Similar Datasets
Project description:This 121-node Boolean regulatory network model that synthesizes mechanosensitive signaling that links anchorage and matrix stiffness to proliferation and migration, and cell density to contact inhibition. It can reproduce anchorage dependence and anoikis, detachment-induced cytokinesis errors, the effect of matrix stiffness on proliferation, and contact inhibition of proliferation and migration by two mechanisms that converge on the YAP transcription factor. In addition, this model offers testable predictions related to cell cycle-dependent sensitivity to anoikis, the molecular requirements for abolishing contact inhibition, substrate stiffness-dependent expression of the catalytic subunit of PI3K, heterogeneity of migratory and non-migratory phenotypes in sub-confluent monolayers, and linked inhibition but semi-independent induction of proliferation versus migration as a function of cell density and mitogenic stimulation.
The model is an extended version of the growth signaling, cell cycle and apoptosis model published in Sizek et al, PLoS Comp. Biol. 15(3): e1006402, 2019.
2020-08-26 | MODEL2006170001 | BioModels
Project description:A Bidirectional Single-Cell Migration and Retrieval Chip for Quantitative Study of Dendritic Cell Migration
| PRJNA856333 | ENA
Project description:<p>Energy metabolism is highly interdependent with adaptive cell migration <em>in vivo</em>. Mechanical confinement is a critical physical cue that induces switchable migration modes of the mesenchymal-to-amoeboid transition (MAT). However, the energy states in distinct migration modes, especially amoeboid-like stable bleb (A2) movement, remain unclear. In this report, we developed multivalent DNA framework-based nanomachines to explore strategical mitochondrial trafficking and differential ATP levels during cell migration in mechanically heterogeneous microenvironments. Through single-particle tracking and metabolomic analysis, we revealed that fast A2-moving cells driven by biomimetic confinement recruited back-end positioning of mitochondria for powering highly polarized cytoskeletal networks, preferentially adopting an energy-saving mode compared with a mesenchymal mode of cell migration. We present a versatile DNA nanotool for cellular energy exploration and highlight that adaptive energy strategies coordinately support switchable migration modes for facilitating efficient metastatic escape, offering a new perspective for therapeutic interventions in cancer metastasis.</p>
2024-03-25 | MTBLS9657 | MetaboLights
Project description:Shifting the optimal stiffness for cell migration
| PRJNA377905 | ENA
Project description:MicroRNA effects on breast cancer cell migration
| PRJNA669871 | ENA
Project description:The efficiency of T cell based immunotherapies is affected by the insufficient migration and activity of tumor specific effector T cells in the tumor. Aim of this phase I/II clinical trial is to evaluate whether a neoadjuvant, low dose radiotherapy can improve T cell connected anti tumor immune response in colorectal liver metastases.
The primary endpoint is the number of tumor infiltrating T cells. Furthermore the T cell activity in situ, the number of regulatory T cells and the frequency of tumor reactive T cells in the blood and bone marrow will be examined.
| 2094317 | ecrin-mdr-crc
Project description:Reiterer2013 - pseudophosphatase STYX role in
ERK signalling
This model is described in the article:
Pseudophosphatase STYX
modulates cell-fate decisions and cell migration by
spatiotemporal regulation of ERK1/2.
Reiterer V, Fey D, Kolch W,
Kholodenko BN, Farhan H.
Proc. Natl. Acad. Sci. U.S.A. 2013 Jul;
110(31): E2934-43
Abstract:
Serine/threonine/tyrosine-interacting protein (STYX) is a
catalytically inactive member of the dual-specificity
phosphatases (DUSPs) family. Whereas the role of DUSPs in
cellular signaling is well explored, the function of STYX is
still unknown. Here, we identify STYX as a spatial regulator of
ERK signaling. We used predictive-model simulation to test
several hypotheses for possible modes of STYX action. We show
that STYX localizes to the nucleus, competes with nuclear DUSP4
for binding to ERK, and acts as a nuclear anchor that regulates
ERK nuclear export. Depletion of STYX increases ERK activity in
both cytosol and nucleus. Importantly, depletion of STYX causes
an ERK-dependent fragmentation of the Golgi apparatus and
inhibits Golgi polarization and directional cell migration.
Finally, we show that overexpression of STYX reduces ERK1/2
activation, thereby blocking PC12 cell differentiation.
Overall, our results identify STYX as an important regulator of
ERK1/2 signaling critical for cell migration and PC12 cell
differentiation.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000557.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000557 | BioModels