instruction:
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".
question:
Paragraph: The major biochemical and thermodynamic features of nucelocapsid protein of SARS coronavirus (SARS _ NP) were characterized by use of non-denatured gel electrophoresis, size-exclusion chromatographic and surface plasmon resonance (SPR) techniques. The results showed that SARS _ NP existed in vitro as oligomer, more probably dimer, as the basic functional unit. This protein shows its maximum conformational stability near pH 9.0, and it seems that its oligomer dissociation and protein unfolding occur simultaneously. Thermal-induced unfolding for SARS _ NP was totally irreversible. Both the thermal and chemical denaturant-induced denaturation analyses showed that oligomeric SARS _ NP unfolds and refolds through a two-state model, and the electrostatic interactions among the charge groups of SARS _ NP made a significant contribution to its conformational stability. D Abbreviations: SARS _ CoV, severe acute respiratory syndrome coronavirus; SARS _ NP, nucleocapsid protein of SARS; SPR, surface plasmon resonance; GuHCl, guanidine hydrochloride; CD, circular dichroism; T m and C m , transition midpoints of thermal and chemical denaturations; IPTG, isopropyl-h-d-thiogalasctopyranoside; N and U, native and unfolded states. 
 Title: In vitro biochemical and thermodynamic characterization of nucleocapsid protein of SARS
answer:
False


question:
Paragraph: CD13/Aminopeptidase N (CD13) is known to play an important role in tumour cell invasion. We examined whether basic fibroblast growth factor (bFGF) is involved in the regulation of CD13 expression in human melanoma cells. 1F6 human melanoma cells were stably transfected with constructs encoding either the 18 kDa (18kD) or all (ALL) bFGF isoform proteins. We observed highly increased CD13 mRNA and protein expression in the 1F6 clones regardless of the overexpression of either the 18kD or all isoform proteins. Neutral aminopeptidase activity was increased five-fold and could be inhibited by bestatin and the CD13-neutralising antibody WM15. The enhanced invasion through Matrigel, but not migration in a wound assay, was efficiently abrogated by both bestatin and WM15. Upregulation of CD13 expression was the result of increased epithelial and myeloid promoter activity up to 4.5fold in 1F6-18kD and 1F6-ALL clones. Interestingly, in a panel of human melanoma cell lines, a significant correlation (r 2 ¼ 0.883, Po0.05) between bFGF and CD13 mRNA and protein expression was detected. High bFGF and CD13 expression were clearly related with an aggressive phenotype. Taken together, our data indicate that high bFGF expression upregulates CD13 expression in human melanoma cells by activating both the myeloid and the epithelial CD13 promoter. In addition, we show that high bFGF and CD13 expression results in enhanced invasive capacity and metastatic behaviour of human melanoma cells. 
 Title: CD13/Aminopeptidase N overexpression by basic fibroblast growth factor mediates enhanced invasiveness of 1F6 human melanoma cells
answer:
False


question:
Paragraph: word count: 359 20 Text word count: 4423 21 22 All rights reserved. No reuse allowed without permission. ABSTRACT 23 The 3¢-to-5¢ exoribonuclease in coronavirus (CoV) nonstructural protein 14 (nsp14-ExoN) 24 mediates RNA proofreading during genome replication. ExoN catalytic residues are arranged in 25 three motifs: I (DE), II (E), III (D). Alanine substitution of the motif I residues (AA-E-D, four 26 nucleotide substitutions) in murine hepatitis virus (MHV) and SARS-CoV yields viable mutants 27 with impaired replication and fitness, increased mutation rates, and attenuated virulence in vivo. 28 Despite these impairments, MHV-and SARS-CoV ExoN motif I AA mutants (ExoN-AA) have 29 not reverted at motif I in diverse in vitro and in vivo environments, suggesting that profound 30 fitness barriers prevent motif I reversion. To test this hypothesis, we engineered MHV-ExoN-AA 31 with 1, 2 or 3 nucleotide mutations along genetic pathways to AA-to-DE reversion. We show 32 that engineered intermediate revertants were viable but had no increased replication or 33 competitive fitness compared to MHV-ExoN-AA. In contrast, a low passage (P10) MHV-ExoN-34 AA showed increased replication and competitive fitness without reversion of ExoN-AA. 35 Finally, engineered reversion of ExoN-AA to ExoN-DE in the presence of ExoN-AA passage-36 adaptive mutations resulted in significant fitness loss. These results demonstrate that while 37 reversion is possible, at least one alternative adaptive pathway is more rapidly advantageous than 38 intermediate revertants and may alter the genetic background to render reversion detrimental to 39 fitness. Our results provide an evolutionary rationale for lack of ExoN-AA reversion, illuminate 40 potential multi-protein replicase interactions and coevolution, and support future studies aimed at 41 stabilizing attenuated CoV ExoN-AA mutants. 42 43 All rights reserved. No reuse allowed without permission. The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. . https://doi.org/10.1101/618249 doi: bioRxiv preprint Coronaviruses encode an exoribonuclease (ExoN) that is important for viral replication, fitness, 45 and virulence, yet coronaviruses with a defective ExoN (ExoN-AA) have not reverted under 46 diverse experimental conditions. In this study, we identify multiple impediments to MHV-ExoN-47 AA reversion. We show that ExoN-AA reversion is possible but evolutionarily unfavorable. 48 Instead, compensatory mutations outside of ExoN-AA motif I are more accessible and beneficial 49 than partial reversion. We also show that coevolution between replicase proteins over long-term 50 passage partially compensates for ExoN-AA motif I but renders the virus inhospitable to a 51 reverted ExoN. Our results reveal the evolutionary basis for the genetic stability of ExoN-52 inactivating mutations, illuminate complex functional and evolutionary relationships between 53 coronavirus replicase proteins, and identify potential mechanisms for stabilization of ExoN-AA 54 coronavirus mutants. 55 All rights reserved. No reuse allowed without permission. 
 Title: Fitness barriers limit reversion of a proofreading-deficient coronavirus 1 2
answer:

False