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2010 panc sco h37rvma derivative (ATCC)

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ATCC 2010 panc sco h37rvma derivative
2010 Panc Sco H37rvma Derivative, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1018 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/2010+derivative/JB6+Cl+41-5a/pmc05153693__id6b00150_si_001-56-21-13
Average 96 stars, based on 1018 article reviews

2010 panc sco h37rvma derivative - by Bioz Stars, 2026-10

96/100 stars

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Southern Blot:

Article Title: Role of the Carboxy Terminus of SecA in Iron Acquisition, Protein Translocation, and Virulence of the Bacterial Pathogen Acinetobacter baumannii
Article Snippet: In our preliminary 301 study (9), we reported that the A. baumannii ATCC 19606 T 2010 isogenic insertion derivative, 302 which was isolated because of its inability to grow in the presence of the synthetic iron chelator 303 DIP, harbors an EZ::TN insertion 140 nucleotides from the 3’end of a 2,724-304 nucleotide gene (ORF 2 in Fig. 1A). .. Detection by Southern blotting of a single 2.4-kb KpnI-305 PvuII restriction fragment, the size of which was increased by 2 kb because of the transposon 306 insertion in the 2010 derivative (Fig. 1B and C), indicates that this is the only ATCC 19606 T 307 coding region disrupted by the transposition insertion. .. Further in silico analyses including the 308 information available at the Broad Institute as part of the Human Microbiome Project 309 (http://www.broadinstitute.org/) showed that the gene interrupted in the 2010 derivative is a 310 canonical secA, which was annotated as HMPREF0010_02761.1.

Article Title: Role of the Carboxy Terminus of SecA in Iron Acquisition, Protein Translocation, and Virulence of the Bacterial Pathogen Acinetobacter baumannii
Article Snippet: In our preliminary study ( 9 ), we reported that the A. baumannii ATCC 19606 T 2010 isogenic insertion derivative, which was isolated because of its inability to grow in the presence of the synthetic iron chelator DIP, harbors an EZ::TN insertion 140 nucleotides from the 3′ end of a 2,724-nucleotide gene (open reading frame [ORF] 2 in ). .. Detection by Southern blotting of a single 2.4-kb KpnI-PvuII restriction fragment, the size of which was increased by 2 kb because of the transposon insertion in the 2010 derivative ( and ), indicates that this is the only ATCC 19606 T coding region disrupted by the transposition insertion. .. Further in silico analyses including the information available at the Broad Institute as part of the Human Microbiome Project ( http://www.broadinstitute.org/ ) showed that the gene interrupted in the 2010 derivative is a canonical secA , which was annotated as HMPREF0010_02761.1.

Article Title: Role of the Carboxy Terminus of SecA in Iron Acquisition, Protein Translocation, and Virulence of the Bacterial Pathogen Acinetobacter baumannii
Article Snippet: The three long black horizontal bars represent cloned DNA regions used as probes in Southern blotting (pMU734), to complement the 2010 insertion derivative (pMU472), or to overproduce a His-tagged SecA derivative (pMU481). .. The short black horizontal bar flanked by primer numbers indicate the 5′-end secA region used to test transcriptional expression by qRT-PCR. (B and C) Southern blotting of KpnI-PvuII-digested total DNA isolated from the ATCC 19606 T parental strain (lanes 2) and the 2010 derivative (lanes 3) probed with pMU734 (B) or the aph gene (C). (D) Western blotting of cytoplasmic proteins isolated from the ATCC 19606 T parental strain (lane 1) and the 2010 derivative (lane 2) probed with anti-SecA antibodies. .. The white arrow indicates the truncated SecA protein produced in the 2010 insertion derivative.

Isolation:

Article Title: Role of the Carboxy Terminus of SecA in Iron Acquisition, Protein Translocation, and Virulence of the Bacterial Pathogen Acinetobacter baumannii
Article Snippet: .. Our preliminary study ( 9 ) reporting the isolation of the 2010 derivative under nonselective conditions and growth data collected during this work ( ) showed that there were not statistically significant differences between the growth rates of the parental ATCC 19606 T strain and the 2010 isogenic derivative when cultured in LB broth. .. However, incubation of 2010 cells in LB broth containing 200 μM DIP resulted in a drastic growth reduction ( P ≤ 0.001) compared with that of the ATCC 19606 T strain after overnight incubation ( ).

Article Title: Role of the Carboxy Terminus of SecA in Iron Acquisition, Protein Translocation, and Virulence of the Bacterial Pathogen Acinetobacter baumannii
Article Snippet: This analysis showed that although the transposon 350 insertion did not abolish the production of secA transcripts, their abundance in 2010 cells was 351 reduced to 69% (P ≤ 0.001) of that detected in ATCC 19606 T parental bacteria (Fig. 2). .. 352 Our preliminary study (9) reporting the isolation of the 2010 derivative under non-353 selective conditions and growth data collected during this work (Fig. 3A) showed that there were 354 not statistically significant differences between the growth rates of the parental ATCC 19606 T 355 strain and the 2010 isogenic derivative when cultured in LB broth. .. However, incubation of 2010 356 cells in LB broth containing 200 μM DIP resulted in a drastic growth reduction (P ≤ 0.001) when 357 compared with the ATCC 19606 T strain after overnight incubation (Fig. 3B).

Article Title: Role of the Carboxy Terminus of SecA in Iron Acquisition, Protein Translocation, and Virulence of the Bacterial Pathogen Acinetobacter baumannii
Article Snippet: The three long black horizontal bars represent cloned DNA regions used as probes in Southern blotting (pMU734), to complement the 2010 insertion derivative (pMU472), or to overproduce a His-tagged SecA derivative (pMU481). .. The short black horizontal bar flanked by primer numbers indicate the 5′-end secA region used to test transcriptional expression by qRT-PCR. (B and C) Southern blotting of KpnI-PvuII-digested total DNA isolated from the ATCC 19606 T parental strain (lanes 2) and the 2010 derivative (lanes 3) probed with pMU734 (B) or the aph gene (C). (D) Western blotting of cytoplasmic proteins isolated from the ATCC 19606 T parental strain (lane 1) and the 2010 derivative (lane 2) probed with anti-SecA antibodies. .. The white arrow indicates the truncated SecA protein produced in the 2010 insertion derivative.

Article Title: Role of the Carboxy Terminus of SecA in Iron Acquisition, Protein Translocation, and Virulence of the Bacterial Pathogen Acinetobacter baumannii
Article Snippet: The short black horizontal bar flanked by primer numbers 792 indicate the 5’-end secA region used to test transcriptional expression by qRT-PCR. (B and C) 793 Southern blotting of KpnI-PvuII digested total DNA isolated from the ATCC 19606 T parental 794 strain (lane 2) and the 2010 derivative (lane 3) probed with pMU734 (B) or the aph gene (C). .. 795 (D) Western blotting of cytoplasmic proteins isolated from the ATCC 19606 T parental strain 796 (lane 1) and the 2010 derivative (lane 2) probed with anti-SecA antibodies. .. The white arrow 797 indicates the truncated SecA protein produced in the 2010 insertion derivative.

Cell Culture:

Article Title: Role of the Carboxy Terminus of SecA in Iron Acquisition, Protein Translocation, and Virulence of the Bacterial Pathogen Acinetobacter baumannii
Article Snippet: .. Our preliminary study ( 9 ) reporting the isolation of the 2010 derivative under nonselective conditions and growth data collected during this work ( ) showed that there were not statistically significant differences between the growth rates of the parental ATCC 19606 T strain and the 2010 isogenic derivative when cultured in LB broth. .. However, incubation of 2010 cells in LB broth containing 200 μM DIP resulted in a drastic growth reduction ( P ≤ 0.001) compared with that of the ATCC 19606 T strain after overnight incubation ( ).

Article Title: Role of the Carboxy Terminus of SecA in Iron Acquisition, Protein Translocation, and Virulence of the Bacterial Pathogen Acinetobacter baumannii
Article Snippet: This analysis showed that although the transposon 350 insertion did not abolish the production of secA transcripts, their abundance in 2010 cells was 351 reduced to 69% (P ≤ 0.001) of that detected in ATCC 19606 T parental bacteria (Fig. 2). .. 352 Our preliminary study (9) reporting the isolation of the 2010 derivative under non-353 selective conditions and growth data collected during this work (Fig. 3A) showed that there were 354 not statistically significant differences between the growth rates of the parental ATCC 19606 T 355 strain and the 2010 isogenic derivative when cultured in LB broth. .. However, incubation of 2010 356 cells in LB broth containing 200 μM DIP resulted in a drastic growth reduction (P ≤ 0.001) when 357 compared with the ATCC 19606 T strain after overnight incubation (Fig. 3B).

Expressing:

Article Title: Role of the Carboxy Terminus of SecA in Iron Acquisition, Protein Translocation, and Virulence of the Bacterial Pathogen Acinetobacter baumannii
Article Snippet: The three long black horizontal bars represent cloned DNA regions used as probes in Southern blotting (pMU734), to complement the 2010 insertion derivative (pMU472), or to overproduce a His-tagged SecA derivative (pMU481). .. The short black horizontal bar flanked by primer numbers indicate the 5′-end secA region used to test transcriptional expression by qRT-PCR. (B and C) Southern blotting of KpnI-PvuII-digested total DNA isolated from the ATCC 19606 T parental strain (lanes 2) and the 2010 derivative (lanes 3) probed with pMU734 (B) or the aph gene (C). (D) Western blotting of cytoplasmic proteins isolated from the ATCC 19606 T parental strain (lane 1) and the 2010 derivative (lane 2) probed with anti-SecA antibodies. .. The white arrow indicates the truncated SecA protein produced in the 2010 insertion derivative.

Western Blot:

Article Title: Role of the Carboxy Terminus of SecA in Iron Acquisition, Protein Translocation, and Virulence of the Bacterial Pathogen Acinetobacter baumannii
Article Snippet: The three long black horizontal bars represent cloned DNA regions used as probes in Southern blotting (pMU734), to complement the 2010 insertion derivative (pMU472), or to overproduce a His-tagged SecA derivative (pMU481). .. The short black horizontal bar flanked by primer numbers indicate the 5′-end secA region used to test transcriptional expression by qRT-PCR. (B and C) Southern blotting of KpnI-PvuII-digested total DNA isolated from the ATCC 19606 T parental strain (lanes 2) and the 2010 derivative (lanes 3) probed with pMU734 (B) or the aph gene (C). (D) Western blotting of cytoplasmic proteins isolated from the ATCC 19606 T parental strain (lane 1) and the 2010 derivative (lane 2) probed with anti-SecA antibodies. .. The white arrow indicates the truncated SecA protein produced in the 2010 insertion derivative.

Article Title: Role of the Carboxy Terminus of SecA in Iron Acquisition, Protein Translocation, and Virulence of the Bacterial Pathogen Acinetobacter baumannii
Article Snippet: The short black horizontal bar flanked by primer numbers 792 indicate the 5’-end secA region used to test transcriptional expression by qRT-PCR. (B and C) 793 Southern blotting of KpnI-PvuII digested total DNA isolated from the ATCC 19606 T parental 794 strain (lane 2) and the 2010 derivative (lane 3) probed with pMU734 (B) or the aph gene (C). .. 795 (D) Western blotting of cytoplasmic proteins isolated from the ATCC 19606 T parental strain 796 (lane 1) and the 2010 derivative (lane 2) probed with anti-SecA antibodies. .. The white arrow 797 indicates the truncated SecA protein produced in the 2010 insertion derivative.

Image Search Results

Apigenin can downregulate Srx expression in TPA-induced JB6 and A431 cSCC cells. (a) JB6 was treated with control (DMSO), TPA (20 nM), or apigenin (40 or 80 μ M) for different time points (6 h-48 h). Srx expression was detected by western blotting (left). Western blot was served to analyze the expression of Srx while TPA-induced JB6 cells were incubated with apigenin (80 μ M) for different times (6 h-48 h) (right). (b) Human SCC A431 cells were treated with apigenin at different times, and the expression of Srx was detected by WB. (c) The mRNA level of Srx in TPA-induced JB6 and A431 cells was conducted to measure after incubation with 80 μ M apigenin for 6 h and 12 h. (d) Representative images of immunofluorescence staining of Srx in TPA-induced JB6 treated with control (DMSO) or 80 μ M apigenin for 6 h-48 h (left). Quantitative analysis of Srx means fluorescence intensity (MFI) (right) (mean values ± SEM, n = 3). Significant differences were evaluated using a one-way ANOVA. ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 vs. control. For JB6 cells, TPA-induced sample as control.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Apigenin Induced Apoptosis by Downregulating Sulfiredoxin Expression in Cutaneous Squamous Cell Carcinoma

doi: 10.1155/2022/8172866

Figure Lengend Snippet: Apigenin can downregulate Srx expression in TPA-induced JB6 and A431 cSCC cells. (a) JB6 was treated with control (DMSO), TPA (20 nM), or apigenin (40 or 80 μ M) for different time points (6 h-48 h). Srx expression was detected by western blotting (left). Western blot was served to analyze the expression of Srx while TPA-induced JB6 cells were incubated with apigenin (80 μ M) for different times (6 h-48 h) (right). (b) Human SCC A431 cells were treated with apigenin at different times, and the expression of Srx was detected by WB. (c) The mRNA level of Srx in TPA-induced JB6 and A431 cells was conducted to measure after incubation with 80 μ M apigenin for 6 h and 12 h. (d) Representative images of immunofluorescence staining of Srx in TPA-induced JB6 treated with control (DMSO) or 80 μ M apigenin for 6 h-48 h (left). Quantitative analysis of Srx means fluorescence intensity (MFI) (right) (mean values ± SEM, n = 3). Significant differences were evaluated using a one-way ANOVA. ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 vs. control. For JB6 cells, TPA-induced sample as control.

Article Snippet: The mouse epithelial-derived JB6 Cl 41-5a cell was purchased from the American Type Culture Collection (ATCC) and stored in our laboratory [ ].

Techniques: Expressing, Control, Western Blot, Incubation, Immunofluorescence, Staining, Fluorescence

Apigenin can attenuate cell proliferation and migration in cSCC cells. (a) CCK-8 assay was implied to analyze the cell viability after the treatment of TPA-induced JB6 and A431 cells with different concentrations of apigenin (up to 80 μ M) as time gone (mean values ± SEM, n = 6). ∗∗∗∗ p < 0.0001 vs. control by ANOVA. (b) Representative images of colony formation assay in TPA-induced JB6 treated with control (DMSO) or 80 μ M apigenin. (c) Typical pictures (left) and quantitative analysis (right) of wound healing assay in TPA-induced JB6 (up) and A431 (down) cells. Cells were treated with control (DMSO) or 80 μ M apigenin for indicated time points. ns: no statistical significance; ∗∗∗∗ p < 0.0001 vs. control by Student's unpaired t -test.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Apigenin Induced Apoptosis by Downregulating Sulfiredoxin Expression in Cutaneous Squamous Cell Carcinoma

doi: 10.1155/2022/8172866

Figure Lengend Snippet: Apigenin can attenuate cell proliferation and migration in cSCC cells. (a) CCK-8 assay was implied to analyze the cell viability after the treatment of TPA-induced JB6 and A431 cells with different concentrations of apigenin (up to 80 μ M) as time gone (mean values ± SEM, n = 6). ∗∗∗∗ p < 0.0001 vs. control by ANOVA. (b) Representative images of colony formation assay in TPA-induced JB6 treated with control (DMSO) or 80 μ M apigenin. (c) Typical pictures (left) and quantitative analysis (right) of wound healing assay in TPA-induced JB6 (up) and A431 (down) cells. Cells were treated with control (DMSO) or 80 μ M apigenin for indicated time points. ns: no statistical significance; ∗∗∗∗ p < 0.0001 vs. control by Student's unpaired t -test.

Article Snippet: The mouse epithelial-derived JB6 Cl 41-5a cell was purchased from the American Type Culture Collection (ATCC) and stored in our laboratory [ ].

Techniques: Migration, CCK-8 Assay, Control, Colony Assay, Wound Healing Assay

Apigenin induced apoptosis in cSCC cells. (a) Flow cytometry was used to analyze the apoptosis cells. Cells were stained with annexin V and PI to quantify the percentage of apoptotic cells. TPA-induced JB6 cells (upper) or A431 cells (lower) were treated with control (DMSO) or 80 μ M apigenin for different times. (b) A concrete percentage of apoptosis cells in TPA-induced JB6 and A431 cells were evaluated using a one-way ANOVA (mean values ± SEM, n = 3) ∗ p < 0.05, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 vs. control (TPA-induced sample as control for JB6 cells). (c) TPA-induced JB6 cells were incubated with control (DMSO) or 80 μ M apigenin for 6 h-48 h. Western blot was served to analyze the expression of apoptosis-associated proteins (left). The bar graphs on the right showed the intensity of the protein band from each treatment relative to the housekeeping protein ( β -actin). Valued represent the means ± SEM. Significant difference was designed by ANOVA, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 vs. control (only TPA-induced sample). (d) The apoptosis-associated proteins were detected while 80 μ M apigenin was used for treatment for different time-points in A431 cells. The bar graphs showed the intensity quantification of the protein band relative to the housekeeping protein. Significant difference from control by ANOVA, ∗∗∗ p < 0.001 and ∗∗∗∗ p < 0.0001.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Apigenin Induced Apoptosis by Downregulating Sulfiredoxin Expression in Cutaneous Squamous Cell Carcinoma

doi: 10.1155/2022/8172866

Figure Lengend Snippet: Apigenin induced apoptosis in cSCC cells. (a) Flow cytometry was used to analyze the apoptosis cells. Cells were stained with annexin V and PI to quantify the percentage of apoptotic cells. TPA-induced JB6 cells (upper) or A431 cells (lower) were treated with control (DMSO) or 80 μ M apigenin for different times. (b) A concrete percentage of apoptosis cells in TPA-induced JB6 and A431 cells were evaluated using a one-way ANOVA (mean values ± SEM, n = 3) ∗ p < 0.05, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 vs. control (TPA-induced sample as control for JB6 cells). (c) TPA-induced JB6 cells were incubated with control (DMSO) or 80 μ M apigenin for 6 h-48 h. Western blot was served to analyze the expression of apoptosis-associated proteins (left). The bar graphs on the right showed the intensity of the protein band from each treatment relative to the housekeeping protein ( β -actin). Valued represent the means ± SEM. Significant difference was designed by ANOVA, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 vs. control (only TPA-induced sample). (d) The apoptosis-associated proteins were detected while 80 μ M apigenin was used for treatment for different time-points in A431 cells. The bar graphs showed the intensity quantification of the protein band relative to the housekeeping protein. Significant difference from control by ANOVA, ∗∗∗ p < 0.001 and ∗∗∗∗ p < 0.0001.

Article Snippet: The mouse epithelial-derived JB6 Cl 41-5a cell was purchased from the American Type Culture Collection (ATCC) and stored in our laboratory [ ].

Techniques: Flow Cytometry, Staining, Control, Incubation, Western Blot, Expressing

Apigenin activated the MAPK signaling pathway in cSCC in vitro. (a, b) Variation of the MAPK signaling pathway with the treatment of apigenin in TPA-induced JB6 (a) and A431 cells (b). The cells were treated with 80 μ M apigenin for different time points up to 24 h. Western blot was applied to analyze the expression of MAPK pathway-associated proteins, includingp38, ERK1/2 and JNK compared with GAPDH (left). The bar graph on the right showed the intensity of the phosphorylation protein band from each treatment relative to the total protein. Valued represent the means ± SEM. Significant difference was designed by ANOVA, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 vs. control (TPA-induced sample as control for JB6 cells). (c) TPA-induced JB6 cell was incubated with control (DMSO, TPA-alone, and apigenin-alone) or apigenin (40 or 80 μ M) for indicted time points. Western blot was served to analyze the expression of Nrf2. β -Actin was used as the reference for the loading quantity of protein sample. The bar graph indicated the density quantification of the Nrf2 band relative to β -actin. ∗ p < 0.05 and ∗∗∗ p < 0.001 vs. TPA-induced control by ANOVA.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Apigenin Induced Apoptosis by Downregulating Sulfiredoxin Expression in Cutaneous Squamous Cell Carcinoma

doi: 10.1155/2022/8172866

Figure Lengend Snippet: Apigenin activated the MAPK signaling pathway in cSCC in vitro. (a, b) Variation of the MAPK signaling pathway with the treatment of apigenin in TPA-induced JB6 (a) and A431 cells (b). The cells were treated with 80 μ M apigenin for different time points up to 24 h. Western blot was applied to analyze the expression of MAPK pathway-associated proteins, includingp38, ERK1/2 and JNK compared with GAPDH (left). The bar graph on the right showed the intensity of the phosphorylation protein band from each treatment relative to the total protein. Valued represent the means ± SEM. Significant difference was designed by ANOVA, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 vs. control (TPA-induced sample as control for JB6 cells). (c) TPA-induced JB6 cell was incubated with control (DMSO, TPA-alone, and apigenin-alone) or apigenin (40 or 80 μ M) for indicted time points. Western blot was served to analyze the expression of Nrf2. β -Actin was used as the reference for the loading quantity of protein sample. The bar graph indicated the density quantification of the Nrf2 band relative to β -actin. ∗ p < 0.05 and ∗∗∗ p < 0.001 vs. TPA-induced control by ANOVA.

Article Snippet: The mouse epithelial-derived JB6 Cl 41-5a cell was purchased from the American Type Culture Collection (ATCC) and stored in our laboratory [ ].

Techniques: In Vitro, Western Blot, Expressing, Phospho-proteomics, Control, Incubation

Apigenin induced cell apoptosis and inhibited the expression of Srx via regulating the MAPK signaling pathway in cSCC. (a, b) TPA-induced JB6 cells (a) and A431 cells (b) were treated with the combination of apigenin and inhibitor of MEK1/2, Binimetinib (5 or 10 nM), for 8 h. Western blotting was used to analyze the expression of Srx, p-Erk, and the apoptosis-related proteins BAX and Bcl2. Representative images are shown on the left. The bar graph on the right indicated the intensity quantification of the protein band relative to GAPDH or total protein (ERK). Significant difference was designed by ANOVA, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 vs. control (TPA-induced sample as control for JB6 cells). (c) Real-time PCR was conducted to quantify the mRNA expression of Srx in cSCC cell lines while cells were treated for indicated compounds. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 vs control by ANOVA analysis. (d) Representative images of cell apoptosis analysis by flow cytometry after 5 nM Binimetinib (MEK1/2 inhibitor) treatment for 24 h, respectively, in TPA-induced JB6 (up) and A431 (down). The percentage of apoptosis cells after apigenin treatment with or without Binimetinib is shown in the bar graph. ∗∗∗∗ p < 0.0001 vs. control by ANOVA analysis. (e, f) TPA-induced JB6 (e) and A431 (f) were incubated with or without the MEK1/2 inhibitor (5 nM Binimetinib) for 24 h in the presence of 80 μ M apigenin. Whole-cell lysates were subjected to western blotting to detect the apoptosis-associated proteins caspase 3, caspase 8, and PARP. The bar graph showed the intensity quantification of the protein bands from each treatment. Significant difference was designed by ANOVA, ∗∗∗ p < 0.001 and ∗∗∗∗ p < 0.0001 vs. the apigenin-alone group.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Apigenin Induced Apoptosis by Downregulating Sulfiredoxin Expression in Cutaneous Squamous Cell Carcinoma

doi: 10.1155/2022/8172866

Figure Lengend Snippet: Apigenin induced cell apoptosis and inhibited the expression of Srx via regulating the MAPK signaling pathway in cSCC. (a, b) TPA-induced JB6 cells (a) and A431 cells (b) were treated with the combination of apigenin and inhibitor of MEK1/2, Binimetinib (5 or 10 nM), for 8 h. Western blotting was used to analyze the expression of Srx, p-Erk, and the apoptosis-related proteins BAX and Bcl2. Representative images are shown on the left. The bar graph on the right indicated the intensity quantification of the protein band relative to GAPDH or total protein (ERK). Significant difference was designed by ANOVA, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 vs. control (TPA-induced sample as control for JB6 cells). (c) Real-time PCR was conducted to quantify the mRNA expression of Srx in cSCC cell lines while cells were treated for indicated compounds. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 vs control by ANOVA analysis. (d) Representative images of cell apoptosis analysis by flow cytometry after 5 nM Binimetinib (MEK1/2 inhibitor) treatment for 24 h, respectively, in TPA-induced JB6 (up) and A431 (down). The percentage of apoptosis cells after apigenin treatment with or without Binimetinib is shown in the bar graph. ∗∗∗∗ p < 0.0001 vs. control by ANOVA analysis. (e, f) TPA-induced JB6 (e) and A431 (f) were incubated with or without the MEK1/2 inhibitor (5 nM Binimetinib) for 24 h in the presence of 80 μ M apigenin. Whole-cell lysates were subjected to western blotting to detect the apoptosis-associated proteins caspase 3, caspase 8, and PARP. The bar graph showed the intensity quantification of the protein bands from each treatment. Significant difference was designed by ANOVA, ∗∗∗ p < 0.001 and ∗∗∗∗ p < 0.0001 vs. the apigenin-alone group.

Article Snippet: The mouse epithelial-derived JB6 Cl 41-5a cell was purchased from the American Type Culture Collection (ATCC) and stored in our laboratory [ ].

Techniques: Expressing, Western Blot, Control, Real-time Polymerase Chain Reaction, Flow Cytometry, Incubation

Spautin‐1 significantly attenuated proliferation of melanoma cells in a time‐ and dose‐dependent manner. A, Viability analysis after the treatment of A375 and Sk‐Mel‐28 cells with different concentration of spautin‐1 (up to 20 µmol/L) for 0, 24, 48 and 72 h. (Mean values ± SEM, n = 6). B, The IC50 values of spautin‐1 in A375 and Sk‐Mel‐28 were automatically calculated by GraphPad Prism software. C, spautin‐1 inhibited A375 and Sk‐Mel‐28 cell colony formation. The number of colonies normalized to the corresponding untreated cells formed colonies. (Mean values ± SEM, n = 3) Significant differences were evaluated using a one‐way ANOVA. * P < .05 vs control group, # P < .05 vs 2.5 µmol/L. D, Non‐tumorigenic cell lines (HaCaT and JB6) were treated with various concentration of spautin‐1 for 72 h as indicated, and cell viability in the presence of HaCat and JB6 was measured by MTS as described in the Section and analysed by GraphPad Prism software (mean values ± SEM, n = 6)

Journal: Journal of Cellular and Molecular Medicine

Article Title: Potent USP10/13 antagonist spautin‐1 suppresses melanoma growth via ROS‐mediated DNA damage and exhibits synergy with cisplatin

doi: 10.1111/jcmm.15093

Figure Lengend Snippet: Spautin‐1 significantly attenuated proliferation of melanoma cells in a time‐ and dose‐dependent manner. A, Viability analysis after the treatment of A375 and Sk‐Mel‐28 cells with different concentration of spautin‐1 (up to 20 µmol/L) for 0, 24, 48 and 72 h. (Mean values ± SEM, n = 6). B, The IC50 values of spautin‐1 in A375 and Sk‐Mel‐28 were automatically calculated by GraphPad Prism software. C, spautin‐1 inhibited A375 and Sk‐Mel‐28 cell colony formation. The number of colonies normalized to the corresponding untreated cells formed colonies. (Mean values ± SEM, n = 3) Significant differences were evaluated using a one‐way ANOVA. * P < .05 vs control group, # P < .05 vs 2.5 µmol/L. D, Non‐tumorigenic cell lines (HaCaT and JB6) were treated with various concentration of spautin‐1 for 72 h as indicated, and cell viability in the presence of HaCat and JB6 was measured by MTS as described in the Section and analysed by GraphPad Prism software (mean values ± SEM, n = 6)

Article Snippet: The human malignant melanoma cell lines (A375 and SK‐Mel‐28), the human keratinocyte HaCaT and the mouse epidermis‐derived JB6 Cl 41‐5a cells were purchased from the American Type Culture Collection (ATCC).

Techniques: Concentration Assay, Software, Control

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2010 panc sco h37rvma derivative (ATCC)

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