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1 ences would allow precise means for specific genetic intervention.
2 es canonically would allow precise means for genetic intervention.
3 ntion,(1) ushering in a new era of precision genetic intervention.
4 K, or NF-kappaB using pharmacological and/or genetic interventions.
5 tive models and the possibility of precision genetic interventions.
6 llular vectors, as well as pharmacologic and genetic interventions.
7 y the pharmacological and microglia-specific genetic interventions.
8 d CD4 T cells could potentially be used as a genetic intervention against both R5- and X4-tropic HIV-
9 d CD4 T cells could potentially be used as a genetic intervention against both R5- and X4-tropic HIV-
10 transcriptional regulatory-network analyses, genetic interventions and chromatin immunoprecipitation
11 elds in various species will require renewed genetic interventions and dramatic improvement of agricu
12 igrostriatal neurons was examined by using a genetic intervention approach.
13 dustrialized societies unless novel means of genetic intervention are developed.
14 celerate the clinical translatability of CNS genetic interventions are addressed, and we present less
15 nly in developing and mastering endovascular genetic interventions but also in assessing the success
16 ts that quantitative behaviour and precision genetic intervention can be used to manipulate discrete
17  human study designed to determine whether a genetic intervention can prolong the survival of T cells
18                              Muscle-specific genetic interventions can induce systemic effects indire
19 ially reversible, and both environmental and genetic interventions can result in the rejuvenation of
20 tivity ratio by multiple pharmacological and genetic interventions confirms that high ERK/p38 ratio f
21                                              Genetic intervention during mitosis prevented both appre
22  diseases has made the design of therapeutic genetic interventions feasible in these clinical entitie
23  for studying brain development and devising genetic intervention for severe developmental diseases.
24                                              Genetic intervention for the therapy of human disease ha
25                                     Devising genetic interventions for desired cellular phenotypes re
26  (ASOs) have shown promise as individualized genetic interventions for rare genetic diseases.
27 ve Cas9 (dCas9) and offers an alternative to genetic interventions for studying pervasive antisense t
28 ansiently modify lymphocytes, without direct genetic intervention, for adoptive transfer.
29 at mitochondrial disease, both metabolic and genetic interventions have been attempted.
30                                      Several genetic interventions have been found to ameliorate old
31 e 1 (HSV-1) plasmid vectors have promise for genetic intervention in the brain, but several problems
32                                The future of genetic interventions in humans critically depends on th
33 s to develop adenovirus vectors suitable for genetic interventions in humans have identified three ma
34 e the potential to co-limit growth, multiple genetic interventions in source and sink tissues, plus t
35                        In our previous work, genetic interventions in the Lama2(Dy-w) mouse model for
36  testing the efficacy of pharmacological and genetic interventions in vivo.
37                                              Genetic intervention inducing over-enlargement of myofib
38                                              Genetic intervention is increasingly being explored as a
39 be used to screen pharmacological as well as genetic interventions more rapidly for positive effects
40                                 Surgical and genetic interventions of sensory circuits demonstrate th
41 d fluid flow, as well as pharmacological and genetic interventions of specific proteins.
42                                              Genetic interventions on HIF/PHD pathways reveal multipl
43 etween human and animal studies by exploring genetic interventions on network activity in human brain
44                  We found that both of these genetic interventions produced a several-fold increase i
45                                              Genetic interventions promoting longevity are usually qu
46 y toxic NIR light, labeling without need for genetic intervention, rapid kinetics, remote subsurface
47 eted lysine acylation in cells often rely on genetic intervention, recruitment of endogenous acylatio
48  either by Brefeldin A (BFA) treatment or by genetic intervention results in increased intracellular
49                          Pharmacological and genetic interventions revealed that insulin regulates GL
50 mbers by pharmacological (with dithizone) or genetic intervention (SOX9 flox/flox Villin cre+/- mice)
51 bitor-resistant PR was blocked, showing that genetic intervention strategies based on td PRs can be e
52                                       Hence, genetic intervention strategies based on trans-dominant
53  was also observed with a microglia-specific genetic intervention targeting the N-GAPDH cascade.
54                          Pharmacological and genetic interventions targeting several key elements of
55 s was controlled for >3 years after a single genetic intervention that led to persistent production o
56                           Herein, we show by genetic intervention that prostaglandin E(2) in the spin
57              Our study demonstrates a simple genetic intervention that rescues the TIN2-DC disease ph
58                                            A genetic intervention that specifically decreases NADH le
59                                              Genetic interventions that accelerate or retard aging in
60 ing with males or inducing egg retention via genetic interventions that block egg-laying can strongly
61 calable platforms to systematically identify genetic interventions that boost the function of old NSC
62                                 Accordingly, genetic interventions that increase cytoplasmic Mn(2+) l
63                                     Overall, genetic interventions that promote ALMR exopher producti
64 essary for membrane and cellular repair, and genetic interventions that restore MLRs to normal cellul
65  associated with expanded uterus lengths and genetic interventions that suppress ALMR exopher product
66     Consistent with this, pharmacological or genetic interventions that target dysregulated ion chann
67 n beta(s) mice was blunted by immunologic or genetic interventions that target tissue factor, endothe
68 ts provide the ability to tailor the mode of genetic intervention to specific aspects of a disease st
69 x (PFC) neurons and used pharmacological and genetic interventions to block connexin-mediated hemicha
70 advanced techniques -- ranging from targeted genetic interventions to brain imaging -- that are rapid
71                            We designed three genetic interventions to manipulate the actions of gluco
72  signaling pathways, and pharmacological and genetic interventions to rescue arrhythmias in cIRS2-KO
73            The potential of such a molecular genetic intervention was examined by using the Cre-loxP
74                    Using pharmacological and genetic interventions, we found that NF-kB and retinoic
75          Using a combination of chemical and genetic interventions, we identified that HS modulates t
76 viduals and potentially serve as a molecular genetic intervention which can contribute to the treatme
77 rge-scale nonlinear kinetic models to devise genetic interventions while accounting for the network e
78 ithfully recapitulate the effect of multiple genetic interventions would be transformative in our abi