We illustrate our methods potential to find intervention targets for cancer treatment and cell differentiation by applying it to a leukemia signaling network and to the network controlling the differentiation of helper T cells.

To demonstrate the potential of our framework, we choose two types of cell fate reprogramming processes: disease therapeutics and cell differentiation .

Helper T cell differentiation network.

The helper T cell differentiation network under the selected environmental conditions consists of 55 nodes and 121 edges and is shown in Fig 5.

We illustrated our methods potential to find intervention targets for cancer treatment and cell differentiation by applying it to network models of T-LGL leukemia and helper T cell differentiation .

Logical rules, classification of attractors, and analysis of the stable motif succession diagram in the helper T cell differentiation network model.

When a cyanobacteria filament is deprived of combined nitrogen, some vegetative cells differentiate into heterocysts, Which are terminally differentiated nitrogen-fixing cells.

NtcA presents autoregulation [22, 24, 25] and indirectly activates the key gene that controls cell differentiation and pattern formation: hetR [26—28].

The study of cell differentiation and its underlying mechanisms constitutes one of most intriguing problems in biology.

The approach presented here deals With a simple system, heterocyst formation in cyanobacteria filaments, yet compleX enough to capture the main ingredients of some of the mechanisms for cell differentiation and pattern formation under external driving.

However, in the absence of combined nitrogen (cN), a subset of the vegetative cells differentiate into heterocysts, which are terminally differentiated nitrogen-fixing cells.

A chain lacking both PatS and HetN leads to a lethal phenotype in which all cells differentiate [43].

There is compelling evidence that stalled or incomplete cell differentiation is the primary defect that gives rise to this cancer [2—6].

Tyrosine kinase signaling networks play a major role in governing cell differentiation , including in neuroblastoma [16].

The metazoan evolution of multicellular organisms coincided with expansion of tyrosine kinases, protein tyrosine phosphatases, and SH2 domains, which suggests that tyrosine kinase signaling mechanisms play a major role in cell differentiation [20—22].