1 r (VEGF) proximal promoter region contains
a poly G/C-rich element that is essential for basal and in
2 Phase variation of PorA is mediated by
a poly-G repeat tract present within the promoter, leading
3 ces, such as poly-K/R, poly-N/Q, poly-A,
and poly-G residues.
4 mation at presumed endogenous RFBs formed
by poly G/C tracts in the absence of DOG-1.
5 s showed that lgtA, lgtC, and lgtD
contained poly-G tracts within the coding frames, leading to the h
6 In a cohort of 22 patients, we
detect poly-G variants in 91% of tumors.
7 from the pyrG promoter, which contains
eight poly-G RNA bases synthesized using three C bases in the
8 These findings
establish poly-G ODN as a novel type of cancer immunotherapy.
9 We
generate poly-G mutation profiles of spatially separated samples
10 A homopolymeric tract of
Gs (
poly-G) is present in the pgtA gene of many GC strains,
11 tream 3' splice site and downstream
intronic poly-G runs functioned redundantly to protect an exon fr
12 Mechanistically,
poly-G ODN directly induced the phosphorylation of Lck (
13 Intriguingly, the
microsatellite poly G repeat is neither essential nor the site for the
14 The antitumor activity
of poly-G ODN was mediated through CD8 T cells in a TLR9-in
15 RNA polymerase will synthesize a 'ladder'
of poly-G RNA products.
16 nscription assays to determine the length
of poly-G RNA from the pyrG promoter variants.
17 elation was observed between the presence
of poly-G in pgtA and the dissemination of GC infection.
18 matic variation in hypermutable
polyguanine (
poly-G) repeats can provide a rapid and reliable assessm
19 the intratumoral injection of
polyguanosine (
poly-G) oligonucleotides (ODN) has such an effect, boost
20 e, we show that synthetic
polyriboguanosine (
poly G) and oligo-deoxyriboguanosine (oligo G) reduce en
21 tic mutation frequency, suggesting that
some poly-G variants accumulate before the onset of carcinoge
22 Finally, we show
that poly-G mutations can be found in other cancers than colo
23 However, disruption of
the poly G sequence impaired the RFS, potentially due to alt
24 ase pair insertions and deletions within
the poly G:C run there, suggesting that a high affinity PNA
25 s in the number of guanosine residues in
the poly-G tracts might be responsible for the high frequenc
26 ted gonorrhea (UG) patients, pgtA lacked
the poly-G.
27 However, in many other GC, pgtA lacks
the poly-G and is expressed constitutively without Pv.
28 Strikingly, we found that
the poly-G run, a known intronic splicing enhancer, was the
29 We
use poly-G repeat genotyping to study the evolution of colon
30 gene of many GC strains, and this pgtA
with poly-G can undergo phase variation (Pv).