(Genetrank) hits (Def. 6) for the list of reference genes O15304 (SIVA1), P78537 (BLOC1S1), P0CW18 (PRSS56), P53007 (SLC25A1), Q9Y2X8 (UBE2D4), DNM1L(O00429).

(Genetrank) hits (Def. 6) for the list of reference genes O15304 (SIVA1), P78537 (BLOC1S1), P0CW18 (PRSS56), P53007 (SLC25A1), Q9Y2X8 (UBE2D4), DNM1L(O00429).</p

Radar plots for four experimentally validated genes.

The range of values covers the range of log scores observed. The two bullets on a spoke read as follows: blue dot: direction PX ⇝; green dot: direction XP ⇝.</p

(pr-affinity) hits (Def. 6) for the list of reference genes O15304 (SIVA1), P78537 (BLOC1S1), P0CW18 (PRSS56), P53007 (SLC25A1), Q9Y2X8 (UBE2D4), DNM1L(O00429).

(pr-affinity) hits (Def. 6) for the list of reference genes O15304 (SIVA1), P78537 (BLOC1S1), P0CW18 (PRSS56), P53007 (SLC25A1), Q9Y2X8 (UBE2D4), DNM1L(O00429).</p

Example interaction graph and Markov chain: Two structural properties motivating absorbing states and the renormalization of hit probabilities.

Arcs indicate transitions in the Markov chains—transition probabilities are omitted. The set of sources is S = {s1, s2, s3} and the set of targets is T = {t1, t2, t3, t4}. When defining absorbing states, transitions corresponding to blue arcs are removed. This implies that t2 will not be highlighted because t1 or t4 must be visited before any random walk starting from any source s ∈ S. Furthermore, the normalization aims at reducing the importance of t3 in the study (due to its high proximity to the three sources).</p

(Genetrank) saturation plots (Def. 5) for <i>τ</i> = 20.

Values of r processed in decreasing order. (Left column) Saturation index and slices at r = cst and k = cst (See Eq 9) (Right column) Relative saturation index and slices at r = cst and k = cst (See Eq 10).</p

(pr-affinity) saturation plots (Def. 5) for <i>τ</i> = 20.

Values of r processed in decreasing order. (Left column) Saturation index and slices at r = cst and k = cst (See Eq 9) (Right column) Relative saturation index and slices at r = cst and k = cst (See Eq 10).</p

Score radar scatter plot.

The individual radar plots (Fig 6) are assembled in a MA plot. Zooming on a radar reveals the scores for that gene (80 data points per gene in a radar).</p

List of class I PI3K isoform inhibitors and their respective in vitro IC₅₀.

<p>Assays were conducted side by side with 10 µM ATP using the method described previously <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0063907#pone.0063907-Knight1" target="_blank">[22]</a>.</p

IL-1β increases wound closure via a TGF-β1-dependent mechanism in primary human ATII cell monolayers.

<p>(<b>A</b>) IL-1β increases the rate of wound closure in primary human ATII cell monolayers. IL-1β (10 ng/ml) and/or TGF-βscRII or their respective vehicles were added to the monolayers after the scratch. Phase contrast microscopy (20X magnification) immediately after wounding (left panels, t = 0 h) and after 36 h (right panels t = 36 h). Scale bar: 100 µm. (<b>B</b>) TGF-β1 soluble receptor (TGF-βscRII) prevents IL-1β-dependent increase in rate of wound closure of primary human ATII cell monolayers. IL-1β (10 ng/ml) and/or TGF-βscRII or their respective vehicles were added to the monolayers after the scratch. Rate of wound closure was expressed as percent of control 16 h after wounding. *<i>p</i><0.05 from monolayers exposed to IL-1β vehicle. **<i>p</i><0.05 from monolayers exposed to IL-1β.</p

Endogenous HMGB1 released by primary rat ATII cell monolayers after scratch wounds increases alveolar epithelial wound closure via an IL-1β-dependent mechanism.

<p>(<b>A</b>) Supernatant from primary rat ATII monolayers collected 6 hours after multiple scratches (MS Cell Sup) induces an increase in the secretion of IL-1β by primary rat ATII cell monolayers via a TLR4-dependent pathway. MS Cell Sup, a blocking TLR4 antibody or its isotype control IgG were added to the monolayers after the scratch. HMGB1 was depleted from MS Cell Sup by immunoprecipitation using 30 µg/ml of HMGB1 specific Ab (MS Cell Sup IP w/HMGB1 Ab). Controls were MS Cell Sup immunoprecipitated with a control IgG (MS Cell Sup IP w/Cont Ab). IL-1β was measured by ELISA (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0063907#s2" target="_blank">methods</a>) in the cell supernatant. (<b>B</b>) IL-1β receptor antagonist (IL-1RA) prevented the MS Cell Sup-dependent increase in the rate of wound closure of primary rat ATII cell monolayers. MS Cell Sup, and IL-1β receptor antagonist (IL-1RA, 1 µg/ml) or its vehicle were added to the monolayers after the scratch. Rate of wound closure is expressed as percent of control 16 h after wounding. *<i>p</i><0.05 from monolayers exposed to condition media. **<i>p</i><0.05 from monolayers exposed to MS Cell Sup.</p