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CG genes were initially identified because their activation in tumor cells generates the expression of tumor-specific antigens, which can be recognized by cytolytic T lymphocytes [ 12].
S. Scuderi et al. discussed that alternative splicing in PARK2 generates the expression of different PARK2 (Parkin) protein isoforms and leads to selective degeneration of dopaminergic neurons based on evidences in human, rat, and mouse brains.
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It remains unclear whether these regions make different contributions to a single aversive learning process or represent independent learning mechanisms that interact to generate the expression of pain-related behavior.
Genome wide microarray analysis was performed according to Agarwal et al. [ 41], to generate the expression profile of OsPPs.
Genome-wide microarray analysis was performed according to Ray et al. to generate the expression profile of OsARM genes.
In the hidden factor approach, for each cluster, we first generated the expression levels of a single controlling factor z by sampling the standard normal distribution.
This can be clearly seen in the mosaics generated by the expression of Rab11DN in stripes using enGAL4.
In the newly generated strains the expression of PKH2, controlled by the tetO7 promoter, is decreased by addition of doxycycline.
Polyclonal CAR+ γδ T cells have been successfully generated retaining the expression of receptors displaying inherent antitumor activity [ 43, 44].
Mammals have at least 26 different NCS proteins generated by the expression of 14 genes and by differential splicing [ 5].
There might therefore be a common signal generated by the expression of TPS1 and drought stress that leads to the up-regulation of these four genes.
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