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1 PDIMs and PGLs are important effectors of virulence.
2 We performed whole-genome resequencing of a PDIM-deficient clone and identified a spontaneous point
5 ds, and suggest that drugs aimed at blocking PDIM and/or PGL production might synergize with antibiot
7 rulence factors, phthiocerol dimycocerosate (PDIM) and sulfolipid-1 (SL-1), are controlled by the ava
8 he surface lipid phthiocerol dimycocerosate (PDIM) exhibited significant death rates, and consequentl
9 ted lipid called phthiocerol dimycocerosate (PDIM) which is found only in pathogenic mycobacteria.
10 biosynthesis of phthiocerol dimycocerosate (PDIM), a cell wall lipid that is required for full virul
11 in synthesis of phthiocerol dimycocerosate (PDIM), a surface lipid critical for virulence during acu
16 ace-associated phthiocerol dimycoceroserate (PDIM) lipids to mask underlying pathogen-associated mole
19 ppsD(G44C) point mutation is responsible for PDIM deficiency, virulence attenuation in NOS2(-/-) and
20 us, we have identified coordinated roles for PDIM, known to be essential for mycobacterial virulence,
21 son insertions affecting genes implicated in PDIM synthesis; the third has a disruption in a gene enc
28 ads to a mutant that produces only traces of PDIMs and PGLs, has a slight growth yield increase and d
29 e data suggest that in addition to producing PDIMs, the growing phthiocerol product can also be shutt
35 tide-associated protein (Pap) encoded in the PDIM synthesis gene cluster, as well as PapA5 homologs f
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