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Growth curves showing the body weights of the normal and <t>CCI</t> <t>rats.</t>
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Growth curves showing the body weights of the normal and <t>CCI</t> <t>rats.</t>
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The PI3K/Akt/mTOR pathway is essential for HAdV-11 replication in ESCC cell lines. ( A ) Cells were treated with HAdV-11 for 72 h at an MOI of 2 PFU/cell, the mRNA expression levels were determined using quantitative polymerase chain reaction (qPCR). ( B , D , E , F , H and I ) Cells were treated with HAdV-11 for 72 h at an MOI of 2 PFU/cell, and Western blot analysis of mTOR, p-DRP1, PARK2, LC3 and GPX4 expression. ( C ) Cells were pretreated with Temsirolimus <t>(CCI-779)</t> (10 nM) for 2 h, and then infected with HAdV-11 at an MOI of 2 for 48 h. The mitochondrial mass was estimated by MTG staining. ( H ) After pretreatment with 0.5 µM mTOR agonist (MHY1485) for 2 h, cells were infected with HAdV-11 at a MOI of 2 for 48 h. Subsequently, the cells were stained with either C11-BODIPY or Fe 2+ and quantified using flow cytometry. ( J ) Cells were pretreated with CCI-779 for 2 h, and then infected with HAdV-11 at an MOI of 2 for 72 h. Infectious virus production was assessed by titration on JH293 cells and the titer as PFU/cell calculated. The half maximal effective concentration (EC50) for each sample was calculated. Data are cumulative results from 3 experiments ( A , J ) or are representative of 3 independent experiments ( B , C , D , E , F , G , H , I ). Data are presented as mean ± SD ( A , C , E , F , G , H , I , J ). Differences analyzed using a one-way ANOVA with Bonferroni’s post hoc correction ( C , E , F , G , H , I ) or two-tailed t-test ( A , J ) ( n = 3)
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The PI3K/Akt/mTOR pathway is essential for HAdV-11 replication in ESCC cell lines. ( A ) Cells were treated with HAdV-11 for 72 h at an MOI of 2 PFU/cell, the mRNA expression levels were determined using quantitative polymerase chain reaction (qPCR). ( B , D , E , F , H and I ) Cells were treated with HAdV-11 for 72 h at an MOI of 2 PFU/cell, and Western blot analysis of mTOR, p-DRP1, PARK2, LC3 and GPX4 expression. ( C ) Cells were pretreated with Temsirolimus <t>(CCI-779)</t> (10 nM) for 2 h, and then infected with HAdV-11 at an MOI of 2 for 48 h. The mitochondrial mass was estimated by MTG staining. ( H ) After pretreatment with 0.5 µM mTOR agonist (MHY1485) for 2 h, cells were infected with HAdV-11 at a MOI of 2 for 48 h. Subsequently, the cells were stained with either C11-BODIPY or Fe 2+ and quantified using flow cytometry. ( J ) Cells were pretreated with CCI-779 for 2 h, and then infected with HAdV-11 at an MOI of 2 for 72 h. Infectious virus production was assessed by titration on JH293 cells and the titer as PFU/cell calculated. The half maximal effective concentration (EC50) for each sample was calculated. Data are cumulative results from 3 experiments ( A , J ) or are representative of 3 independent experiments ( B , C , D , E , F , G , H , I ). Data are presented as mean ± SD ( A , C , E , F , G , H , I , J ). Differences analyzed using a one-way ANOVA with Bonferroni’s post hoc correction ( C , E , F , G , H , I ) or two-tailed t-test ( A , J ) ( n = 3)
Rotarod Test Before Cci, supplied by AutoMate Scientific Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The PI3K/Akt/mTOR pathway is essential for HAdV-11 replication in ESCC cell lines. ( A ) Cells were treated with HAdV-11 for 72 h at an MOI of 2 PFU/cell, the mRNA expression levels were determined using quantitative polymerase chain reaction (qPCR). ( B , D , E , F , H and I ) Cells were treated with HAdV-11 for 72 h at an MOI of 2 PFU/cell, and Western blot analysis of mTOR, p-DRP1, PARK2, LC3 and GPX4 expression. ( C ) Cells were pretreated with Temsirolimus <t>(CCI-779)</t> (10 nM) for 2 h, and then infected with HAdV-11 at an MOI of 2 for 48 h. The mitochondrial mass was estimated by MTG staining. ( H ) After pretreatment with 0.5 µM mTOR agonist (MHY1485) for 2 h, cells were infected with HAdV-11 at a MOI of 2 for 48 h. Subsequently, the cells were stained with either C11-BODIPY or Fe 2+ and quantified using flow cytometry. ( J ) Cells were pretreated with CCI-779 for 2 h, and then infected with HAdV-11 at an MOI of 2 for 72 h. Infectious virus production was assessed by titration on JH293 cells and the titer as PFU/cell calculated. The half maximal effective concentration (EC50) for each sample was calculated. Data are cumulative results from 3 experiments ( A , J ) or are representative of 3 independent experiments ( B , C , D , E , F , G , H , I ). Data are presented as mean ± SD ( A , C , E , F , G , H , I , J ). Differences analyzed using a one-way ANOVA with Bonferroni’s post hoc correction ( C , E , F , G , H , I ) or two-tailed t-test ( A , J ) ( n = 3)
Card Identification Test, supplied by CogState Ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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DescriptionSuccinyl-CoA synthetase (SCS; succinyl-CoA ligase; succinate thiokinase; EC 6.2.1.5), also known as succinyl-CoA synthetase ligase/succinate thiokinase, is a mitochondrial enzyme. The enzyme catalyzes a substrate-level phosphorylation of GDP or ADP and thus, plays a vital
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Image Search Results


Growth curves showing the body weights of the normal and CCI rats.

Journal: Experimental Animals

Article Title: Establishment of a novel dwarf rat strain: cartilage calcification insufficient (CCI) rats

doi: 10.1538/expanim.14-0072

Figure Lengend Snippet: Growth curves showing the body weights of the normal and CCI rats.

Article Snippet: There was no difference in the incidence of dwarfism between male and female CCI rats (Chi-square test, P =0.689).

Techniques:

Radiographic findings regarding the lengths of the femur (A, B), tibia (A, C), and head (D, E). Both male and female CCI rats exhibited delayed posterior fontanel closing (arrows in D). Data are expressed as mean ± SD values of normal male (n=12), normal female (n=9), CCI male (n=6), and CCI female (n=6) rats. # P <0.01 vs. normal male rats. * P <0.01 vs. normal female rats.

Journal: Experimental Animals

Article Title: Establishment of a novel dwarf rat strain: cartilage calcification insufficient (CCI) rats

doi: 10.1538/expanim.14-0072

Figure Lengend Snippet: Radiographic findings regarding the lengths of the femur (A, B), tibia (A, C), and head (D, E). Both male and female CCI rats exhibited delayed posterior fontanel closing (arrows in D). Data are expressed as mean ± SD values of normal male (n=12), normal female (n=9), CCI male (n=6), and CCI female (n=6) rats. # P <0.01 vs. normal male rats. * P <0.01 vs. normal female rats.

Article Snippet: There was no difference in the incidence of dwarfism between male and female CCI rats (Chi-square test, P =0.689).

Techniques:

Undecalcified sections of the tibial knee joints of a normal rat (A, B) and a CCI rat (C, D) that had been stained with toluidine blue and von Kossa stain. B and D show magnified views of the rectangular areas shown in A and C, respectively. The dotted lines indicate the erosion zone, i.e., the border between the growth plate (GP) and the primary spongiosa (PS). (A, B) A calcified matrix (arrows) was detected in the lowest part of the growth plate (GP), which was contiguous with the bone spicules (BS) in the primary spongiosa (PS). The bone spicules were arranged in an orderly manner along the long axis of the tibia. (C, D) The bone spicules (BS) were arranged randomly and were thicker that those seen in the normal rats. Staining intensity did not differ between the normal and CCI rats (compared with the BS in B). We obtained the same results when we examined three different samples (n=3). Bar=200 µ m

Journal: Experimental Animals

Article Title: Establishment of a novel dwarf rat strain: cartilage calcification insufficient (CCI) rats

doi: 10.1538/expanim.14-0072

Figure Lengend Snippet: Undecalcified sections of the tibial knee joints of a normal rat (A, B) and a CCI rat (C, D) that had been stained with toluidine blue and von Kossa stain. B and D show magnified views of the rectangular areas shown in A and C, respectively. The dotted lines indicate the erosion zone, i.e., the border between the growth plate (GP) and the primary spongiosa (PS). (A, B) A calcified matrix (arrows) was detected in the lowest part of the growth plate (GP), which was contiguous with the bone spicules (BS) in the primary spongiosa (PS). The bone spicules were arranged in an orderly manner along the long axis of the tibia. (C, D) The bone spicules (BS) were arranged randomly and were thicker that those seen in the normal rats. Staining intensity did not differ between the normal and CCI rats (compared with the BS in B). We obtained the same results when we examined three different samples (n=3). Bar=200 µ m

Article Snippet: There was no difference in the incidence of dwarfism between male and female CCI rats (Chi-square test, P =0.689).

Techniques: Staining

Longitudinal sections from the tibial growth plates of normal rats (A, C, D) and CCI rats (B, E, F) that had been stained with toluidine blue (A, B) or immunostaining for aggrecan (C − F). D and F show magnified views of the rectangular areas shown in C and E, respectively. The articular cartilage (AC in A) and growth plate (GP in A) in normal rats were clearly distinguishable, and the architecture of the chondrocyte zones in the growth plate cartilage (two-way arrow) was well established in the normal rats. The secondary ossification center in CCI rats (arrow in B) had not fully formed, and the growth plate (GP, two-way arrow in B) in the CCI rats was longer than that in normal rats (GP in A). The architecture of the chondrocyte zones was irregular or disorganized in the CCI rats. In the normal rats, aggrecan immunostaining (arrows in C) was detected in the articular cartilage (AC in C) and the growth plate (GP in C). At higher magnification, aggrecan immunostaining was evenly distributed throughout the growth plate (arrows in D). In the CCI rats, aggrecan immunostaining (arrows in E) was unevenly distributed throughout the articular cartilage (AC in E) and growth plate (GP in E). At higher magnification, an aggrecan–negative area was also observed (arrow in F). We obtained the same results when we examined three different samples (n=3). Bars=100 µ m

Journal: Experimental Animals

Article Title: Establishment of a novel dwarf rat strain: cartilage calcification insufficient (CCI) rats

doi: 10.1538/expanim.14-0072

Figure Lengend Snippet: Longitudinal sections from the tibial growth plates of normal rats (A, C, D) and CCI rats (B, E, F) that had been stained with toluidine blue (A, B) or immunostaining for aggrecan (C − F). D and F show magnified views of the rectangular areas shown in C and E, respectively. The articular cartilage (AC in A) and growth plate (GP in A) in normal rats were clearly distinguishable, and the architecture of the chondrocyte zones in the growth plate cartilage (two-way arrow) was well established in the normal rats. The secondary ossification center in CCI rats (arrow in B) had not fully formed, and the growth plate (GP, two-way arrow in B) in the CCI rats was longer than that in normal rats (GP in A). The architecture of the chondrocyte zones was irregular or disorganized in the CCI rats. In the normal rats, aggrecan immunostaining (arrows in C) was detected in the articular cartilage (AC in C) and the growth plate (GP in C). At higher magnification, aggrecan immunostaining was evenly distributed throughout the growth plate (arrows in D). In the CCI rats, aggrecan immunostaining (arrows in E) was unevenly distributed throughout the articular cartilage (AC in E) and growth plate (GP in E). At higher magnification, an aggrecan–negative area was also observed (arrow in F). We obtained the same results when we examined three different samples (n=3). Bars=100 µ m

Article Snippet: There was no difference in the incidence of dwarfism between male and female CCI rats (Chi-square test, P =0.689).

Techniques: Staining, Immunostaining

The PI3K/Akt/mTOR pathway is essential for HAdV-11 replication in ESCC cell lines. ( A ) Cells were treated with HAdV-11 for 72 h at an MOI of 2 PFU/cell, the mRNA expression levels were determined using quantitative polymerase chain reaction (qPCR). ( B , D , E , F , H and I ) Cells were treated with HAdV-11 for 72 h at an MOI of 2 PFU/cell, and Western blot analysis of mTOR, p-DRP1, PARK2, LC3 and GPX4 expression. ( C ) Cells were pretreated with Temsirolimus (CCI-779) (10 nM) for 2 h, and then infected with HAdV-11 at an MOI of 2 for 48 h. The mitochondrial mass was estimated by MTG staining. ( H ) After pretreatment with 0.5 µM mTOR agonist (MHY1485) for 2 h, cells were infected with HAdV-11 at a MOI of 2 for 48 h. Subsequently, the cells were stained with either C11-BODIPY or Fe 2+ and quantified using flow cytometry. ( J ) Cells were pretreated with CCI-779 for 2 h, and then infected with HAdV-11 at an MOI of 2 for 72 h. Infectious virus production was assessed by titration on JH293 cells and the titer as PFU/cell calculated. The half maximal effective concentration (EC50) for each sample was calculated. Data are cumulative results from 3 experiments ( A , J ) or are representative of 3 independent experiments ( B , C , D , E , F , G , H , I ). Data are presented as mean ± SD ( A , C , E , F , G , H , I , J ). Differences analyzed using a one-way ANOVA with Bonferroni’s post hoc correction ( C , E , F , G , H , I ) or two-tailed t-test ( A , J ) ( n = 3)

Journal: BMC Cancer

Article Title: Oncolytic adenovirus type 11-induced ferroptosis of esophageal squamous cell carcinoma cells involves in mitochondrial impairment and the mTOR pathway

doi: 10.1186/s12885-026-15735-7

Figure Lengend Snippet: The PI3K/Akt/mTOR pathway is essential for HAdV-11 replication in ESCC cell lines. ( A ) Cells were treated with HAdV-11 for 72 h at an MOI of 2 PFU/cell, the mRNA expression levels were determined using quantitative polymerase chain reaction (qPCR). ( B , D , E , F , H and I ) Cells were treated with HAdV-11 for 72 h at an MOI of 2 PFU/cell, and Western blot analysis of mTOR, p-DRP1, PARK2, LC3 and GPX4 expression. ( C ) Cells were pretreated with Temsirolimus (CCI-779) (10 nM) for 2 h, and then infected with HAdV-11 at an MOI of 2 for 48 h. The mitochondrial mass was estimated by MTG staining. ( H ) After pretreatment with 0.5 µM mTOR agonist (MHY1485) for 2 h, cells were infected with HAdV-11 at a MOI of 2 for 48 h. Subsequently, the cells were stained with either C11-BODIPY or Fe 2+ and quantified using flow cytometry. ( J ) Cells were pretreated with CCI-779 for 2 h, and then infected with HAdV-11 at an MOI of 2 for 72 h. Infectious virus production was assessed by titration on JH293 cells and the titer as PFU/cell calculated. The half maximal effective concentration (EC50) for each sample was calculated. Data are cumulative results from 3 experiments ( A , J ) or are representative of 3 independent experiments ( B , C , D , E , F , G , H , I ). Data are presented as mean ± SD ( A , C , E , F , G , H , I , J ). Differences analyzed using a one-way ANOVA with Bonferroni’s post hoc correction ( C , E , F , G , H , I ) or two-tailed t-test ( A , J ) ( n = 3)

Article Snippet: Mitochondrial division inhibitor 1 (Mdivi-1), Ferrostatin-1, Erastin, MK2206, LY294002 and Temsirolimus (CCI-779) were purchased from MedChem Express (Shanghai, China).

Techniques: Expressing, Real-time Polymerase Chain Reaction, Western Blot, Infection, Staining, Flow Cytometry, Virus, Titration, Concentration Assay, Two Tailed Test