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Non-VLPs
Published in Paul Pumpens, Single-Stranded RNA Phages, 2020
Cao et al. (2013) generated a genetically encoded optogenetic system that activated mRNA translation in mammalian cells in response to light. Blue light induced the reconstitution of an RNA binding domain and a translation initiation domain, thereby activating target mRNA translation downstream of the binding sites. To do this, the MS2 coat was fused to the CIBN domain, an NLS-deficient truncated version of the CIB1 protein. The latter was the basic-helix–loop–helix 1 polypeptide interacting with the Arabidopsis thaliana Cryptochrome 2 (CRY2), protein upon light illumination.
Targeting ubiquitin protein ligase E3 component N-recognin 5 in cancer cells induces a CD8+ T cell mediated immune response
Published in OncoImmunology, 2020
Mei Song, Chao Wang, Huan Wang, Tuo Zhang, Jiuqi Li, Robert Benezra, Lotfi Chouchane, Yin-Hao Sun, Xin-Gang Cui, Xiaojing Ma
An ingenuity pathway analysis (IPA)-based study that we performed (unpublished data) reveals that UBR5 may represent a major signaling hub connecting with many important molecules in various ways such as TP53, argonaute 1 (AGO1), Bcl-2-associated X protein (BAX), calcium and integrin binding 1 (CIB1), growth arrest and DNA damage-inducible 45 (GADD45) proto-oncogene MDM2, poly(A)-binding and interacting protein 2 (PAIP2), progesterone receptor (PGR), protein phosphatase 2 regulatory subunit Balpha (PPP2R2A), and AGTRI, etc., suggesting a broad network of biological pathways regulated by UBR5 through direct or indirect physical interactions. In this study, we present evidence that UBR5 gene amplifications are common occurrence in human breast cancers and that high UBR5 expression is adversely associated with disease progression and patient survival. Targeting UBR5 in the mammary tumor through gene editing or expression silencing causes paracrine effects that trigger the activation of CD8+ T cells, which help control the tumor growth. The antigenic specificities of this response are presently unknown. We have shown that Raet1e expression was upregulated in Ubr5−/- tumor, which may stimulate an anti-tumor response. This response is unlikely to be of NK cell origin since depletion of NK cells did not have an impact on the anti-tumor response (data not shown). It remains to be determined if γδ T cells are involved.18 Given UBR5’s demonstrated essential role for G(1)/S and intra S phase DNA damage checkpoint activation and for the maintenance of G(2)/M arrest and genome integrity after double-strand DNA breaks,21 it is conceivable that deletion of Ubr5 may cause genomic instability and the induction of “neoantigens” that attract T cell-mediated immune responses. Further studies in this area may lead to the identification of these neoantigens for potential applications as novel cancer vaccine and immunotherapy targets.