1 We demonstrate that alpha
1C antisense ODNs abolish the increase in Gm in response to
2 In contrast, gamma
2 antisense ODN treatments of cell cultures increased the
3 Administration of Kir6.
2 antisense ODN significantly attenuated apomorphine-induc
4 s, treatment of granule neurons with alpha
6 antisense ODNs caused a decrease in GABA-induced maximal
5 The pharmacodynamic effects of CGP
69846A antisense ODNs are therefore limited by the duration of
6 iPLA(2)beta or cPLA(2)
alpha antisense ODN-treated adoptively transferred mouse monoc
7 Only the
alpha2A antisense ODNs significantly change the hypnotic respons
8 At
an antisense ODN concentration of 0.2 mumol/L, p42 MAPK pro
9 ense ODNs to neogenin and restin, but not
an antisense ODN to rap1GAP, were effective in inhibiting O
10 In siRNA
and antisense ODN databases, positive correlations are obser
11 the target gene is actively transcribed
and antisense ODN is more active than sense ODN.
12 the considerations for RNA interference
and antisense ODNs are reported.
13 re measured after infusion of BDNF sense
and antisense ODNs with or without BDNF coinfusion, using th
14 gested for the design of efficient siRNA
and antisense ODNs and the design of antisense ODNs is more
15 electively decreased only by the
appropriate antisense ODNs and not by the "scrambled" ODNs.
16 prepared from cells treated with alpha 1B-
AR antisense ODN demonstrated that alpha 1B-AR protein expr
17 i observed in cells treated with alpha 1A-
AR antisense ODNs was reduced by 42%.
18 ned treatment with alpha 1A- and alpha 1B-
AR antisense ODNs and antagonists additively inhibits PHE-i
19 observed with cells treated with alpha 1D-
AR antisense ODNs or the alpha 1D-AR antagonist BMY 7378 co
20 Furthermore,
BDNF antisense ODN infusions into the CeA or MeA, but not int
21 Here we report that
BDNF antisense ODN infusions into the CeA and MeA, but not BL
22 transfect the monocytes and found that
both antisense ODNs inhibited expression of their target prot
23 ivity of cortical cells was not disrupted
by antisense ODN treatment in mature animals, indicating de
24 phages whose MR expression was suppressed
by antisense ODN treatment.
25 Inhibition of Cux-1 expression
by antisense ODNs was verified by reverse transcription-PCR
26 ion of DCs transduced with anti-CD80 or
CD86 antisense ODN significantly prolonged the survival of he
27 , and transduced with anti-CD80 or anti-
CD86 antisense ODNs (base-mismatched ODNs as controls).
28 ve RNase H recognition site) afford
chimeric antisense ODNs that retain the ability to inhibit steroi
29 In contrast,
CREB antisense ODN-infused rats exhibited significantly impai
30 .e., short term memory) were similar in
CREB antisense ODN and control groups.
31 We
designed antisense ODNs complementary to the initiation codon reg
32 Using human c-myc-
directed antisense ODNs as a model for the application of this ap
33 Transient MCAO in rats infused with
EAAC1 antisense ODNs had no significant effect on any of these
34 e ODN efficacy, but such that more
effective antisense ODNs appear to target mRNA regions with greate
35 rovide a useful tool for selecting
effective antisense ODNs in antisense research.
36 anslocation of Calpha triggered by
exogenous antisense ODN treatment mirrors that observed in cells e
37 fficient siRNA, but the opposite is true
for antisense ODNs.
38 The c-
fos antisense ODN, however, failed to suppress MMP-1 or MMP-
39 When neocortical slices were prepared
from antisense ODN-treated rats and incubated for 1 to 2 h in
40 pha 6 receptor subunit protein after a 48-
hr antisense ODN treatment was assessed with the use of imm
41 Importantly,
antisense ODN treatment did not impair visually driven a
42 al horn neurons were dramatically reduced
in antisense ODN injected PSNL rats 1 week after injection.
43 difficult to avoid target self-structure
in antisense ODN design.
44 Thus, we have shown that the
iNOS antisense ODN specifically blocked iNOS expression and a
45 Efficacy of the
KOR antisense ODN treatment was behaviorally evaluated by as
46 These studies suggest
KSR1 antisense ODNs as a treatment for Ras-dependent human ma
47 tes were incubated with linear and stem-
loop antisense ODNs targeted to Syk mRNA.
48 These results suggest that the use of
mdr1 antisense ODNs in combination with standard antineoplast
49 Moreover,
antisense ODN did not significantly affect IGFBP-4 prote
50 GF cell line was inhibited by 4 microM c-
myc antisense ODN (14% decrease; P < or = 0.006) and 8 micro
51 decrease; P < or = 0.006) and 8 microM c-
myc antisense ODN (approximately 80% decrease; P < or = 0.00
52 expressing breast cancer cells with HER2/
neu antisense ODNs and conventional chemotherapeutic agents
53 urvival mechanisms and suggest that HER2/
neu antisense ODNs may be of use in cancer therapeutics.
54 greatly enhanced the biological activity
of antisense ODN.
55 Moreover, administration
of antisense ODN 1 day after training did not affect subseq
56 ocumented that pressure-mediated delivery
of antisense ODN can functionally inhibit target gene expre
57 The effect
of antisense ODN on phenotype was examined by flow cytometr
58 3 was observed 10 d after the termination
of antisense ODN treatment.
59 Because the use
of antisense ODN in human disease is already established in
60 se of electroporation to enhance delivery
of antisense ODNs is a promising new approach towards ex vi
61 t siRNA and antisense ODNs and the design
of antisense ODNs is more challenging.
62 promising lead analog for the development
of antisense ODNs with increased potency.
63 e self-structure correlations to efficacy
of antisense ODNs, conversely, are insignificant.
64 Inclusion
of antisense ODNs, derived from the phosphotyrosine kinase
65 Five-day infusions
of antisense ODNs (5 and 10 nmol/day) in rats decreased imm
66 y improves the cellular uptake properties
of antisense ODNs, as well as plasmid DNA.
67 CD spectra
of antisense ODNs exhibited specific responses to divalent
68 ng novel polyamines to facilitate the use
of antisense ODNs for controlling HER-2 gene expression.
69 This agent expands the utility
of antisense ODNs for their use in understanding gene funct
70 A
phosphorothioate antisense ODN against Bcl-2 reduced the AMPA-stimulated
71 Phosphorothioate antisense ODNs targeted against accessible sites reduced
72 Conventional
PKC-
antisense ODN treatment completely and significantly inh
73 PKCbeta-
antisense ODN caused 89.2% inhibition of chemotaxis at i
74 A 15-mer phosphorothioate (
PS)
antisense ODN (erbB1AS15) induced a concentration-depend
75 of A10 cells to ISIS 11061, an active C-
Raf antisense ODN, resulted in a potent, dose-dependent inhi
76 ent exposure of TGF-alpha or IGF-I and c-
ret antisense ODN explants caused partial recovery from the
77 ramatic effects were observed with the c-
ret antisense ODN.
78 Both c-ros and c-
ret antisense ODNs reduced the gene expression and biosynthe
79 unocytochemistry that treatment with
RIalpha antisense ODN induces translocation of the Calpha subuni
80 ional PKC family, and next by using
specific antisense ODN for PKCalpha and PKCbeta.
81 Transfection of MNCs with
Src antisense ODNs blocked H-2g-induced MNC recruitment into
82 n, during cell-attached patch-clamp
studies,
antisense ODNs to alpha1c completely blocked the swellin
83 Such antisense ODNs suppress HER2/neu mRNA and protein levels
84 The stem-loop
Syk antisense ODN at a concentration of 0.2 microM inhibited
85 data indicate the efficacy of stem-loop
Syk antisense ODN for targeting and degrading Syk mRNA and p
86 In addition, stem-loop
Syk antisense ODN inhibited Fc gamma RI and Fc gamma RIIIA-m
87 lexed with cationic liposomes, stem-loop
Syk antisense ODN with phosphorothioate modification exhibit
88 The
Syk antisense ODNs did not change beta-actin mRNA levels and
89 The antisense ODN treatment significantly reduced the clinic
90 The antisense ODN was administered intraventricularly to mic
91 n for efficient gene repair exhibited by
the antisense ODN is its increased accessibility to the non-
92 phate were also significantly reduced by
the antisense ODN treatment.
93 itric oxide synthase was not affected by
the antisense ODN.
94 nimals killed to determine the effect of
the antisense ODN on Kir6.2 mRNA.
95 In the presence of
the antisense ODN, but not sense or scrambled ODNs, the toxi
96 at we have targeted for disruption using
the antisense ODN strategy one that has been of particular i
97 was unaffected in the same rats in which
the antisense ODN effectively knocked-down the KOR as assess
98 Furthermore,
the antisense ODNs to Jak2 and Tyk2 both inhibited the induc
99 as not affected by treatment with any of
the antisense ODNs.
100 These antisense ODNs were then administered three times, on al
101 altered mice and the rats treated with
TLR4 antisense ODN displayed significantly attenuated behavio
102 Injection of
TNF antisense ODN on days 1 through 7 increased the area of
103 Group 2 received a daily injection of
TNF antisense ODN or control on days 5 through 15 post-lesio
104 the day following the last injection of
TNF antisense ODN.
105 control (reverse sense) ODN treatment or
to antisense ODN injections targeted anterior or posterior
106 ry rate of Raf-1 mRNA after cell exposure
to antisense ODNs as the half-life (t1/2 approximately 50 h
107 Moreover, inhibition of MDM2
using antisense ODNs also triggered MM cell apoptosis as evide
108 ture in the target appears to correlate
with antisense ODN efficacy, but such that more effective ant
109 increase was abolished by pretreatment
with antisense ODN.
110 Transduction
with antisense ODN targeting CD80 or CD86mRNA is a feasible a
111 completely abolished by prior treatment
with antisense ODN, which had no effect on its own.
112 Compared
with antisense ODNs targeting of individual oncogenes, downre
113 NA that are accessible to hybridization
with antisense ODNs.
114 to acetylcholine, whereas pretreatment
with antisense ODNs blocked this effect.
115 Embryos treated
with antisense ODNs cleave normally and initiate gastrulation
116 or effects following systemic treatment
with antisense ODNs plus doxorubicin in nude mice bearing hum