Review

anti prkcg (Bioss)

Bioss is a verified supplier

Bioss manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Bioss anti prkcg
Anti Prkcg, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+prkcg/PKC+gamma+SCA14+Polyclonal+Antibody/pmc12407310-302-45-48
Average 94 stars, based on 2 article reviews

anti prkcg - by Bioz Stars, 2026-10

94/100 stars

Images

Incubation:

Article Title: β‐Mangostin Attenuates TET2‐Mediated DNA Demethylation of Prkcg in the Prevention of Intervertebral Disc Degeneration
Article Snippet: .. After dewaxing and antigen retrieval, the slides were blocked with 3% BSA for 30 min. Then, the slides were incubated with anti‐Pink1 (1:200, 23274‐1‐AP, Proteintech, China), anti‐Parkin (1:100, 14060‐1‐AP, Proteintech, China) and anti‐Prkcg (1:100, bs3626R, Bioss, China) overnight at 4 °C. .. Afterward, the slides were incubated with CY3‐conjugated goat anti‐rabbit antibody (1:300, GB21303, Servicebio, China) in the dark at room temperature for 50 min, followed by DAPI (C0065, Solarbio, China) staining for 5 min to label the cell nuclei.

Article Title: β‐Mangostin Attenuates TET2‐Mediated DNA Demethylation of Prkcg in the Prevention of Intervertebral Disc Degeneration
Article Snippet: .. After washing with TBS, the sections were blocked with 10% goat serum (Boster, China) for 1 h. Then, the sections were incubated overnight at 4 °C with the anti‐Collagen2α1(1:800, 28459‐1‐AP, Proteintech, China), anti‐MMP13 (1:100, 18165‐1‐AP, Proteintech, China), anti‐INOS (1:100, A14031, Abclonal, China), anti‐Prkcg (1:100, bs3626R, Bioss, China), anti‐TET2 (1:100, a5682, Abclonal, China). .. The HRP‐conjugated secondary antibody (RGAR011, Proteintech, China) was applied to the corresponding primary antibody.

Article Title: β-Mangostin Attenuates TET2-Mediated DNA Demethylation of Prkcg in the Prevention of Intervertebral Disc Degeneration.
Article Snippet: The isolated proteins were separated by sodium dodecyl sulfatepolyacrylamide gel electrophoresis (SDS-PAGE) and transferred onto a PVDF membrane (Millipore, USA). .. The membrane was then blocked with 5% milk for 1 h. The membrane was then incubated with the anti-β-actin (1:50 000, AC026, Abclonal, China), anti-Collagen2α1(1:500, A19308, Abclonal, China), anti-Aggrecan (1:1000, A8536, Abclonal, China), anti-MMP13 (1:1000, A1606, Abclonal, China), anti-ADAMTS5 (1:1000, A2836, abalone, China), anti-INOS (1:1000, 18985-1-AP, Proteintech, China), anti-COX-2 (1:1000, 12375-1-AP, Proteintech, China), anti-Prkcg (1:1000, bs3626R, Bioss, China), anti-TET2 (1:1000, a5682, Abclonal, China), anti-Pink1 (1:1000, 23274-1-AP, Proteintech, China), anti-Parkin (1:1000, 14060-1-AP, Proteintech, China), anti-LC3B (1:1000, 14600-1-AP, Proteintech, China), anti-SQSTM1 (1:1000, 18420-1-AP, Proteintech, China) overnight. .. The membrane was then incubated with HRP-conjugated Goat anti-Rabbit IgG (1:2000, Abclonal, AS014, China) for 1 h. The membranes were visualized using ECL Plus (Thermo Fisher Scientific, USA).

Article Title: β‐Mangostin Attenuates TET2‐Mediated DNA Demethylation of Prkcg in the Prevention of Intervertebral Disc Degeneration
Article Snippet: The isolated proteins were separated by sodium dodecyl sulfate‐polyacrylamide gel electrophoresis (SDS‐PAGE) and transferred onto a PVDF membrane (Millipore, USA). .. The membrane was then blocked with 5% milk for 1 h. The membrane was then incubated with the anti‐β‐actin (1:50 000, AC026, Abclonal, China), anti‐Collagen2α1(1:500, A19308, Abclonal, China), anti‐Aggrecan (1:1000, A8536, Abclonal, China), anti‐MMP13 (1:1000, A1606, Abclonal, China), anti‐ADAMTS5 (1:1000, A2836, abalone, China), anti‐INOS (1:1000, 18985‐1‐AP, Proteintech, China), anti‐COX‐2 (1:1000, 12375‐1‐AP, Proteintech, China), anti‐Prkcg (1:1000, bs3626R, Bioss, China), anti‐TET2 (1:1000, a5682, Abclonal, China), anti‐Pink1 (1:1000, 23274‐1‐AP, Proteintech, China), anti‐Parkin (1:1000, 14060‐1‐AP, Proteintech, China), anti‐LC3B (1:1000, 14600‐1‐AP, Proteintech, China), anti‐SQSTM1 (1:1000, 18420‐1‐AP, Proteintech, China) overnight. .. The membrane was then incubated with HRP‐conjugated Goat anti‐Rabbit IgG (1:2000, Abclonal, AS014, China) for 1 h. The membranes were visualized using ECL Plus (Thermo Fisher Scientific, USA).

Article Title: β-Mangostin Attenuates TET2-Mediated DNA Demethylation of Prkcg in the Prevention of Intervertebral Disc Degeneration.
Article Snippet: .. IF Staining (IVD): After dewaxing and antigen retrieval, the slides were blocked with 3% BSA for 30 min. Then, the slides were incubated with anti-Pink1 (1:200, 23274-1-AP, Proteintech, China), anti-Parkin (1:100, 14060-1-AP, Proteintech, China) and anti-Prkcg (1:100, bs3626R, Bioss, Adv. ..

Article Title: β-Mangostin Attenuates TET2-Mediated DNA Demethylation of Prkcg in the Prevention of Intervertebral Disc Degeneration.
Article Snippet: .. After washingwith TBS, the sections were blocked with 10% goat serum (Boster, China) for 1 h. Then, the sections were incubated overnight at 4 °C with the anti-Collagen2α1(1:800, 28459-1-AP, Proteintech, China), anti-MMP13 (1:100, 18165-1-AP, Proteintech, China), anti-INOS (1:100, A14031, Abclonal, China), anti-Prkcg (1:100, bs3626R, Bioss, China), anti-TET2 (1:100, a5682, Abclonal, China). .. The HRP-conjugated secondary antibody (RGAR011, Proteintech, China) was applied to the corresponding primary antibody.

Blocking Assay:

Article Title: β‐Mangostin Attenuates TET2‐Mediated DNA Demethylation of Prkcg in the Prevention of Intervertebral Disc Degeneration
Article Snippet: Add 500 μL of 4% paraformaldehyde to each well and fix the cells for 20 min. Then, add 500 μL of 0.5% Triton X‐100 (Sigma, USA) to each well to permeabilize the cells for 10 min. .. Afterward, add 1 mL of 5% BSA (Sigma, USA) to each well and block the cells for 1 h. Add anti‐Collagen‐2α1 (1:100, A19308, Abclonal, China), anti‐MMP‐13 (1:100, A1606, Abclonal, China), anti‐INOS (1:100, 18985‐1‐AP, Proteintech, China), anti‐Pink1 (1:200, 23274‐1‐AP, Proteintech, China), anti‐Parkin (1:100, 14060‐1‐AP, Proteintech, China), anti‐Prkcg (1:100, bs3626R, Bioss, China), anti‐TET2 (1:100, a5682, Abclonal, China). to each well and incubate overnight at 4 °C in the dark. .. Then, add FITC‐conjugated goat anti‐rabbit secondary antibody (1:100, Solarbio, China) and incubate in the dark at room temperature for 1 h. Wash the cells three times with PBS, then stain the cytoskeleton with Rhodamine‐labeled phalloidin (1:200, Solarbio, China) for 1 h. Finally, wash the cells with PBS three times.

Membrane:

Staining:

Image Search Results

WDFY4 is up‐regulated in ox‐LDL‐treated HAEC and inhibits cell viability. HAECs were treated with 0 μg/mL, 25 μg/mL, 50 μg/mL, 100 μg/mL, 150 μg/mL and 200 μg/mL ox‐LDL for 24 h. (A) The effects of different concentrations of ox‐LDL on the activity of HAEC were detected. (B) The expression level of WDFY4 protein in HAEC treated with different concentrations of ox‐LDL was detected. (C) The expression of WDFY4 mRNA in HAEC treated with different concentrations of ox‐LDL was detected. (D) The expression of WDFY4 was detected by immunofluorescence. Scale bar, 25 μm. n = 4. One‐way ANOVA was used for comparison between multiple groups. Data are presented as mean ± SD. * p < 0.05 and ** p < 0.01.

Journal: Journal of Cellular and Molecular Medicine

Article Title: WDFY4 Promotes the Progression of Atherosclerosis by Regulating Ferroptosis Mediated by the LAPTM5 / CDC42 / mTOR / 4EBP1 / SLC7A11 Pathway

doi: 10.1111/jcmm.70729

Figure Lengend Snippet: WDFY4 is up‐regulated in ox‐LDL‐treated HAEC and inhibits cell viability. HAECs were treated with 0 μg/mL, 25 μg/mL, 50 μg/mL, 100 μg/mL, 150 μg/mL and 200 μg/mL ox‐LDL for 24 h. (A) The effects of different concentrations of ox‐LDL on the activity of HAEC were detected. (B) The expression level of WDFY4 protein in HAEC treated with different concentrations of ox‐LDL was detected. (C) The expression of WDFY4 mRNA in HAEC treated with different concentrations of ox‐LDL was detected. (D) The expression of WDFY4 was detected by immunofluorescence. Scale bar, 25 μm. n = 4. One‐way ANOVA was used for comparison between multiple groups. Data are presented as mean ± SD. * p < 0.05 and ** p < 0.01.

Article Snippet: Proteins were separated by SDS‐PAGE, transferred to PVDF membrane (Millipore, Billerica, MA, USA) and blocked with 5% skimmed milk powder (1 g skimmed milk powder: 20 mL 1 × TBST reagent) for 2 h. Subsequently, membranes were incubated overnight at 4°C with primary antibodies: WDFY4 (1: 500, orb512258, Biorbyt, UK), LAPTM5 (1: 1000, PA5‐23585, Thermo Fisher), GPX4 (1: 500, ab125066, Abcam, UK), SLC7A11 (1: 500, ab307601, Abcam), ACSL4 (1: 500, ab155282, Abcam), CDC42 (1: 500, ab187643, Abcam), mTOR (1:500, ab134903, Abcam), 4EBP1 (1: 500, ab32024, Abcam) and GAPDH (1: 1000, ab181602, Abcam).

Techniques: Activity Assay, Expressing, Immunofluorescence, Comparison

Knockdown of WDFY4 inhibits ox‐LDL‐induced ferroptosis in HAECs. After HAECs were treated with 100 μg/mL ox‐LDL for 24 h, HAECs were transfected with sh‐WDFY4. (A) RT‐qPCR was used to detect the expression level of WDFY4 mRNA in HAECs. (B) Western blotting was used to detect the expression level of WDFY4 protein in HAECs. (C) CCK‐8 was used to detect the activity of HAECs. (D) The level of lipid ROS in HAECs was detected by DCFH‐DA fluorescent probe method. Scale bar, 100 μm. (E) MDA content was detected with MDA assay kit. (F) GSH level was detected with GSH assay kit. (G) ELISA was used to detect Fe 2+ content in HAECs. (H) Western blotting was used to detect the level of ferroptosis‐related proteins. (I) Representative transmission electron microscopy pictures of mitochondria ultrastructure in HAECs were showed. Scale bar, 1 μm. n = 4. One‐way ANOVA or Two‐way ANOVA was used for comparison between multiple groups. ** p < 0.01.

Journal: Journal of Cellular and Molecular Medicine

Article Title: WDFY4 Promotes the Progression of Atherosclerosis by Regulating Ferroptosis Mediated by the LAPTM5 / CDC42 / mTOR / 4EBP1 / SLC7A11 Pathway

doi: 10.1111/jcmm.70729

Figure Lengend Snippet: Knockdown of WDFY4 inhibits ox‐LDL‐induced ferroptosis in HAECs. After HAECs were treated with 100 μg/mL ox‐LDL for 24 h, HAECs were transfected with sh‐WDFY4. (A) RT‐qPCR was used to detect the expression level of WDFY4 mRNA in HAECs. (B) Western blotting was used to detect the expression level of WDFY4 protein in HAECs. (C) CCK‐8 was used to detect the activity of HAECs. (D) The level of lipid ROS in HAECs was detected by DCFH‐DA fluorescent probe method. Scale bar, 100 μm. (E) MDA content was detected with MDA assay kit. (F) GSH level was detected with GSH assay kit. (G) ELISA was used to detect Fe 2+ content in HAECs. (H) Western blotting was used to detect the level of ferroptosis‐related proteins. (I) Representative transmission electron microscopy pictures of mitochondria ultrastructure in HAECs were showed. Scale bar, 1 μm. n = 4. One‐way ANOVA or Two‐way ANOVA was used for comparison between multiple groups. ** p < 0.01.

Techniques: Knockdown, Transfection, Quantitative RT-PCR, Expressing, Western Blot, CCK-8 Assay, Activity Assay, Multiple Displacement Amplification, GSH Assay, Enzyme-linked Immunosorbent Assay, Transmission Assay, Electron Microscopy, Comparison

Interference with WDFY4 reduces ox‐LDL induced HAEC cell death and inflammatory response. After HAECs were treated with 100 μg/mL ox‐LDL for 24 h, HAECs were transfected with sh‐WDFY4. (A) The concentration of endothelial cell function marker NO in the supernatant of HAEC cells was detected by NO assay kit. (B) The activity of endothelial cell function marker eNOS in HAECs supernatant was detected by ELISA. (C) The level of endothelial cell function marker ET‐1 in the supernatant of HAECs was detected by ELISA. (D–F) The secretion level of inflammatory factors (TNF‐α, IL‐6 and IL‐1β) in the supernatant of HAECs was detected by ELISA. (G, H) PI staining was used to detect the mortality of HAECs treated with ox‐LDL. Scale bar, 100 μm. n = 4. One‐way ANOVA was used for comparison between multiple groups. * p < 0.05, ** p < 0.01.

Journal: Journal of Cellular and Molecular Medicine

Article Title: WDFY4 Promotes the Progression of Atherosclerosis by Regulating Ferroptosis Mediated by the LAPTM5 / CDC42 / mTOR / 4EBP1 / SLC7A11 Pathway

doi: 10.1111/jcmm.70729

Figure Lengend Snippet: Interference with WDFY4 reduces ox‐LDL induced HAEC cell death and inflammatory response. After HAECs were treated with 100 μg/mL ox‐LDL for 24 h, HAECs were transfected with sh‐WDFY4. (A) The concentration of endothelial cell function marker NO in the supernatant of HAEC cells was detected by NO assay kit. (B) The activity of endothelial cell function marker eNOS in HAECs supernatant was detected by ELISA. (C) The level of endothelial cell function marker ET‐1 in the supernatant of HAECs was detected by ELISA. (D–F) The secretion level of inflammatory factors (TNF‐α, IL‐6 and IL‐1β) in the supernatant of HAECs was detected by ELISA. (G, H) PI staining was used to detect the mortality of HAECs treated with ox‐LDL. Scale bar, 100 μm. n = 4. One‐way ANOVA was used for comparison between multiple groups. * p < 0.05, ** p < 0.01.

Techniques: Transfection, Concentration Assay, Cell Function Assay, Marker, Activity Assay, Enzyme-linked Immunosorbent Assay, Staining, Comparison

WDFY4 interacts with LAPTM5 to promote LAPTM5 expression. After HAECs were treated with 100 μg/mL ox‐LDL for 24 h, HAECs were transfected with sh‐WDFY4. (A) WDFY4 interacting proteins were predicted. (B) Immunofluorescence staining of WDFY4 and LAPTM5 was showed. Scale bar, 25 μm. (C) Co‐IP assay was used to verify the interaction between WDFY4 and LAPTM5. (D) The effect of WDFY4 knockdown on the expression of LAPTM5 protein in HAEC was detected by Western blotting. n = 4. One‐way ANOVA was used for comparison between multiple groups. * p < 0.05, ** p < 0.01.

Journal: Journal of Cellular and Molecular Medicine

Article Title: WDFY4 Promotes the Progression of Atherosclerosis by Regulating Ferroptosis Mediated by the LAPTM5 / CDC42 / mTOR / 4EBP1 / SLC7A11 Pathway

doi: 10.1111/jcmm.70729

Figure Lengend Snippet: WDFY4 interacts with LAPTM5 to promote LAPTM5 expression. After HAECs were treated with 100 μg/mL ox‐LDL for 24 h, HAECs were transfected with sh‐WDFY4. (A) WDFY4 interacting proteins were predicted. (B) Immunofluorescence staining of WDFY4 and LAPTM5 was showed. Scale bar, 25 μm. (C) Co‐IP assay was used to verify the interaction between WDFY4 and LAPTM5. (D) The effect of WDFY4 knockdown on the expression of LAPTM5 protein in HAEC was detected by Western blotting. n = 4. One‐way ANOVA was used for comparison between multiple groups. * p < 0.05, ** p < 0.01.

Techniques: Expressing, Transfection, Immunofluorescence, Staining, Co-Immunoprecipitation Assay, Knockdown, Western Blot, Comparison

WDFY4 interacts with LAPTM5 and promotes ferroptosis in HAEC by inhibiting CDC42/mTOR/4EBP1/SLC7A11 pathway. After HAECs were treated with 100 μg/mL ox‐LDL for 24 h. ox‐LDL treated HAECs were transfected with sh‐WDFY4 and pcDNA‐LAPTM5 or treated with 10 μM ML141. (A) Western blotting was used to detect the expression level of WDFY4 protein in HAECs. (B) CCK‐8 was used to detect the activity of HAECs. (C) Western blotting was used to detect the expression level of CDC42, mTOR and 4EBP1 protein in HAECs. (D) ELISA was used to detect Fe 2+ content in HAECs. (E) The level of lipid ROS in HAEC was detected by DCFH‐DA fluorescent probe method. Scale bar, 100 μm. (F) MDA content was detected with MDA assay kit. (G) GSH level was detected with GSH assay kit. (H) Western blotting was used to detect the level of ferroptosis‐related proteins. (I) Representative transmission electron microscopy pictures of mitochondria ultrastructure in HAECs were showed. Scale bar, 1 μm. n = 4. One‐way ANOVA or Two‐way ANOVA was used for comparison between multiple groups. ** p < 0.01, and ns means non‐significant.

Journal: Journal of Cellular and Molecular Medicine

Article Title: WDFY4 Promotes the Progression of Atherosclerosis by Regulating Ferroptosis Mediated by the LAPTM5 / CDC42 / mTOR / 4EBP1 / SLC7A11 Pathway

doi: 10.1111/jcmm.70729

Figure Lengend Snippet: WDFY4 interacts with LAPTM5 and promotes ferroptosis in HAEC by inhibiting CDC42/mTOR/4EBP1/SLC7A11 pathway. After HAECs were treated with 100 μg/mL ox‐LDL for 24 h. ox‐LDL treated HAECs were transfected with sh‐WDFY4 and pcDNA‐LAPTM5 or treated with 10 μM ML141. (A) Western blotting was used to detect the expression level of WDFY4 protein in HAECs. (B) CCK‐8 was used to detect the activity of HAECs. (C) Western blotting was used to detect the expression level of CDC42, mTOR and 4EBP1 protein in HAECs. (D) ELISA was used to detect Fe 2+ content in HAECs. (E) The level of lipid ROS in HAEC was detected by DCFH‐DA fluorescent probe method. Scale bar, 100 μm. (F) MDA content was detected with MDA assay kit. (G) GSH level was detected with GSH assay kit. (H) Western blotting was used to detect the level of ferroptosis‐related proteins. (I) Representative transmission electron microscopy pictures of mitochondria ultrastructure in HAECs were showed. Scale bar, 1 μm. n = 4. One‐way ANOVA or Two‐way ANOVA was used for comparison between multiple groups. ** p < 0.01, and ns means non‐significant.

Techniques: Transfection, Western Blot, Expressing, CCK-8 Assay, Activity Assay, Enzyme-linked Immunosorbent Assay, Multiple Displacement Amplification, GSH Assay, Transmission Assay, Electron Microscopy, Comparison

LAPTM5 and ML141 reversed the alleviation effect of sh‐WDFY4 on cell injury and inflammatory response in AS model cells. After HAECs were treated with 100 μg/mL ox‐LDL for 24 h. ox‐LDL treated HAECs were transfected with sh‐WDFY4 and pcDNA‐LAPTM5 or treated with 10 μM ML141. (A) The concentration of endothelial cell function marker NO in the supernatant of HAEC cells was detected by NO assay kit. (B) The activity of endothelial cell function marker eNOS in HAECs supernatant was detected by ELISA. (C) The level of endothelial cell function marker ET‐1 in the supernatant of HAECs was detected by ELISA. (D–F) The secretion level of inflammatory factors (TNF‐α, IL‐6 and IL‐1β) in the supernatant of HAECs was detected by ELISA. (G) PI staining was used to detect the mortality of HAECs treated with ox‐LDL. Scale bar, 100 μm. n = 4. One‐way ANOVA was used for comparison between multiple groups. ** p < 0.01.

Journal: Journal of Cellular and Molecular Medicine

Article Title: WDFY4 Promotes the Progression of Atherosclerosis by Regulating Ferroptosis Mediated by the LAPTM5 / CDC42 / mTOR / 4EBP1 / SLC7A11 Pathway

doi: 10.1111/jcmm.70729

Figure Lengend Snippet: LAPTM5 and ML141 reversed the alleviation effect of sh‐WDFY4 on cell injury and inflammatory response in AS model cells. After HAECs were treated with 100 μg/mL ox‐LDL for 24 h. ox‐LDL treated HAECs were transfected with sh‐WDFY4 and pcDNA‐LAPTM5 or treated with 10 μM ML141. (A) The concentration of endothelial cell function marker NO in the supernatant of HAEC cells was detected by NO assay kit. (B) The activity of endothelial cell function marker eNOS in HAECs supernatant was detected by ELISA. (C) The level of endothelial cell function marker ET‐1 in the supernatant of HAECs was detected by ELISA. (D–F) The secretion level of inflammatory factors (TNF‐α, IL‐6 and IL‐1β) in the supernatant of HAECs was detected by ELISA. (G) PI staining was used to detect the mortality of HAECs treated with ox‐LDL. Scale bar, 100 μm. n = 4. One‐way ANOVA was used for comparison between multiple groups. ** p < 0.01.

Techniques: Transfection, Concentration Assay, Cell Function Assay, Marker, Activity Assay, Enzyme-linked Immunosorbent Assay, Staining, Comparison

Fluorescence co‐localization of WDFY4 and LAPTM5 In vivo. ApoE −/− mice were fed a high‐fat diet and injected with sh‐WDFY4, sh‐LAPTM5 or sh‐NC lentivirus every other day. Immunofluorescence staining of WDFY4 and LAPTM5 in the diseased area of the aortic root in mice were showed, and the fluorescence intensity was quantified. Scale bar, 25 μm. n = 8. One‐way ANOVA was used for comparison between multiple groups. ** p < 0.01, and ns means non‐significant.

Journal: Journal of Cellular and Molecular Medicine

Article Title: WDFY4 Promotes the Progression of Atherosclerosis by Regulating Ferroptosis Mediated by the LAPTM5 / CDC42 / mTOR / 4EBP1 / SLC7A11 Pathway

doi: 10.1111/jcmm.70729

Figure Lengend Snippet: Fluorescence co‐localization of WDFY4 and LAPTM5 In vivo. ApoE −/− mice were fed a high‐fat diet and injected with sh‐WDFY4, sh‐LAPTM5 or sh‐NC lentivirus every other day. Immunofluorescence staining of WDFY4 and LAPTM5 in the diseased area of the aortic root in mice were showed, and the fluorescence intensity was quantified. Scale bar, 25 μm. n = 8. One‐way ANOVA was used for comparison between multiple groups. ** p < 0.01, and ns means non‐significant.

Techniques: Fluorescence, In Vivo, Injection, Immunofluorescence, Staining, Comparison

Knockdown of WDFY4 and LAPTM5 alleviates AS associated with ferroptosis. ApoE −/− mice were fed a high‐fat diet and injected with sh‐WDFY4, sh‐LAPTM5 or sh‐NC lentivirus every other day. (A) Western blotting was used to detect the expression levels of WDFY4, LAPTM5 and ferroptosis‐related proteins in mouse aortic tissue. (B) ELISA was used to detect the Fe 2+ level in serum of mice. (C) The level of ROS in serum of mice was detected. (D) The expression levels of inflammatory factors TNF‐α and IL‐1β mRNA in serum of mice were detected by qPCR. (E) Oil red O staining was used to detect the degree of arterial plaque. Scale bar, 50 μm. (F) HE staining was used for pathological analysis of arterial tissue. Scale bar, 50 μm. (G) The serum TC, TG, LDL and HDL levels were detected by ELISA. n = 8. One‐way ANOVA was used for comparison between multiple groups. ** p < 0.01, and ns means non‐significant.

Journal: Journal of Cellular and Molecular Medicine

Article Title: WDFY4 Promotes the Progression of Atherosclerosis by Regulating Ferroptosis Mediated by the LAPTM5 / CDC42 / mTOR / 4EBP1 / SLC7A11 Pathway

doi: 10.1111/jcmm.70729

Figure Lengend Snippet: Knockdown of WDFY4 and LAPTM5 alleviates AS associated with ferroptosis. ApoE −/− mice were fed a high‐fat diet and injected with sh‐WDFY4, sh‐LAPTM5 or sh‐NC lentivirus every other day. (A) Western blotting was used to detect the expression levels of WDFY4, LAPTM5 and ferroptosis‐related proteins in mouse aortic tissue. (B) ELISA was used to detect the Fe 2+ level in serum of mice. (C) The level of ROS in serum of mice was detected. (D) The expression levels of inflammatory factors TNF‐α and IL‐1β mRNA in serum of mice were detected by qPCR. (E) Oil red O staining was used to detect the degree of arterial plaque. Scale bar, 50 μm. (F) HE staining was used for pathological analysis of arterial tissue. Scale bar, 50 μm. (G) The serum TC, TG, LDL and HDL levels were detected by ELISA. n = 8. One‐way ANOVA was used for comparison between multiple groups. ** p < 0.01, and ns means non‐significant.

Techniques: Knockdown, Injection, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Staining, Comparison

Review

anti prkcg (Bioss)

Structured Review

Images

Related Articles

Incubation:

Blocking Assay:

Membrane:

Staining:

Similar Products

Image Search Results