China
Africa
Explore chapters and articles related to this topic
Order Blubervirales: Core Protein
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
The native HBc protein interacted with virus-suppressing proteins such as Np95/ICBP90-like RING finger protein (NIRF), a novel E3 ubiquitin ligase (Qian et al. 2012, 2015), and cytidine deaminase APOBEC3A (Zhao D et al. 2010; Lucifora et al. 2014), and packed them into the HBc nucleocapsids. Some other proteins, such as the MxA protein, an interferon-inducible cytoplasmic dynamin-like GTPase that possesses anti-HBV activity, might interfere with the HBc self-assembly (Li N et al. 2012). Finally, the proper self-assembly and release of the HBc capsids depended on functional Rab33B, a GTPase participating in autophagosome formation via interaction with the Atg5-Atg12/Atg16L1 complex (Döring and Prange 2015).
MiR-34b regulates cervical cancer cell proliferation and apoptosis
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Zhen Cao, Gong Zhang, Conghua Xie, Yunfeng Zhou
Several studies have demonstrated that miR-34b was reduced or lost in a number of cancers, including breast cancer, epithelial ovarian cancer and Gastric Cancer [12–14]. The association between a polymorphism in miR-34b and risk of cancer was also reported in independent studies and meta-analyses [15,16]. There were also some studies focusing on the effect of miR-34b in the development of cervical cancer. In a study including 88 cervical cancer cases, it was reported that miR-34b-3p were found to be frequently downregulated in cancers suggesting miRNA-mediated deregulation of APOBEC3A expression in cancer patients harbouring this particular deletion polymorphism [17]. MiR-34b was also reported to distinguish the high-grade CIN specimens from normal cervical epithelium [18]. However, a fundamental question was whether miR-34b has therapeutic potential for cervical cancer. In addition, the signalling mechanisms by which miR-34b functions remain to be determined. Thus we conducted this study to detect the expression pattern of miR-34b in cervical cancers and demonstrate the regulation effect of miR-34b through in-vitro studies.
Extracellular vesicles mediate the horizontal transfer of an active LINE-1 retrotransposon
Published in Journal of Extracellular Vesicles, 2019
Yumi Kawamura, Anna Sanchez Calle, Yusuke Yamamoto, Taka-Aki Sato, Takahiro Ochiya
Therefore, we next examined whether host mechanisms regulating L1 activity could be affecting the rate of L1-EGFP retrotransposition in recipient cells. APOBEC3 (apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like protein 3) is a well-known example of an intrinsic factor that inhibits L1 retrotransposition by cytidine deaminase activity [39–41] and deamination-independent mechanisms such as sequestration of retrotransposon RNPs and targeting to cytoplasmic stress granules and processing bodies for degradation [33,36,42–44]. To investigate whether L1-EGFP retrotransposition is inhibited by endogenous APOBEC3 activity, we performed qRT-PCR analysis on total RNA from L1-EGFP cells and recipient cells co-cultured with L1-EGFP cells exposed to L1-EGFP EVs. Increased expression of APOBEC3B (A3B) and APOBEC3C (A3C) was detected in both MM231 L1-EGFP and HCT116 L1-EGFP cells (Figure S5A). APOBEC3F (A3F) expression was increased in HCT116 L1-EGFP cells, but not in MM231 L1-EGFP cells (Figure S5A). APOBEC3A (A3A) was not expressed in both cell lines (Figure S5A). More notably, a significant increase in the expression of A3B, A3C, and A3F was observed in MM231 recipient cells exposed to L1-EGFP EVs (Figure 5(a)). The gradual increase of corresponding proteins was also observed from day 5 to day 14 in recipient cells (Figure 5(d)). These findings indicate that A3B, A3C, and A3F in MM231 recipient cells are activated in response to increased exposure to L1-EGFP RNA.
Viral subversion of APOBEC3s: Lessons for anti-tumor immunity and tumor immunotherapy
Published in International Reviews of Immunology, 2018
Faezeh Borzooee, Mahdi Asgharpour, Emma Quinlan, Michael D. Grant, Mani Larijani
The APOBEC3 family of 7 members (APOBEC3A, B, C, D, F, G, H) are endogenous DNA-editing enzymes that mutate viral and cellular genomes.1 Since their discovery 15 years ago, and in the ensuing time, A3s have been intensively studied as anti-viral factors of the innate immune arm. This is because they are constitutively expressed in immune cells and function to mutate and incapacitate the genomic sequences of invading retroviruses, such as HIV.2 Subsequent work revealed that the relationship between A3 and HIV is double-edged in that the A3s are not strictly anti-viral but rather carry two significant pro-viral activities: first, A3-induced mutagenesis of the HIV genome was shown to yield drug-resistance variants, and second, A3 activity is now recognized as a source of mutations that result in HIV evading cytotoxic T cell (CTL) recognition.3,4