In this task, you're given a paragraph and title from the research paper. Your task is to classify whether the given title is suitable or not for the research paper based on the given paragraph. Return "True" if title is proper according to paragraph else "False".
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Question: Paragraph: Human cytomegalovirus (HCMV) is a ubiquitous betaherpesvirus that frequently causes morbidity and mortality in individuals with insufficient immunity, such as transplant recipients, AIDS patients, and congenitally infected newborns. Several antiviral drugs are approved to treat HCMV infections. However, resistant HCMV mutants can arise in patients receiving long-term therapy. Additionally, side effects and the risk to cause birth defects limit the use of currently approved antivirals against HCMV. Therefore, the identification of new drug targets is of clinical relevance. Recent work identified DNA-damage binding protein 1 (DDB1) and the family of the cellular cullin (Cul) RING ubiquitin (Ub) ligases (CRLs) as host-derived factors that are relevant for the replication of human and mouse cytomegaloviruses. The first-in-class CRL inhibitory compound Pevonedistat (also called MLN4924) is currently under investigation as an anti-tumor drug in several clinical trials. Cytomegaloviruses exploit CRLs to regulate the abundance of viral proteins, and to induce the proteasomal degradation of host restriction factors involved in innate and intrinsic immunity. Accordingly, pharmacological blockade of CRL activity diminishes viral replication in cell culture. In this review, we summarize the current knowledge concerning the relevance of DDB1 and CRLs during cytomegalovirus replication and discuss chances and drawbacks of CRL inhibitory drugs as potential antiviral treatment against HCMV.
Title: Molecular Sciences Cellular Cullin RING Ubiquitin Ligases: Druggable Host Dependency Factors of Cytomegaloviruses

Answer: True

Question: Paragraph: We aimed to test the hypothesis that gene silencing of tumor necrosis factor alpha converting enzyme (TACE) may attenuate lesion inflammation and positive vascular remodeling and enhance plaque stability in a rabbit model of atherosclerosis. Lentivirus-mediated TACE shRNA was injected into the abdominal aortic plaques of rabbits which effectively down-regulated TACE expression and activities from week 8 to week 16. TACE gene silencing reduced remodeling index and plaque burden, and diminished the content of macrophages and lipids while increased that of smooth muscle cells and collagen in the aortic plaques. In addition, TACE gene silencing attenuated the local expression of P65, iNOS, ICAM-1, VEGF and Flt-1 and activities of MMP9 and MMP2 while increased the local expression of TGF-1 together with reduced number of neovessels in the aorta. TACE shRNA treatment resulted in down-regulated expression of TACE in macrophages and blunted ERK-P38 phosphorylation and tube formation of co-cultured mouse vascular smooth muscle cells or human umbilical vein endothelial cells. In conclusion, gene silencing of TACE enhanced plaque stability and improved vascular positive remodeling. The mechanisms may involve attenuated local inflammation, neovascularization and MMP activation, as well as enhanced collagen production probably via down-regulated ERK-NF-B and upregulated TGF-1 signaling pathways. Tumor necrosis factor alpha converting enzyme (TACE), also known as ADAM17 (A disintegrin and A metalloproteinase 17), was initially discovered as a protease that cleaves the 26-kDa precursor of TNF- and sheds transmembrane TNF- to generate a soluble form of TNF- that can bind to TNF- receptors to induce inflammatory response 1 . Recently it has been recognized that TACE is a type I transmembrane protein and a member of a superfamily of Zn dependent metalloproteases. The major physiological role of TACE is to regulate the proteolytic release of a number of growth factors, cytokines, adhesion molecules and cleavage enzymes from cellular membrane 2,3 . The major pro-inflammatory cytokine processed by TACE is TNF- which is produced by macrophages, monocytes and T-cells, and acts as a major player in the pathogenesis of inflammation. It has been increasingly recognized that TACE-mediated shedding is involved in a variety of diseases such as ischemia, heart failure, arthritis, atherosclerosis, diabetes, cancer, neurological and immune diseases 3-5 . Ashley EA et al. provided functional evidence for TACE as a candidate gene of atherosclerosis susceptibility and found that polymorphisms of the TACE genes had relation to cardiovascular mortality in humans 6 . Canault M et al. found that TACE expression was associated with lesion formation in atherosclerosis-prone sites of apolipoprotein E-knockout (ApoE -/-) mice 7 . Oksala N demonstrated that TACE was upregulated in advanced human atherosclerotic lesions in samples from carotid, aortic, and femoral arteries compared to samples from internal thoracic artery free of atherosclerotic plaques 8 . In addition, Stoehr R et al. showed that loss of TIMP3, an endogenous inhibitor of TACE, exacerbated atherosclerosis 1
Title: Gene silencing of TACE enhances plaque stability and improves vascular remodeling in a rabbit model of atherosclerosis

Answer: False

Question: Paragraph: corona-, toro-and roniviruses are evolutionarily related positive-strand RNA viruses, united in the order Nidovirales. The best studied nidoviruses, the corona-and arteriviruses, employ a unique transcription mechanism, which involves discontinuous RNA synthesis, a process resembling similarityassisted copy-choice RNA recombination. During infection, multiple subgenomic (sg) mRNAs are transcribed from a mirror set of sg negative-strand RNA templates. The sg mRNAs all possess a short 5 common leader sequence, derived from the 5 end of the genomic RNA. The joining of the non-contiguous leader' and'body' sequences presumably occurs during minus-strand synthesis. To study whether toroviruses use a similar transcription mechanism, we characterized the 5 termini of the genome and the four sg mRNAs of Berne virus (BEV). We show that BEV mRNAs 35 lack a leader sequence. Surprisingly, however, RNA 2 does contain a leader, identical to the 5-terminal 18 residues of the genome. Apparently, BEV combines discontinuous and nondiscontinous RNA synthesis to produce its sg mRNAs. Our ®️ndings have important implications for the understanding of the mechanism and evolution of nidovirus transcription.
Title: Discontinuous and non-discontinuous subgenomic RNA transcription in a nidovirus

Answer:
True