Inventorship and Authorship.

Ownership of a U.S. patent is based on inventorship. In the United States, an inventor is the owner of the claimed invention unless it is assigned to another entity. The correct naming of inventors is important, and the improper naming of inventors in a patent can be grounds for rendering the patent unenforceable. Each inventor must make an intellectual contribution, solely or jointly, to at least one element of a claim in the patent. This is in contrast to authorship of a research article, where authors may be named to acknowledge contribution to the reported research rather than an intellectual contribution. Thus, identifying inventors for a patent is not the same as identifying authors for a publication.

CD28 regulates the translation of Bcl-xL via the phosphatidylinositol 3-kinase/mammalian target of rapamycin pathway.

In concert with the TCR, CD28 promotes T cell survival by regulating the expression of the antiapoptotic protein Bcl-x(L). The mechanism by which CD28 mediates the induction of Bcl-x(L) remains unknown. We show that although signaling through the TCR is sufficient to stimulate transcription of Bcl-x(L) mRNA, CD28, by activating PI3K and mammalian target of rapamycin, provides a critical signal that regulates the translation of Bcl-x(L) transcripts. We observe that CD28 induced 4E-binding protein-1 phosphorylation, an inhibitor of the translational machinery, and that CD28 costimulation directly augmented the translation of a Bcl-x(L) 5'-untranslated region reporter construct. Lastly, costimulation by CD28 shifted the distribution of Bcl-x(L) mRNA transcripts from the pretranslation complex to the translationally active polyribosomes. These results demonstrate that CD28 relieves the translational inhibition of Bcl-x(L) in a PI3K/mammalian target of rapamycin-dependent manner.