Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Q: Context: Reduction-oxidation (redox) signaling, the translation of an oxidative intracellular environment into a cellular response, is mediated by the reversible oxidation of specific cysteine thiols. The latter can result in disulfide formation between protein hetero- or homodimers that alter protein function until the local cellular redox environment has returned to the basal state. We have previously shown that this mechanism promotes the nuclear localization and activity of the Forkhead Box O4 (FOXO4) transcription factor.', 'In this study, we sought to investigate whether redox signaling differentially controls the human FOXO3 and FOXO4 paralogs.', 'We present evidence that FOXO3 and FOXO4 have acquired paralog-specific cysteines throughout vertebrate evolution. Using a proteome-wide screen, we identified previously unknown redox-dependent FOXO3 interaction partners. The nuclear import receptors Importin-7 (IPO7) and Importin-8 (IPO8) form a disulfide-dependent heterodimer with FOXO3, which is required for its reactive oxygen species-induced nuclear translocation. FOXO4 does not interact with IPO7 or IPO8.
Answer: IPO7 and IPO8 control the nuclear import of FOXO3, but not FOXO4, in a redox-sensitive and disulfide-dependent manner. Our findings suggest that evolutionary acquisition of cysteines has contributed to regulatory divergence of FOXO paralogs, and that phylogenetic analysis can aid in the identification of cysteines involved in redox signaling.

A: Does evolutionary acquisition of cysteines determine FOXO paralog-specific redox signaling?
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Q: Context: Pandemic strains of HIV-1 (group M) encode a total of nine structural (gag, pol, env), regulatory (rev, tat) and accessory (vif, vpr, vpu, nef) genes. However, some subtype A and C viruses exhibit an unusual gene arrangement in which the first exon of rev (rev1) and the vpu gene are placed in the same open reading frame. Although this rev1-vpu gene fusion is present in a considerable fraction of HIV-1 strains, its functional significance is unknown.', 'Examining infectious molecular clones (IMCs) of HIV-1 that encode the rev1-vpu polymorphism, we show that a fusion protein is expressed in infected cells. Due to the splicing pattern of viral mRNA, however, these same IMCs also express a regular Vpu protein, which is produced at much higher levels. To investigate the function of the fusion gene, we characterized isogenic IMC pairs differing only in their ability to express a Rev1-Vpu protein. Analysis in transfected HEK293T and infected CD4+ T cells showed that all of these viruses were equally active in known Vpu functions, such as down-modulation of CD4 or counteraction of tetherin. Furthermore, the polymorphism did not affect Vpu-mediated inhibition of NF-кB activation or Rev-dependent nuclear export of incompletely spliced viral mRNAs. There was also no evidence for enhanced replication of Rev1-Vpu expressing viruses in primary PBMCs or ex vivo infected human lymphoid tissues. Finally, the frequency of HIV-1 quasispecies members that encoded a rev1-vpu fusion gene did not change in HIV-1 infected individuals over time.
Answer: Expression of a rev1-vpu fusion gene does not affect regular Rev and Vpu functions or alter HIV-1 replication in primary target cells. Since there is no evidence for increased replication fitness of rev1-vpu encoding viruses, this polymorphism likely emerged in the context of other mutations within and/or outside the rev1-vpu intergenic region, and may have a neutral phenotype.

A: Does a Naturally Occurring rev1-vpu Fusion Gene Confer a Fitness Advantage to HIV-1?
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Q: Context: This study was performed to examine the association between household food insecurity, self-efficacy and infant feeding styles in mothers with children under 2 years old in Varamin, Iran.', "In this cross-sectional study, 423 mothers aged 17-40 years from different areas of Varamin were selected by a multistage sampling methods from October 2013 to February 2014. The questionnaires consisted of three valid instruments, including: Household Food Insecurity Access Scale, Comprehensive Feeding Practices Questionnaire and Mother's Self-Efficacy Questionnaire. Data were analyzed using Chi-square, t tests, ANOVA, Pearson correlations and multiple linear regressions. Structural equation modeling was also used.", "Mild and moderate-severe food insecurity was observed in 39.5 and 12.8 % of the households respectively. Mean score of mother's self-efficacy in food secure households was 32.5 ± 3.7; while in mild food insecure and moderate-severe food insecure households were 31.9 ± 3.1 and 28.4 ± 4.0, respectively (P = 0.001). There was a significant negative correlation between household food insecurity and mother's self-efficacy (r = -0.297, P < 0.01). Significant correlation was seen between mother's self-efficacy and the maternal infant feeding styles. Household food insecurity and mother's self-efficacy had significant relationship with mother-infant feeding styles: control of home food access [β (SE)] = [-0.015(0.004), P = 0.001]; restriction for weight control [β = 0.038(0.013), P = 0.003]; restriction for health [β = 0.019(0.008), P = 0.027] and encouragement [=0.018(0.006), P = 0.001]. The model had sufficient fitness with data of the research (CFI = 0.927, RMSEA = 0.076).
Answer: Our findings suggest that performing interventions in order to enhance mother's self-efficacy in food insecure households can lead to improve positive maternal feeding behaviors.

A:
Does mother 's Self-Efficacy mediate the Relationship Between Household Food Insecurity and Maternal Infant Feeding Styles?
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