The 3′-end-processing factor CPSF is required for the splicing of single-intron pre-mRNAs in vivo

Li, Yongzhong; Chen, Zhongying; Wang, Weirong; Baker, Carl C.; Krug, Robert M.

doi:10.1017/s1355838201010226

Cited by 117 publications

(115 citation statements)

References 39 publications

(35 reference statements)

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“…However, it is possible that the truncation disrupted or reduced the binding of PABII to NS1 that is required to prevent the export of cellular premRNAs from the nucleus in infected cells (37). Disruption of this feature may be responsible for the attenuation of the rNS1-trunc virus in tissue culture and the increase in MLD 50 in infected mice.…”

Section: Discussionmentioning

confidence: 99%

A new influenza virus virulence determinant: The NS1 protein four C-terminal residues modulate pathogenicity

Jackson

Hossain

Hickman

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

365

306

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The virulence of influenza virus is a multigenic trait. One determinant of virulence is the multifunctional NS1 protein that functions in several ways to defeat the cellular innate immune response. Recent large-scale genome sequence analysis of avian influenza virus isolates indicated that four C-terminal residues of the NS1 protein is a PDZ ligand domain of the X-S/T-X-V type and it was speculated that it may represent a virulence determinant. To test this hypothesis, by using mice as a model system, the four Cterminal amino acid residues of a number of influenza virus strains were engineered into the

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Section: Discussionmentioning

confidence: 99%

A new influenza virus virulence determinant: The NS1 protein four C-terminal residues modulate pathogenicity

Jackson

Hossain

Hickman

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

365

306

View full text Add to dashboard Cite

show abstract

“…ZF1 and ZF4 of Yth1p interact with the N-terminal region of Brr5p/Ysh1p [125]. Influenza virus attenuates host antiviral response by blocking the function of CPSF-30 with its NS1 protein [127][128][129].…”

Section: Cpsf-30 (Yth1p)mentioning

confidence: 99%

Protein factors in pre-mRNA 3′-end processing

Mandel

Bai

Tong

2007

Cell. Mol. Life Sci.

358

482

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Most eukaryotic mRNA precursors (pre-mRNAs) must undergo extensive processing, including cleavage and polyadenylation at the 3′-end. Processing at the 3′-end is controlled by sequence elements in the pre-mRNA (cis elements) as well as protein factors. Despite the seeming biochemical simplicity of the processing reactions, more than 14 proteins have been identified for the mammalian complex, and more than 20 proteins have been identified for the yeast complex. The 3′-end processing machinery also has important roles in transcription and splicing. The mammalian machinery contains several sub-complexes, including cleavage and polyadenylation specificity factor (CPSF), cleavage stimulation factor (CstF), cleavage factor I (CF I m ), and cleavage factor II (CF II m ). Additional protein factors include poly(A) polymerase (PAP), poly(A) binding protein (PABP), symplekin, and the C-terminal domain (CTD) of RNA polymerase II largest subunit. The yeast machinery includes cleavage factor IA (CF IA), cleavage factor IB (CF IB), and cleavage and polyadenylation factor (CPF).

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“…Viral IFN antagonists are often multifunctional proteins and their different properties may vary in importance at different stages of the virus replication cycle. For example, the NS1 protein of most strains of influenza A virus blocks expression of cellular genes by interfering with stability, processing or export of mRNA from the nucleus (Fortes et al, 1994;Chen et al, 1999;Li et al, 2001b;Kim et al, 2002;Noah et al, 2003;Satterly et al, 2007). However, the NS1 protein of some influenza virus strains also inhibits RIG-I-mediated inhibition of the IFN pathway (Guo et al, 2006;Opitz et al, 2006;Pichlmair et al, 2006;Mibayashi et al, 2007).…”

mentioning

confidence: 99%

Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures

Randall

Goodbourn

2008

Journal of General Virology

1,389

1,420

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The interferon (IFN) system is an extremely powerful antiviral response that is capable of controlling most, if not all, virus infections in the absence of adaptive immunity. However, viruses can still replicate and cause disease in vivo, because they have some strategy for at least partially circumventing the IFN response. We reviewed this topic in 2000 [Goodbourn, S., Didcock, L. & Randall, R. E. (2000). J Gen Virol 81, 2341-2364] but, since then, a great deal has been discovered about the molecular mechanisms of the IFN response and how different viruses circumvent it. This information is of fundamental interest, but may also have practical application in the design and manufacture of attenuated virus vaccines and the development of novel antiviral drugs. In the first part of this review, we describe how viruses activate the IFN system, how IFNs induce transcription of their target genes and the mechanism of action of IFN-induced proteins with antiviral action. In the second part, we describe how viruses circumvent the IFN response. Here, we reflect upon possible consequences for both the virus and host of the different strategies that viruses have evolved and discuss whether certain viruses have exploited the IFN response to modulate their life cycle (e.g. to establish and maintain persistent/latent infections), whether perturbation of the IFN response by persistent infections can lead to chronic disease, and the importance of the IFN system as a species barrier to virus infections. Lastly, we briefly describe applied aspects that arise from an increase in our knowledge in this area, including vaccine design and manufacture, the development of novel antiviral drugs and the use of IFN-sensitive oncolytic viruses in the treatment of cancer. Biology of the interferon systemThe interferons (IFNs) are a group of secreted cytokines that elicit distinct antiviral effects. They are grouped into three classes called type I, II and III IFNs, according to their amino acid sequence. Type I IFNs (discovered in 1957;Isaacs & Lindenmann, 1957) comprise a large group of molecules; mammals have multiple distinct IFN-a genes (13 in man), one to three IFN-b genes (one in man) and other genes, such as IFN-v, -e, -t, -d and -k. The IFN-a and -b genes are induced directly in response to viral infection, whereas IFN-v, -e, -d and -k play less well-defined roles, such as regulators of maternal recognition in pregnancy. Thus, rather than use the term 'type I IFN', we will use IFN-a/b when referring to the virally induced cytokines. Although the multigenic nature of IFN-a has been known for over 20 years, the significance of this is still debatedi.e. whether these genes are expressed differentially in distinct cell types, whether they are inducible by different types of viruses or whether they are functionally specialized (Brideau-Andersen et al., 2007). For the rest of this review, we will not distinguish between IFN-a subtypes. Type III IFNs have been described more recently and comprise IFNl1, -l2 and -l3, also referred to as IL-2...

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The 3′-end-processing factor CPSF is required for the splicing of single-intron pre-mRNAs in vivo

Cited by 117 publications

References 39 publications

A new influenza virus virulence determinant: The NS1 protein four C-terminal residues modulate pathogenicity

A new influenza virus virulence determinant: The NS1 protein four C-terminal residues modulate pathogenicity

Protein factors in pre-mRNA 3′-end processing

Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures

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