Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

[EX Q]: Atg8-family proteins are the best-studied proteins of the core autophagic machinery. They are essential for the elongation and closure of the phagophore into a proper autophagosome. Moreover, Atg8-family proteins are associated with the phagophore from the initiation of the autophagic process to, or just prior to, the fusion between autophagosomes with lysosomes. In addition to their implication in autophagosome biogenesis, they are crucial for selective autophagy through their ability to interact with selective autophagy receptor proteins necessary for the specific targeting of substrates for autophagic degradation. In the past few years it has been revealed that Atg8-interacting proteins include not only receptors but also components of the core autophagic machinery, proteins associated with vesicles and their transport, and specific proteins that are selectively degraded by autophagy. Atg8-interacting proteins contain a short linear LC3-interacting region/LC3 recognition sequence/Atg8-interacting motif (LIR/LRS/AIM) motif which is responsible for their interaction with Atg8-family proteins. These proteins are referred to as LIR-containing proteins (LIRCPs). So far, many experimental efforts have been carried out to identify new LIRCPs, leading to the characterization of some of them in the past 10years. Given the need for the identification of LIRCPs in various organisms, we developed the iLIR database ( [Link] ) as a freely available web resource, listing all the putative canonical LIRCPs identified in silico in the proteomes of 8 model organisms using the iLIR server, combined with a Gene Ontology (GO) term analysis. Additionally, a curated text-mining analysis of the literature permitted us to identify novel putative LICRPs in mammals that have not previously been associated with autophagy.
[EX A]: Which web resource for LIR motif-containing proteins in eukaryotes has been developed?

[EX Q]: Our objective was to evaluate the diagnostic value of computed tomography angiography (CTA) and ventilation perfusion (V/Q) scan in the assessment of pulmonary embolism (PE) by means of a Bayesian statistical model. Wells criteria defined pretest probability. Sensitivity and specificity of CTA and V/Q scan for PE were derived from pooled meta-analysis data. Likelihood ratios calculated for CTA and V/Q were inserted in the nomogram. Absolute (ADG) and relative diagnostic gains (RDG) were analyzed comparing post- and pretest probability. Comparative gain difference was calculated for CTA ADG over V/Q scan integrating ANOVA p value set at 0.05. The sensitivity for CT was 86.0% (95% CI: 80.2%, 92.1%) and specificity of 93.7% (95% CI: 91.1%, 96.3%). The V/Q scan yielded a sensitivity of 96% (95% CI: 95%, 97%) and a specificity of 97% (95% CI: 96%, 98%). Bayes nomogram results for CTA were low risk and yielded a posttest probability of 71.1%, an ADG of 56.1%, and an RDG of 374%, moderate-risk posttest probability was 85.1%, an ADG of 56.1%, and an RDG of 193.4%, and high-risk posttest probability was 95.2%, an ADG of 36.2%, and an RDG of 61.35%. The comparative gain difference for low-risk population was 46.1%; in moderate-risk 41.6%; and in high-risk a 22.1% superiority. ANOVA analysis for LR+ and LR- showed no significant difference (p=0.8745, p=0.9841 respectively). This Bayesian model demonstrated a superiority of CTA when compared to V/Q scan for the diagnosis of pulmonary embolism. Low-risk patients are recognized to have a superior overall comparative gain favoring CTA.
[EX A]: What can be predicted with the Wells criteria?

[EX Q]: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a vascular dementing disease caused by mutations in the NOTCH3 gene, most which are missense mutations leading to an uneven number of cysteine residues in epidermal growth factor-like repeats in the extracellular domain of Notch3 receptor (N3ECD). CADASIL is characterized by degeneration of vascular smooth muscle cells (VSMC) and accumulation of N3ECD on the VSMCs of small and middle-sized arteries. Recent studies have demonstrated that impairment of Notch3 signaling is not the primary cause of the disease. In the present study we used proteomic analysis to characterize the protein expression pattern of a unique material of genetically genuine cultured human CADASIL VSMCs. We identified 11 differentially expressed proteins, which are involved in protein degradation and folding, contraction of VSMCs, and cellular stress. Our findings indicate that misfolding of Notch3 may cause endoplasmic reticulum stress and activation of unfolded protein response, leading to increased reactive oxygen species and inhibition of cell proliferation. In addition, upregulation of contractile proteins suggests an alteration in the signaling system of VSMC contraction. The accumulation of N3ECD on the cell surface possibly upregulates the angiotensin II regulatory feedback loop and thereby enhances the readiness of the cells to respond to angiotensin II stimulation.
[EX A]:
Which gene is involved in CADASIL?