Journal: Molecular Systems Biology

Article Title: A tool for modeling gene regulatory networks (GRN_modeler) and its applications to synthetic biology

doi: 10.1038/s44320-025-00148-8

Figure Lengend Snippet: I) The repressilator ( A ) Topology of the repressilator. ( B ) Topology of the circuit in the interface generated by the make_graph() method: the red dots N 1 , N 2 , and N 3 represent the nodes in the circuit. The red arrows denote the directed edges of the graph, illustrating the repression interactions between nodes. Additionally, the yellow dots N 1 ∣ − N 3 , N 2 ∣ − N 1 , and N 3 ∣ − N 2 represent the regulatory interactions. For example, N 1 ∣ − N 3 denotes that node N 1 is repressed by N 3 . ( C ) Deterministic and ( D ) stochastic simulations of the repressilator using the Elowitz model, as described in Appendix Table in the . The detailed information about the model is available in the file “repressilator.html". II) Redesigned repressilator for an independent modulation of amplitude and frequency. ( A ) Topology of the redesigned repressilator. “C" and “L" are proteases, “I 1 " and “I 2 " external inducers, “U" and “Y" transcription factors activating N 4 and N 2 , respectively. The dotted gray lines indicate which proteins are degraded by the proteases. ( B ) Topology of the circuit in the interface. ( C ) The effect of the inducers on the amplitude of N 4 . ( D ) The effect of the inducers on the time period of N 4 . The detailed information about the model is available in the file “Tomazou.html". III) The CRISPRlator circuit. ( A ) Topology of the CRISPRlator. ( B ) Topology of the circuit in the interface. For example, N 1 NOHILL∣-N 3 denotes that node N 1 is repressed by N 3 through an input named NOHILL, which corresponds to the CRISPRi interaction in the node model. This repression is incorporated into the system by introducing new reactions (R 6 and R 7 in Appendix Table ), where the dCas:sgRNA N3 complex binds to DNA N1 , inhibiting transcription at node N 1 . ( C ) Deterministic and ( D ) stochastic simulations of the CRISPRlator generated by the model detailed in Appendix Table in the . The detailed information about the model is available in the file “CRISPR.html”. The deterministic simulations were fulfilled with the “ode15s” solver of MATLAB, while the stochastic simulations were performed using the “adaptivesa” solver of COPASI in every case.

Article Snippet: We conducted deterministic simulations using MATLAB’s ode15s and sundials solvers with the SimBiology toolbox.

Techniques: Generated, CRISPR

Journal: Sensors (Basel, Switzerland)

Article Title: Method to Develop Legs for Underwater Robots: From Multibody Dynamics with Experimental Data to Mechatronic Implementation

doi: 10.3390/s22218462

Figure Lengend Snippet: Simscape block parameters for sphere-to-plane contact.

Article Snippet: The multibody model was simulated on a CPU with a sixth-generation Core i7 processor running Windows NT 10.0, and a 32 GB RAM memory board, with Simulink release 2020b and configuration parameters of a maximum step size of 0.008 and solver ode 15 s with a Simscape inventor integration.

Techniques: Blocking Assay

Journal: British Journal of Pharmacology

Article Title: Systems analysis of phosphorylation‐regulated Bcl‐2 interactions establishes a model to reconcile the controversy over the significance of Bcl‐2 phosphorylation

doi: 10.1111/bph.14555

Figure Lengend Snippet: The pBcl‐2/Bcl‐2 model predicts the MOMP in response to ABT‐199 or etoposide. (A, B) The experimentally derived CI values for the ABT‐199/paclitaxel combination were plotted against those predicted from the pBcl‐2/Bcl‐2 model, using MDA‐MB‐231 (A) and T49D cells (B), with and without SP600125. Data are the mean ± SD (n = 5). Spearman's correlation (r) and P values are shown. (C, D) Upper panel: Expression of p‐PKCα/β, p‐ERK and Bcl‐2 proteins in the five AML cell lines (A) before and after ABT‐199 treatment (0.2 μM for OCI‐AML2 and KG‐1; 4 μM for THP‐1 and NB4; 10 μM for OCI‐AML3; 24 h) and in the five colorectal cancer cell lines (B) before or after etoposide treatment (1 μM for LoVo and HCT‐116; 2 μM for SW480; 4 μM for DLD1 and HT29; 24 h). Equal loading was confirmed by stripping the immunoblot and reprobing it for actin. Lower panel: The experimental IC50 values for apoptosis induced by ABT‐199 or etoposide treatment after 48 h were plotted against the dose ω predicted by the pBcl‐2/Bcl‐2 model or the Bcl‐2 model Correlations (r values shown) between the experimental IC50 values and the predicted dose ω predicted by pBcl‐2/Bcl‐2 model were statistically significant whereas those using the Bcl‐2 model were not significant .

Article Snippet: Subsequently, ODEs were solved using MATLAB 7.3 (MathWorks, R2007b) function ode 15 s at time point t = 300 min. Materials Paclitaxel, ABT‐199 and etoposide were purchased from Selleck Chemicals (S1150, S8048 and S1225, Houston, TX, USA).

Techniques: Derivative Assay, Expressing, Stripping Membranes, Western Blot