Insertional mutagens allow for relatively unbiased, genome-wide, identification of both novel cancer genes and collaborations between genes involved in cancer.
After placing gene correlation estimation onto gene networks, we construct a weighted graph whose nodes cover all genes, and whose edges reflect the first-order collaboration probability between genes.
As proved by Nadler et al. [33], the diffusion distance (eq. 3) can be accurately approximated by the Euclidean distance in the new space, i.e., <img src="http://journals.plos.org/plosone/article/asset?id=info?doi/10.1371/journal.pone.0013748.e034.PNG" class= inline-graphic"/> The diffusion distance (eqs. 3–4) negatively reflects the collaboration relationship between genes.
Functional collaboration between different genes may contribute to their high frequency of co-amplification in the 11q13 locus.
Newborn Pim-1 transgenic mice infected with mMuLV with activation of MYC developed T-cell lymphomas with a latency of only 7 8 weeks, evidencing a very strong oncogenic collaboration between these genes.
In a collaboration between the Gene Ontology (GO) Consortium and the muscle biology community, we have made large-scale additions to the GO biological process and cellular component ontologies.
Collaboration between various sophisticated gene regulatory mechanisms enables evolutionary novelties by fine-tuning gene expression and depends on location, timing and cell type, notably with respect to the developmental history of the cell.
The study of collaboration, conflict, and cheating between genes, sub-cellular organelles (apparently once-separate organisms), and cells as well as between separate organisms is a fascinating aspect of recent evolutionary biology, and Mr Wright effectively pulls the ideas together under the rubric of non-zero-sumness.
It is thought that co-expressed genes are co-regulated by similar regulatory mechanisms; hence, possible functional collaborations between co-expressed genes have been proposed.
Reprogramming resulted from repression of Pax5 by C/EBP to silence B-cell identity and collaboration between C/EBP and PU.1 to activate myeloid genes (Feng et al, 2008; Xie et al, 2004).
