Degradation of many toxic compounds using decontaminating enzymes fused with cellulose-binding CBMs has been reported, which enabled a single-step purification and immobilization of fusion proteins into different cellulosic materials (Xu et al. 2002).
Techniques are reported which enable errors in strain range to be identified and quantified using simple relations.
In a previous study, a single nucleotide polymorphism (SNP) diagnostic system named the SMart Amplification Process version 2 (SMAP 2) was reported, which enabled rapid gene diagnostics from crude samples such as whole blood.
This simple concept, which has not been reported before, enables to investigate evolutionary relationship between isolates or species.
There have been numerous mechanisms reported which can enable castration resistant growth including intracrine synthesis of androgen, upregulation of the androgen receptor (AR), co-activation of the AR by other pathways, or complete bypass of androgen signaling through the activation of other pathways [ 4- 6].
An additional transporter specific to the three CC genomes (XAC3198) is an alkanesulfonate transporter substrate-binding subunit, which is reported to enable E. coli to use sulfonates other than taurine [ 37].
In DNA damage response, the function of hnRNP K in p53 activation has been reported to be modulated by sumoylation, which enables the protein to function as p53 cofactor or prevents HDM2-dependent ubiquitination and proteasomal degradation of hnRNP K.
In Homo sapiens, Mus musculus, Drosophila melanogaster and Arabidopsis thaliana, alternative splicing has been reported to occur in many genes, which enables these organisms to enlarge their proteome diversity by increasing transcript variations in their genome [ 10- 15].
Additionally, cisplatin has also been reported to induce protective autophagy in esophageal cancer cells, which enabled them to escape from cisplatin-induced apoptosis [11].
Homothallic (same sex) mating of diploids has also been reported in strains lacking the Bar1 protease which inactivates α-pheromone, enabling autocrine signaling (Alby et al., 2009).
