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Vigene Biosciences c jun
C Jun, supplied by Vigene Biosciences, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Article Title: MicroRNA-139-5p upregulation is associated with diabetic endothelial cell dysfunction by targeting c-jun
Article Snippet: C-jun siRNA were purchased from GenePharma (Shanghai, China), and c-jun plasmids were purchased from Vigene (Jinan, China).

Article Title: Positive feedback loop of FAM83A/PI3K/AKT/c-Jun induces migration, invasion and metastasis in hepatocellular carcinoma.
Article Snippet: Plasmids for c-JUN were purchased from Vigene Biosciences (Shandong, China).

Article Title: MicroRNA-3613-5p Promotes Lung Adenocarcinoma Cell Proliferation through a RELA and AKT/MAPK Positive Feedback Loop
Article Snippet: RELA and JUN plasmids were purchased from Vigene Biosciences (Shandong, P.R.

Article Title: miR‐5188 augments glioma growth, migration and invasion through an SP1‐modulated FOXO1‐PI3K/AKT‐c‐JUN‐positive feedback circuit
Article Snippet: The siRNA targeting FOXO1 and c‐JUN or mimics and inhibitors of hsa‐miR‐5188 were purchased from RiboBio Corporation (as shown in Table ). c‐JUN, SP1 and FOXO1 plasmids were obtained from Vigene Biosciences Corporation.

Article Title: ENKUR expression induced by chemically synthesized cinobufotalin suppresses malignant activities of hepatocellular carcinoma by modulating β-catenin/c-Jun/MYH9/USP7/c-Myc axis
Article Snippet: ENKUR and C-Jun plasmids were obtained from GeneChem (Shanghai, China) and Vigene Biosciences (Shangdong, China), respectively. siRNAs were purchased from Guangzhou RiboBio Co. Ltd (Guangzhou, China) ( ).

Construct:

Article Title: DNASE1L3 functions as a significant metastatic suppressor by attenuating MYH9/β-catenin/c-Jun/LncRNA-KDM4A-induced E-cadherin ubiquitination degradation in nasopharyngeal carcinoma.
Article Snippet: .. The β-catenin, c-Jun and MYH9 plasmids were constructed by Vigene Biosciences (Shangdong, China). .. MYH9 domain plasmids were sourced from BersinBio (Guangzhou, China), and for more information refer to our previous report[40].



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AP-1 (c-FOS and <t>c-JUN)</t> is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by <t>CD.</t> <t>β-Actin</t> served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.
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AP-1 (c-FOS and <t>c-JUN)</t> is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by <t>CD.</t> <t>β-Actin</t> served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.
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AP-1 (c-FOS and <t>c-JUN)</t> is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by <t>CD.</t> <t>β-Actin</t> served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.
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AP-1 (c-FOS and <t>c-JUN)</t> is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by <t>CD.</t> <t>β-Actin</t> served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.
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AP-1 (c-FOS and <t>c-JUN)</t> is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by <t>CD.</t> <t>β-Actin</t> served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.
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AP-1 (c-FOS and <t>c-JUN)</t> is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by <t>CD.</t> <t>β-Actin</t> served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.
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AP-1 (c-FOS and <t>c-JUN)</t> is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by <t>CD.</t> <t>β-Actin</t> served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.
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AP-1 (c-FOS and <t>c-JUN)</t> is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by <t>CD.</t> <t>β-Actin</t> served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.
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AP-1 (c-FOS and c-JUN) is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by CD. β-Actin served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.

Journal: Life Medicine

Article Title: HDAC8-selective inhibitor PCI-34051 protects against aortic dissection by attenuating ferroptosis of vascular smooth muscle cells

doi: 10.1093/lifemedi/lnag013

Figure Lengend Snippet: AP-1 (c-FOS and c-JUN) is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by CD. β-Actin served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.

Article Snippet: The antibodies applied in this study were: β-Actin (AC026, ABclonal), FSP1 (20886-1-AP, Proteintech), GPX4 (ab125066, Abcam), c-JUN (T55290F, ABmart), c-FOS (T56596F, ABmart), Flag (F1804, Sigma-Aldrich), HDAC8 (17548-1-AP, Proteintech), SLC7A11 (26864-1-AP, Proteintech), 4-HNE (MAB3249-SP, Bio-techne), CD86 (13395-1-AP, Proteintech), α-SMA (ab7817, Abcam), α-SMA (GTX100034, Genetex), GST (AE001, Abclonal).

Techniques: Gene Expression, Western Blot, Control, Immunoprecipitation

AP-1 (c-FOS and c-JUN) eliminated the effects of PCI-34051 on HASMC ferroptosis. All HASMCs were infected with lenti-Flag and lenti-c-FOS + lenti-c-JUN, and then these HASMCs were used for subsequent experiments. (A, B) The protein level of AP-1 (c-JUN and c-FOS) was detected by Western blot in HASMCs infected with lenti-Flag and lenti-c-JUN + lenti-c-FOS ( n = 4 per group). (C, D) The CCK8 assay showing the relative viability of HASMCs treated with DMSO and PCI-34051 after CD (C) and IKE (D) stimulation for the indicated time ( n = 5 per group). (E, F) Flow cytometry with propidium iodide (PI) staining displaying the percentage of PI-positive cells of HASMCs after treatment as described above ( n = 4 per group). (G, H) The LDH assay indicating the relative cell damage rate of HASMCs treated with described above ( n = 5 per group). (I–L) The ratio of oxidized BODIPY-C11/non-oxidized BODIPY-C11 fluorescence revealing the level of ROS of HASMCs treated with described above ( n = 4 per group). (M–P). 4-HNE immunofluorescence staining and quantitative analysis exhibiting the content of 4-HNE in HASMCs after treatment as described above ( n = 4 per group). (Q–T) Western-blot analysis and quantification performed to assess the protein levels of GPX4, FSP1, and SLC7A11 in AP-1 overexpressed HASMCs after DMSO and PCI-34051 treatment along with CD or IKE induction. β-Actin served as a loading control ( n = 4 per group). Values are means ± SD; *** P < 0.001, ** P < 0.01, * P < 0.05.

Journal: Life Medicine

Article Title: HDAC8-selective inhibitor PCI-34051 protects against aortic dissection by attenuating ferroptosis of vascular smooth muscle cells

doi: 10.1093/lifemedi/lnag013

Figure Lengend Snippet: AP-1 (c-FOS and c-JUN) eliminated the effects of PCI-34051 on HASMC ferroptosis. All HASMCs were infected with lenti-Flag and lenti-c-FOS + lenti-c-JUN, and then these HASMCs were used for subsequent experiments. (A, B) The protein level of AP-1 (c-JUN and c-FOS) was detected by Western blot in HASMCs infected with lenti-Flag and lenti-c-JUN + lenti-c-FOS ( n = 4 per group). (C, D) The CCK8 assay showing the relative viability of HASMCs treated with DMSO and PCI-34051 after CD (C) and IKE (D) stimulation for the indicated time ( n = 5 per group). (E, F) Flow cytometry with propidium iodide (PI) staining displaying the percentage of PI-positive cells of HASMCs after treatment as described above ( n = 4 per group). (G, H) The LDH assay indicating the relative cell damage rate of HASMCs treated with described above ( n = 5 per group). (I–L) The ratio of oxidized BODIPY-C11/non-oxidized BODIPY-C11 fluorescence revealing the level of ROS of HASMCs treated with described above ( n = 4 per group). (M–P). 4-HNE immunofluorescence staining and quantitative analysis exhibiting the content of 4-HNE in HASMCs after treatment as described above ( n = 4 per group). (Q–T) Western-blot analysis and quantification performed to assess the protein levels of GPX4, FSP1, and SLC7A11 in AP-1 overexpressed HASMCs after DMSO and PCI-34051 treatment along with CD or IKE induction. β-Actin served as a loading control ( n = 4 per group). Values are means ± SD; *** P < 0.001, ** P < 0.01, * P < 0.05.

Article Snippet: The antibodies applied in this study were: β-Actin (AC026, ABclonal), FSP1 (20886-1-AP, Proteintech), GPX4 (ab125066, Abcam), c-JUN (T55290F, ABmart), c-FOS (T56596F, ABmart), Flag (F1804, Sigma-Aldrich), HDAC8 (17548-1-AP, Proteintech), SLC7A11 (26864-1-AP, Proteintech), 4-HNE (MAB3249-SP, Bio-techne), CD86 (13395-1-AP, Proteintech), α-SMA (ab7817, Abcam), α-SMA (GTX100034, Genetex), GST (AE001, Abclonal).

Techniques: Infection, Western Blot, CCK-8 Assay, Flow Cytometry, Staining, Lactate Dehydrogenase Assay, Fluorescence, Immunofluorescence, Control

The working model of PCI-34051 regulating HASMC ferroptosis and aortic dissection in mice. PCI-34051 inhibits the ferroptosis of HASMC by affecting the interaction between HDAC8 and AP-1 (c-FOS and c-JUN) and further suppresses the occurrence and development of BAPN-induced aortic dissection in mice. (This figure is created with Biorender).

Journal: Life Medicine

Article Title: HDAC8-selective inhibitor PCI-34051 protects against aortic dissection by attenuating ferroptosis of vascular smooth muscle cells

doi: 10.1093/lifemedi/lnag013

Figure Lengend Snippet: The working model of PCI-34051 regulating HASMC ferroptosis and aortic dissection in mice. PCI-34051 inhibits the ferroptosis of HASMC by affecting the interaction between HDAC8 and AP-1 (c-FOS and c-JUN) and further suppresses the occurrence and development of BAPN-induced aortic dissection in mice. (This figure is created with Biorender).

Article Snippet: The antibodies applied in this study were: β-Actin (AC026, ABclonal), FSP1 (20886-1-AP, Proteintech), GPX4 (ab125066, Abcam), c-JUN (T55290F, ABmart), c-FOS (T56596F, ABmart), Flag (F1804, Sigma-Aldrich), HDAC8 (17548-1-AP, Proteintech), SLC7A11 (26864-1-AP, Proteintech), 4-HNE (MAB3249-SP, Bio-techne), CD86 (13395-1-AP, Proteintech), α-SMA (ab7817, Abcam), α-SMA (GTX100034, Genetex), GST (AE001, Abclonal).

Techniques: Dissection