF3IP2KD , compared to U87 SCR showed that silencing TRA3IP2 increases ROS levels ( E ). Protein expression of LKB1, p-LKB1, AMPK, p-AMPK in transduced U87, U118, and KNS glioblastoma cell lines (F). Triplicate experiments, (* P < 0.05)

Article Snippet: Phospho-p53 (Ser392) , 9281 , Cell Signaling Technology, Danvers MA.

Techniques: Western Blot, Immunohistochemical staining, Derivative Assay, Expressing, Control

Geranyl acetate (GA) mitigates para-phenylenediamine (PPD)-induced DNA damage response (DDR) signaling in HaCaT cells: A – D, HaCaT cells were seeded in 100 mm dishes (2 × 10 5 cells/dish) and incubated for 24 hours, followed by treatment with GA (0 - 500 μM), in the presence or absence of PPD (250 μM) for 48 hours. Protein expression levels of the DDR-related proteins, including ataxia telangiectasia and Rad3 related protein (ATR), p-ATR, p53, p-p53, p38, p-p38, c-Jun N-terminal kinases (JNK), p-JNK, extracellular signal-regulated kinases (ERK), and p-ERK, were analyzed by Western blotting. The β-Actin was used as a loading control. Protein band intensities were quantified using ImageJ software (version 1.53t). Data are presented as mean ± standard deviation (SD, n = 3). Statistical significance was determined by one-way analysis of variance (ANOVA) followed by Tukey’s post-hoc test (## P < 0.01 and ### P < 0.001 compared with the solvent-treated vehicle control group. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the PPD-treated negative control group).

Journal: Iranian Journal of Pharmaceutical Research : IJPR

Article Title: Geranyl Acetate Attenuates Para-phenylenediamine-induced Cytotoxicity, DNA Damage, Apoptosis, and Inflammation in HaCaT Keratinocytes

doi: 10.5812/ijpr-164379

Figure Lengend Snippet: Geranyl acetate (GA) mitigates para-phenylenediamine (PPD)-induced DNA damage response (DDR) signaling in HaCaT cells: A – D, HaCaT cells were seeded in 100 mm dishes (2 × 10 5 cells/dish) and incubated for 24 hours, followed by treatment with GA (0 - 500 μM), in the presence or absence of PPD (250 μM) for 48 hours. Protein expression levels of the DDR-related proteins, including ataxia telangiectasia and Rad3 related protein (ATR), p-ATR, p53, p-p53, p38, p-p38, c-Jun N-terminal kinases (JNK), p-JNK, extracellular signal-regulated kinases (ERK), and p-ERK, were analyzed by Western blotting. The β-Actin was used as a loading control. Protein band intensities were quantified using ImageJ software (version 1.53t). Data are presented as mean ± standard deviation (SD, n = 3). Statistical significance was determined by one-way analysis of variance (ANOVA) followed by Tukey’s post-hoc test (## P < 0.01 and ### P < 0.001 compared with the solvent-treated vehicle control group. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the PPD-treated negative control group).

Article Snippet: p-p53 (Ser392) , Rabbit , 1:1000 , CST (#9281).

Techniques: Incubation, Expressing, Western Blot, Control, Software, Standard Deviation, Solvent, Negative Control

Geranyl acetate (GA) improves para-phenylenediamine (PPD)-induced apoptosis and inflammation signaling in HaCaT cells: A and B, HaCaT cells were seeded in 100 mm dishes (2 × 10 5 cells/dish) and incubated for 24 hours, followed by treatment with GA (0 - 500 μM), in the presence or absence of PPD (250 μM) for 48 hours. Protein expression levels of the (A) apoptosis-related proteins [BAX, p53 upregulated modulator of apoptosis (PUMA), cytochrome c, and cleaved PARP] and (B) inflammation-related proteins [signal transducer and activator of transcription 3 (STAT3), p-STAT3, p65, p-p65, NF-kappa-B inhibitor alpha (IκB-α), and p-IκB-α] were analyzed by Western blotting. The β-Actin was used as a loading control. Protein band intensities were quantified using ImageJ software (version 1.53t). Data are presented as mean ± standard deviation (SD, n = 3). Statistical significance was determined by one-way analysis of variance (ANOVA) followed by Tukey’s post-hoc test (### P < 0.001 compared with the solvent-treated vehicle control group. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the PPD-treated negative control group).

Journal: Iranian Journal of Pharmaceutical Research : IJPR

Article Title: Geranyl Acetate Attenuates Para-phenylenediamine-induced Cytotoxicity, DNA Damage, Apoptosis, and Inflammation in HaCaT Keratinocytes

doi: 10.5812/ijpr-164379

Figure Lengend Snippet: Geranyl acetate (GA) improves para-phenylenediamine (PPD)-induced apoptosis and inflammation signaling in HaCaT cells: A and B, HaCaT cells were seeded in 100 mm dishes (2 × 10 5 cells/dish) and incubated for 24 hours, followed by treatment with GA (0 - 500 μM), in the presence or absence of PPD (250 μM) for 48 hours. Protein expression levels of the (A) apoptosis-related proteins [BAX, p53 upregulated modulator of apoptosis (PUMA), cytochrome c, and cleaved PARP] and (B) inflammation-related proteins [signal transducer and activator of transcription 3 (STAT3), p-STAT3, p65, p-p65, NF-kappa-B inhibitor alpha (IκB-α), and p-IκB-α] were analyzed by Western blotting. The β-Actin was used as a loading control. Protein band intensities were quantified using ImageJ software (version 1.53t). Data are presented as mean ± standard deviation (SD, n = 3). Statistical significance was determined by one-way analysis of variance (ANOVA) followed by Tukey’s post-hoc test (### P < 0.001 compared with the solvent-treated vehicle control group. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the PPD-treated negative control group).

Article Snippet: p-p53 (Ser392) , Rabbit , 1:1000 , CST (#9281).

Techniques: Incubation, Expressing, Western Blot, Control, Software, Standard Deviation, Solvent, Negative Control