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1 irus - its ability to enter the nucleus of a nondividing cell.
2 to stabilize the active form of a gene in a nondividing cell.
3 on factor binding may be a characteristic of nondividing cells.
4 eplicates only in terminally differentiated, nondividing cells.
5 d more sensitive to VEGF(121)/rGel than were nondividing cells.
6 enes that effectively kill both dividing and nondividing cells.
7 resuscitate from starvation, leaving intact nondividing cells.
8 required for maintaining a silenced state in nondividing cells.
9 egrating their viral DNA into the genomes of nondividing cells.
10 owed by rapid apoptosis in both dividing and nondividing cells.
11 l for virus replication in both dividing and nondividing cells.
12 ed gene delivery and long-term expression in nondividing cells.
13 st, adenoviruses (Ad) can efficiently infect nondividing cells.
14 is essential for the productive infection of nondividing cells.
15 a gene therapy vector to transfer genes into nondividing cells.
16 virus (SNV), which are capable of infecting nondividing cells.
17 transfer systems for delivery of genes into nondividing cells.
18 ites, which are highly toxic to dividing and nondividing cells.
19 -modified HIV-1 particles are able to infect nondividing cells.
20 t gene delivery to a variety of dividing and nondividing cells.
21 en pathway for generating mutant proteins in nondividing cells.
22 ead to viral- and lipid-free transfection of nondividing cells.
23 1-derived vectors is their ability to infect nondividing cells.
24 cells and their isolated lipids relative to nondividing cells.
25 essory gene expression in either dividing or nondividing cells.
26 entivirus vectors can transduce dividing and nondividing cells.
27 mited in certain cell types, particularly in nondividing cells.
28 is defined as the age-dependent viability of nondividing cells.
29 ence of antigenic stimulation and persist as nondividing cells.
30 f high-level gene transfer and expression in nondividing cells.
31 port of the viral genome into the nucleus of nondividing cells.
32 ency virus type 1 (HIV-1) that can transduce nondividing cells.
33 at high titers and infect both dividing and nondividing cells.
34 gene transfer agents because they can infect nondividing cells.
35 type 1 (HIV-1) vectors to deliver genes into nondividing cells.
36 etrotransposons and retroviruses that infect nondividing cells.
37 nescence associated with the accumulation of nondividing cells.
38 e only types of mismatches that can arise in nondividing cells.
39 in cells undergoing DNA replication than in nondividing cells.
40 ly been thought of as metabolically dormant, nondividing cells.
41 s is limited by their inability to transduce nondividing cells.
42 play an important role in viral infection of nondividing cells.
43 essing indels caused by NHEJ in dividing and nondividing cells.
44 cidification and extensive protein damage in nondividing cells.
45 for MMR in helping create new phenotypes in nondividing cells.
46 gesting that R2 is able to retrotranspose in nondividing cells.
47 ds to HIV-1 CA, regulates HIV-1 infection of nondividing cells.
48 mage and genomic instability during aging in nondividing cells.
49 t-proliferating progenitor-like cells and to nondividing cells.
50 ) CA abrogate the ability of HIV-1 to infect nondividing cells.
51 ich binds to HIV-1 CA, on HIV-1 infection of nondividing cells.
52 es can enter the nuclei of both dividing and nondividing cells.
53 , allowing examination of HIV-1 infection of nondividing cells.
54 homologous recombination is not essential in nondividing cells.
55 mine effects of growth factor stimulation on nondividing cells.
56 Rad17, and Chk1 protein expression in these nondividing cells.
57 ficiency virus, by their inability to infect nondividing cells.
58 different half-lives in rapidly dividing or nondividing cells.
59 cript abundance limits retrotransposition in nondividing cells.
60 s prevents replication of diverse viruses in nondividing cells.
61 TDP1), repairs single-stranded DNA breaks in nondividing cells.
62 yeast by measuring the long-term survival of nondividing cells.
63 n of these foci was seen most prominently in nondividing cells.
64 eine also inhibits efficient transduction of nondividing cells.
65 curing of [PSI+] cells in both dividing and nondividing cells.
66 NA-PKcs) that are expressed predominately in nondividing cells.
67 cells are more vulnerable to apoptosis than nondividing cells.
68 on of human immunodeficiency virus type 1 in nondividing cells.
69 ween HIV and MLV in the ability to transduce nondividing cells.
70 uses is their ability to productively infect nondividing cells.
71 protein (CA) in the infectious phenotype in nondividing cells.
72 MLV) loses the ability to efficiently infect nondividing cells.
73 ility to stably integrate into the genome of nondividing cells.
74 d maintenance of phosphoinositide balance in nondividing cells.
75 stricted infection of this chimeric virus in nondividing cells.
76 rabidopsis culture cells than in stationary, nondividing cells.
77 ave the potential to change the phenotype of nondividing cells.
78 ion, thereby facilitating HIV replication in nondividing cells.
79 lls (HSCs) due to their ability to transduce nondividing cells.
80 sistence may be adequate for gene therapy of nondividing cells, a very high MOI or improvements in ba
81 phase) mutagenesis is a phenomenon by which nondividing cells acquire beneficial mutations as a resp
84 77 impairs viral infectivity in dividing and nondividing cells, although the assembly of these Ser mu
85 vectors that express the transduced gene in nondividing cells and (b) increasing the frequency of st
86 a demonstrate essential roles for cohesin in nondividing cells and also introduce a powerful tool by
87 ty of adenoviruses to transduce dividing and nondividing cells and because of their high transduction
88 ribute to the formation of tumors arising in nondividing cells and could also contribute to mutagenes
89 in that is critical for HIV-1 replication in nondividing cells and induces cell cycle arrest and apop
90 eting of the viral preintegration complex in nondividing cells and induces G(2) cell cycle arrest in
92 herefore is linked to higher virus yields in nondividing cells and potentially higher virulence in ex
93 This increased the efficiency of infecting nondividing cells and was sufficient to endow the virus
95 DNA, (iii) enabling analysis in individual, nondividing cells, and (iv) uncoupling other potential f
96 n E1A that preclude efficient replication in nondividing cells, and a deletion of the E3 genes which
97 The extrachromosomal circle is maintained in nondividing cells, and a gene located on such a circle c
98 cantly impaired (1,000-fold lower titers) in nondividing cells, and plaque-forming ability was severe
99 heir low pathogenicity, ability to transduce nondividing cells, and potential for long-term gene expr
100 or that determines retrovirus infectivity in nondividing cells, and several mutations in HIV type 1 (
101 5-Aza-2'-deoxycytidine-treated and untreated nondividing cells, and their mRNA transcripts were down-
104 andomly into the genome of both dividing and nondividing cells as determined by fluorescence in situ
105 t reversibility is not a passive property of nondividing cells, because enforced cell cycle arrest fo
106 /1107) that prevent efficient replication in nondividing cells but allow replication in dividing canc
107 t is unclear how repeats are destabilized in nondividing cells, but it cannot involve DNA replication
108 sed lentiviral vectors efficiently transduce nondividing cells, but present complex safety concerns.
109 ved in the nuclear import of viral genome in nondividing cells, but the mechanism remains poorly unde
110 This modification facilitates infection of nondividing cells by allowing for the recruitment of the
112 ein 1 (SAMHD1) inhibits HIV-1 replication in nondividing cells by reducing the intracellular dNTP poo
113 AMHD1), a dNTPase, prevents the infection of nondividing cells by retroviruses, including HIV, by dep
115 ke the gammaretroviruses, are able to infect nondividing cells by transiting through nuclear pores to
116 s for efficient transduction of dividing and nondividing cells by vector particles based on FIV, a se
117 nds of mitochondria which replicate, even in nondividing cells, by means of a relatively error-prone
118 cells and during transcription initiation in nondividing cells can culminate in genome instability.
119 ncy virus (FIV) is a lentivirus that infects nondividing cells, causes progressive CD4(+) T-cell depl
120 se transcription complex into the nucleus of nondividing cells, cellular differentiation including ce
121 omal rearrangement frequency during aging of nondividing cells compared with that generated during th
123 w that the stability of gene expression in a nondividing cell could be caused by the local entrapment
124 The capacity of mutant virions to transduce nondividing cells could help to elucidate incompletely u
125 viral vectors to deliver genes in vivo into nondividing cells could increase the applicability of re
127 as human immunodeficiency virus, that infect nondividing cells generate integration precursors that m
128 ause they achieve efficient integration into nondividing cell genomes and successful long-term expres
129 mine whether DNA nanoparticles can transfect nondividing cells, growth-arrested neuroblastoma and hep
130 Compared with proliferating hRPE cells, the nondividing cells had lower intracellular GSH, GSSG, and
131 r mitotic spindles along the tubule, whereas nondividing cells improperly position their centrosomes.
133 Lat1 is also a limiting longevity factor in nondividing cells in that overexpressing Lat1 extends ce
137 ts demonstrate the efficient transduction of nondividing cells in vitro by a multiply attenuated FIV
141 but was independent of MinC and continued in nondividing cells in which FtsZ function was inhibited.
145 rus type 1 (HIV-1) infection of dividing and nondividing cells involves regulatory interactions with
146 human immunodeficiency virus (HIV) to infect nondividing cells is a fundamental property by which HIV
147 act nuclear envelope and productively infect nondividing cells is a salient feature of human immunode
149 deficiency virus type 1 (HIV-1) to transduce nondividing cells is key to infecting terminally differe
150 the predominant repeat-mediated mutation in nondividing cells is large-scale deletions encompassing
152 raries via iterative retroviral infection of nondividing cells led to the identification of a novel v
153 DNA repair is especially understudied in nondividing cells like neurons, limiting the efficiency
154 re efficient than MLV vectors at transducing nondividing cell lines as well as human CD34(+) cells an
155 egrate into the host genome and to transduce nondividing cells makes them attractive as vehicles for
156 curs on a largely unmethylated genome and in nondividing cells, making it a highly informative model
157 proaches capable of transducing dividing and nondividing cells may improve the durability of treatmen
158 -long terminal repeat circle accumulation in nondividing cell nuclei was also equivalent to that of L
160 rt models in which UV-induced mutagenesis in nondividing cells occurs during the Pol zeta-dependent f
161 al origin revealed that only differentiated, nondividing cells of the epidermis expressed interferon-
163 Of all mutations originating de novo in nondividing cells, only those in the transcribed (noncod
164 itially reported to function specifically in nondividing cells, other recently identified sequences a
166 ses of sensitivity to DNA-damaging agents in nondividing cell populations, such as cochlear hair and
167 rigin of double nonsilent CpG transitions in nondividing cells predicts a significant excess of the h
168 nodeficiency virus type 1 (HIV-1) can infect nondividing cells productively because the nuclear impor
171 ize that inhibition of retrotransposition in nondividing cells protects somatic tissues from accumula
172 splice variants are expressed highly only in nondividing cells, quiescent cells would be afforded a m
173 feration could reduce the number of residual nondividing cells remaining after imatinib treatment.
174 n a replication strand-independent manner in nondividing cells, resulting in either fully wild-type o
176 abolishes the ability of the virus to infect nondividing cells, serving as a tool to examine cell cyc
177 ts genomic content, followed by entry into a nondividing cell state to protect DNA integrity and ensu
178 ucleoprotein complex facilitate infection of nondividing cells such as macrophages and quiescent T ly
179 virus type 1 (HIV-1) is capable of infecting nondividing cells such as macrophages because the viral
180 gammaretroviruses by their ability to infect nondividing cells such as macrophages, an important vira
183 lity to efficiently infect both dividing and nondividing cells, such as activated T cells and macroph
184 mutations of vpr are unable to replicate in nondividing cells, such as macaque monocyte-derived macr
185 unodeficiency virus type 1 is able to infect nondividing cells, such as macrophages, and the viral Vp
187 ity differ dramatically between dividing and nondividing cells, suggesting that distinct repeat-media
188 ormation, especially during the infection of nondividing cells, suggesting that the function of small
189 iral capsids restrict HIV-1 more potently in nondividing cells than in dividing cells, thus rendering
190 nsgene, we demonstrate that differentiating, nondividing cells that express MEK1 stimulate adjacent t
191 -specific restriction of HIV-1 CA mutants in nondividing cells that is dependent on CypA-CA interacti
193 g mitosis, similar to retroviruses infecting nondividing cells, the cDNA produced must be translocate
194 of these vectors to infect both dividing and nondividing cells, their use as a therapeutic tool for t
195 Because lentiviruses are able to infect nondividing cells, these viruses might be utilized in ge
199 diated nuclear translocation of MoMLV DNA in nondividing cells was not sufficient for stable transduc
200 mammalian cell types, including primary and nondividing cells, we are developing lentiviral short ha
201 avel the mechanisms of repeat instability in nondividing cells, we created an experimental system to
202 y of HIV-based vectors to deliver genes into nondividing cells, we have generated replication-defecti
203 s persistence in myofibers and perhaps other nondividing cells whereby cells that survive infection c
204 lation of superoxide-dependent DNA damage in nondividing cells, which induces error-prone DNA repair
205 replicated productively in both dividing and nondividing cells, while viruses with a mutation at IN-V
206 ith the cell cycle, typically resulting in a nondividing cell with a unique differentiated morphology
207 ating vector in directing gene expression in nondividing cells, with the proper choice of an internal