Flow diagram representing methodology implemented in UniDrug-Target server to identify potential pathogen-specific drug targets.

<p>Flow diagram representing methodology implemented in UniDrug-Target server to identify potential pathogen-specific drug targets.</p

Sample analysis report of one of the pathogen-specific protein (gi:15607938) of <i>M. tuberculosis</i> to determine domain-level conserveness in low-matching sequences between pathogen-specific and non-pathogenic protein sequences^ζ.

ζ<p>For detail see Algorithm section in ‘<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0032833#s2" target="_blank">Material and Methods</a>’.</p>φ<p>Residue, +, blank and - indicate identity, similarity, dissimilarity and gap, respectively w.r.t. corresponding residues in pathogenic sequences in equivalent positions.</p>ψ<p>Different residues forming a given pocket are represented by a number, i.e. 0 indicates biggest size pocket in a protein.</p

Metabolic paths identified until end metabolite synthesis in pyrimidine metabolism (00240) connected pathways starting from the reaction (R00978) catalyzed by the enzyme, dihydropyrimidine dehydrogenase (NADP+ [EC: 1.3.1.2], KEGG Orthologous Id: K00207).

<p>Metabolic paths identified until end metabolite synthesis in pyrimidine metabolism (00240) connected pathways starting from the reaction (R00978) catalyzed by the enzyme, dihydropyrimidine dehydrogenase (NADP+ [EC: 1.3.1.2], KEGG Orthologous Id: K00207).</p

UniDrug-Target predicted pocket forming residues (<b>Table 2</b>) of gi:15607942 (PDBID: 2VZZ).

<p>Visualization through VMD (<a href="http://www.ks.uiuc.edu/Research/vmd/" target="_blank">www.ks.uiuc.edu/Research/vmd/</a>) showed that above residues forming a pocket. Pocket forming residues shown in the surface representation.</p

Identified pocket residues of pathogen-specific protein, gi:15607942, matching with residues forming similar pocket in nonpathogenic sequences of different organisms ^*.

*<p>The number indicates the gi: number. Residue, +, blank and - indicate identity, similarity, dissimilarity and gap, respectively w.r.t. corresponding residues in pathogenic sequences in equivalent positions.</p>#<p>gi:15607942 is having an X-ray crystallographic structure with 2VZZ. The predicted residues are forming pocket equivalent to 2VI7.</p

Expression status of iridoid (a, b) and phenylpropanoid (c, d) pathway genes in field grown tissues (FGS: Field grown shoots having 2.7% P-I and FGR: Field grown roots having 0.4% P-II) w.r.t. tissue cultured shoots (TCS having 0.01% P-I) and roots (TCR having 0.0% P-II).

<p>Expression status of iridoid (a, b) and phenylpropanoid (c, d) pathway genes in field grown tissues (FGS: Field grown shoots having 2.7% P-I and FGR: Field grown roots having 0.4% P-II) w.r.t. tissue cultured shoots (TCS having 0.01% P-I) and roots (TCR having 0.0% P-II).</p

Effect of actinomycin D on expression of significant genes of Picroside-I biosynthetic pathway in <i>Picrorhiza kurroa</i>.

<p>Effect of actinomycin D on expression of significant genes of Picroside-I biosynthetic pathway in <i>Picrorhiza kurroa</i>.</p

Inhibition profiles of enzyme inhibitors on Picroside-I biosynthesis in <i>Picrorhiza kurroa</i>.

<p>Inhibition profiles of enzyme inhibitors on Picroside-I biosynthesis in <i>Picrorhiza kurroa</i>.</p

Effect of inhibitors, fosmidomycin, mevinolin, glyphosate and AOA on transcript levels of target as well as upstream and downstream genes in Picroside-I biosynthesis in <i>Picrorhiza kurroa</i>.

<p>Effect of inhibitors, fosmidomycin, mevinolin, glyphosate and AOA on transcript levels of target as well as upstream and downstream genes in Picroside-I biosynthesis in <i>Picrorhiza kurroa</i>.</p

Expression status of all genes depicted as fold increase, for P-I and P-II biosynthetic pathways in <i>Picrorhiza kurroa</i>: MVA and MEP pathway genes data from Pandit et al. (2012).

<p>Expression status of all genes depicted as fold increase, for P-I and P-II biosynthetic pathways in <i>Picrorhiza kurroa</i>: MVA and MEP pathway genes data from Pandit et al. (2012).</p