model rapamycin  (MedChemExpress)

Journal: Molecular Medicine Reports

Article Title: Role and mechanism of tetrahedral DNA nanostructures in the repair of urethral injury in rats

doi: 10.3892/mmr.2026.13815

Figure Lengend Snippet: (A) Urethral tissue collection images from the control, model, model + rapamycin, and model + TDN group. (B) Body weight monitoring curves for rats in all groups over time. (C) Urethrographic imaging results for each group, with red arrows indicating the location of urethral injury model establishment. (D) Hematoxylin and eosin staining results for urethral tissues from each group. Red arrows indicate urethral lumen narrowing and associated fibrotic changes in the injured urethra. Scale bar, 500 µm (left) and 50 µm (right). TDN, tetrahedral DNA nanostructure.

Article Snippet: The rats were randomly divided into four groups: Control (n=6; intraperitoneal injection of an equal volume of saline every other day; injection volume, 0.2 ml per rat), model (n=6; urethral injury followed by intraperitoneal injection of saline every other day; injection volume, 0.2 ml per rat), model + rapamycin [n=6; 2.0 mg/kg of rapamycin (cat. no. HY-10219; MedChemExpress) injected intraperitoneally every other day after injury] and model + TDN (n=6; 10 nmol/day TDN administered via tail vein injection daily after injury; injection volume, 0.2 ml per rat).

Techniques: Control, Imaging, Staining

Journal: Molecular Medicine Reports

Article Title: Role and mechanism of tetrahedral DNA nanostructures in the repair of urethral injury in rats

doi: 10.3892/mmr.2026.13815

Figure Lengend Snippet: (A) PCA results. Different colors represent different treatment groups. (B) Sample correlation heatmap. The color intensity corresponds to correlation values. (C) Combined volcano plot showing the distribution of FCs in differentially expressed genes in the three group comparisons (model vs. control; model + rapamycin vs. model; model + TDN vs. model), with yellow dots representing upregulated genes and green dots representing downregulated genes. (D) Bar chart of differential gene counts showing the number of differential genes in the three group comparisons. (E) Venn diagram of differential genes displaying the distribution of differential genes in the three group comparisons. The numbers in different areas represent specific intersections or unique differential genes. (F) Heatmap showing the expression patterns of 25 common differentially expressed genes identified from three pairwise comparisons, displayed across four experimental groups (Control, Model, Model + rapamycin, and Model + TDN). Each row represents one gene and each column represents an individual sample. Color gradients indicate normalized gene expression levels. (G) KEGG pathway enrichment analysis of differentially expressed genes from the three pairwise comparisons (model vs. control; model + rapamycin vs. model; model + TDN vs. model). Enrichment results are presented as dot plots. The x-axis represents the GeneRatio, and the size of each dot reflects the proportion of genes enriched in the corresponding pathway. Dot color indicates the statistical significance expressed as -log10(P-value). KEGG pathways are displayed consistently across the three comparisons to facilitate direct visual comparison. KEGG, Kyoto Encyclopedia of Genes and Genomes; TDN, tetrahedral DNA nanostructure; FC, fold change; PCA, principal component analysis.

Article Snippet: The rats were randomly divided into four groups: Control (n=6; intraperitoneal injection of an equal volume of saline every other day; injection volume, 0.2 ml per rat), model (n=6; urethral injury followed by intraperitoneal injection of saline every other day; injection volume, 0.2 ml per rat), model + rapamycin [n=6; 2.0 mg/kg of rapamycin (cat. no. HY-10219; MedChemExpress) injected intraperitoneally every other day after injury] and model + TDN (n=6; 10 nmol/day TDN administered via tail vein injection daily after injury; injection volume, 0.2 ml per rat).

Techniques: Control, Expressing, Gene Expression, Comparison

Journal: Journal of theoretical biology

Article Title: Dynamic modeling of signal transduction by mTOR complexes in cancer.

doi: 10.1016/j.jtbi.2019.109992

Figure Lengend Snippet: Fig. 1. mTOR complex organization and functions. mTOR plays its role in signal integration through two distinct complexes (mTORC1 and mTORC2). Each of these compo- nents is responsible for transducing appropriate signals into distinct responses.

Article Snippet: Contents lists available at ScienceDirect Journal of Theoretical Biology journal homepage: www.elsevier.com/locate/jtb Dynamic modeling of signal transduction by mTOR complexes in cancer Mohammadreza Dorvash a , b , 1 , Mohammad Farahmandnia b , c , 1 , Pouria Mosaddeghi a , b , c , 1 , Mitra Farahmandnejad a , b , c , Hosein Saber a , c , Mohammadhossein Khorraminejad-Shirazi b , c , Amir Azadi a , d , Iman Tavassoly e , ∗ a Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran b Cell and Molecular Medicine Student Research Group, Faculty of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran c Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran d Department of Pharmaceutics, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran e Department of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, 1425 Madison Ave, New York, NY 10029, USA a r t i c l e i n f o Article history: Received 10 May 2019 Revised 5 August 2019 Accepted 2 September 2019 Available online 4 September 2019 Keywords: Cell Signaling Mathematical Model mTOR Rapamycin Systems Biology Systems pharmacology a b s t r a c t Signal integration has a crucial role in the cell fate decision and dysregulation of the cellular signaling pathways is a primary characteristic of cancer.

Techniques:

Journal: Journal of theoretical biology

Article Title: Dynamic modeling of signal transduction by mTOR complexes in cancer.

doi: 10.1016/j.jtbi.2019.109992

Figure Lengend Snippet: Fig. 2. The schematic interaction diagram representing the mechanism of inhibition of mTOR by rapamycin. (Thicker arrows represent higher rate constant for that direction).

Article Snippet: Contents lists available at ScienceDirect Journal of Theoretical Biology journal homepage: www.elsevier.com/locate/jtb Dynamic modeling of signal transduction by mTOR complexes in cancer Mohammadreza Dorvash a , b , 1 , Mohammad Farahmandnia b , c , 1 , Pouria Mosaddeghi a , b , c , 1 , Mitra Farahmandnejad a , b , c , Hosein Saber a , c , Mohammadhossein Khorraminejad-Shirazi b , c , Amir Azadi a , d , Iman Tavassoly e , ∗ a Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran b Cell and Molecular Medicine Student Research Group, Faculty of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran c Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran d Department of Pharmaceutics, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran e Department of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, 1425 Madison Ave, New York, NY 10029, USA a r t i c l e i n f o Article history: Received 10 May 2019 Revised 5 August 2019 Accepted 2 September 2019 Available online 4 September 2019 Keywords: Cell Signaling Mathematical Model mTOR Rapamycin Systems Biology Systems pharmacology a b s t r a c t Signal integration has a crucial role in the cell fate decision and dysregulation of the cellular signaling pathways is a primary characteristic of cancer.

Techniques: Inhibition

Journal: Journal of theoretical biology

Article Title: Dynamic modeling of signal transduction by mTOR complexes in cancer.

doi: 10.1016/j.jtbi.2019.109992

Figure Lengend Snippet: Fig. 3. Temporal concentration of rapamycin for regimens I–IV. Since the plasma protein binding of the rapamycin is set aside, the concentration of free Cytosolic rapamycin is equal to its total concentration. Each regimen is simulated while scanning the “amount ± 20%” area (linearly stepped) around the dose administered. (A) Regimen Ⅰ : 8.0 × 10 −20 ± 20% mole/Day; (B) Regimen Ⅱ : 5.6 × 10 −19 ± 20% mole/Day; (C) Regimen Ⅲ : 5.6 × 10 −19 ± 20% mole/Week; and (D) Regimen Ⅳ : 2.24 × 10 −18 ± 20% mole/ Week.

Article Snippet: Contents lists available at ScienceDirect Journal of Theoretical Biology journal homepage: www.elsevier.com/locate/jtb Dynamic modeling of signal transduction by mTOR complexes in cancer Mohammadreza Dorvash a , b , 1 , Mohammad Farahmandnia b , c , 1 , Pouria Mosaddeghi a , b , c , 1 , Mitra Farahmandnejad a , b , c , Hosein Saber a , c , Mohammadhossein Khorraminejad-Shirazi b , c , Amir Azadi a , d , Iman Tavassoly e , ∗ a Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran b Cell and Molecular Medicine Student Research Group, Faculty of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran c Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran d Department of Pharmaceutics, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran e Department of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, 1425 Madison Ave, New York, NY 10029, USA a r t i c l e i n f o Article history: Received 10 May 2019 Revised 5 August 2019 Accepted 2 September 2019 Available online 4 September 2019 Keywords: Cell Signaling Mathematical Model mTOR Rapamycin Systems Biology Systems pharmacology a b s t r a c t Signal integration has a crucial role in the cell fate decision and dysregulation of the cellular signaling pathways is a primary characteristic of cancer.

Techniques: Concentration Assay, Clinical Proteomics, Protein Binding

Journal: Journal of theoretical biology

Article Title: Dynamic modeling of signal transduction by mTOR complexes in cancer.

doi: 10.1016/j.jtbi.2019.109992

Figure Lengend Snippet: Fig. 5. Temporal concentration of rapamycin, mTORC1, and mTORC2 for different absorption and elimination rate constants (macro-constants) of rapamycin: the K abs@Rapam and K el@Rapam were scanned jointly in an area within a percentage range logarithmically spaced from −2 logs to + 2 logs using three steps each, making nine possible combinations for these kinetic parameters. The reference dose used for this parameter scan is 5.0 × 10 −19 mole/Day (regimen Ⅱ ). The plot at the center is where the K abs@Rapam and K el@Rapam are at their initial values. (K abs@Rapam = absorption rate constant; K el@Rapam = elimination rate constant).

Article Snippet: Contents lists available at ScienceDirect Journal of Theoretical Biology journal homepage: www.elsevier.com/locate/jtb Dynamic modeling of signal transduction by mTOR complexes in cancer Mohammadreza Dorvash a , b , 1 , Mohammad Farahmandnia b , c , 1 , Pouria Mosaddeghi a , b , c , 1 , Mitra Farahmandnejad a , b , c , Hosein Saber a , c , Mohammadhossein Khorraminejad-Shirazi b , c , Amir Azadi a , d , Iman Tavassoly e , ∗ a Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran b Cell and Molecular Medicine Student Research Group, Faculty of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran c Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran d Department of Pharmaceutics, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran e Department of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, 1425 Madison Ave, New York, NY 10029, USA a r t i c l e i n f o Article history: Received 10 May 2019 Revised 5 August 2019 Accepted 2 September 2019 Available online 4 September 2019 Keywords: Cell Signaling Mathematical Model mTOR Rapamycin Systems Biology Systems pharmacology a b s t r a c t Signal integration has a crucial role in the cell fate decision and dysregulation of the cellular signaling pathways is a primary characteristic of cancer.

Techniques: Concentration Assay