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1 sustaining complexes normally concentrate in nuclear foci.
2  the accumulation of gamma-H2AX and 53BP1 in nuclear foci.
3 located in proximity to H3 K79 dimethylation nuclear foci.
4 ther viral DNA replication proteins in large nuclear foci.
5 ination of FANCD2 and the assembly of FANCD2 nuclear foci.
6 ted, SSBP2 remains associated with E1B55K in nuclear foci.
7 L1 that is sequestered in the CUG-containing nuclear foci.
8 domain also promotes ssDNA but fails to form nuclear foci.
9 e modifier (SUMO)-1 conjugates into distinct nuclear foci.
10 ith PCNA (early) and RPA2 (late) in discrete nuclear foci.
11        H2AX became phosphorylated and formed nuclear foci.
12 d NBS1) underwent phosphorylation and formed nuclear foci.
13  diverse membrane compartments as well as in nuclear foci.
14 on and the formation of gamma-H2AX and 53BP1 nuclear foci.
15 FANCD2, targeting FANCD2 to BRCA1-containing nuclear foci.
16 videnced by induction of gammaH2AX and 53BP1 nuclear foci.
17 ction, and localized the protein to punctate nuclear foci.
18 ed activation of caspase 3, and reduction of nuclear foci.
19 h SMRT results in colocalization at discrete nuclear foci.
20 ese proteins colocalized to several distinct nuclear foci.
21                  AtSIZ1-GFP was localized to nuclear foci.
22 and the assembly of damage-associated FANCD2 nuclear foci.
23 PA and Mre11 to discrete detergent-resistant nuclear foci.
24 n the nucleoplasm, R288P Maf was enriched in nuclear foci.
25 th paraspeckle protein NonO to form residual nuclear foci.
26 as well as other interaction partners to the nuclear foci.
27  FANCD2, resulting in the assembly of FANCD2 nuclear foci.
28  association with ionizing radiation-induced nuclear foci.
29 .nibrin complex relocalizes to form punctate nuclear foci.
30  pathogenic RNA molecules that accumulate in nuclear foci.
31 zes with BRCA1 and RAD51 in S-phase-specific nuclear foci.
32  radiation (IR), 53BP1 localized at discreet nuclear foci.
33  resulting in targeting of this protein into nuclear foci.
34 lization pattern and is enriched in specific nuclear foci.
35                p220 is localized to discrete nuclear foci.
36 ludes the sequestration of many factors into nuclear foci.
37 nd photoperiodic pathways in transcriptional nuclear foci.
38 DR machinery colocalized with LT in distinct nuclear foci.
39 -Thr68 phosphorylation and accumulation into nuclear foci.
40            The pathogenic RNA is retained in nuclear foci.
41 DDR pathways accumulate in MCPyV LT-positive nuclear foci.
42 d protein phosphorylation that generates sub-nuclear foci.
43 arge aggregate-like assemblies visualized as nuclear foci.
44  sequesters PTIP away from radiation-induced nuclear foci.
45  factors, resulting in formation of discrete nuclear foci.
46 rotein, these activities became localized to nuclear foci.
47 A to form spontaneous and DNA damage-induced nuclear foci.
48 P1- and phospho-H2AX (gamma-H2AX)-containing nuclear foci, a marker of DNA damage.
49 ence of BRCA1, FANCJ colocalizes with RPA in nuclear foci after DNA damage.
50 uired for recruitment of repair factors into nuclear foci after DNA damage.
51 irect immunofluorescence and formed discrete nuclear foci after exposure to IR, UV radiation, and hyd
52 e, does not support localization of Rad51 to nuclear foci after exposure to UV or treatment with ioni
53 xth, FANCD2, which colocalizes with BRCA1 in nuclear foci after genotoxic stress.
54 RPA protein inhibited the formation of RAD51 nuclear foci after hydroxyurea-induced replication stall
55                   pol mu also forms discrete nuclear foci after IR, and these foci are largely coinci
56 uired for the assembly or stability of XRCC1 nuclear foci after oxidative DNA damage and suggest that
57 ein XRCC1 is rapidly assembled into discrete nuclear foci after oxidative DNA damage at sites of poly
58 efective for the formation of ATR-containing nuclear foci after UV irradiation, suggesting that hMCM7
59 otifs are also required for Polkappa to form nuclear foci after UV radiation.
60 the accumulation of replication protein A in nuclear foci, an indication that Vpr likely induces stal
61  damage response factors Rfa1 and Mre11 into nuclear foci and activation of the Rad53 DNA damage chec
62 ted region (3'-UTR) transcripts aggregate in nuclear foci and are thought to impose dominant-negative
63 ocalizes with ARGONAUTE 4 (AGO4) in punctate nuclear foci and binds AGO4 and RNA transcripts.
64 odes a zinc finger protein that localizes to nuclear foci and binds the promoters of let-60/RAS, lin-
65 scopy-based screening for proteins that form nuclear foci and characterized their localizations using
66            Phosphorylated FANCE assembles in nuclear foci and colocalizes with FANCD2.
67                      Mms22 forms spontaneous nuclear foci and colocalizes with Rad22 in cells treated
68      The toxic RNA typically aggregates into nuclear foci and contributes to disease pathogenesis.
69 olongs the resolution of gammaH2AX and Rad51 nuclear foci and delays DNA repair.
70 ired for the recruitment of p53 into MLL-ELL nuclear foci and is both necessary and sufficient for th
71 ification on H2AK15ub, pUbT12 accumulates in nuclear foci and is increased upon DNA damage.
72                          ATRX accumulates in nuclear foci and is required for therapy-induced senesce
73     This (iCUG)480 transcript accumulates in nuclear foci and its expression leads to muscle wasting
74                  The localization of TREX in nuclear foci and its loading on piRNA precursor transcri
75 ed (ATR) kinase and poleta accumulation into nuclear foci and localization to individual telomeres, c
76                                 TopBP1 forms nuclear foci and localizes to the sites of DNA damage or
77                           This complex forms nuclear foci and may be a sensor of double-strand breaks
78 inhibition and DNA damage by relocalizing to nuclear foci and physically associating with CCT, sugges
79 ral papillomavirus types localize to defined nuclear foci and result in growth suppression of the hos
80             Moreover, recruitment of Ddc2 to nuclear foci and subsequent activation of the Rad53 kina
81 chromatin-bound BRCA2 colocalizes with BCCIP nuclear foci and that most radiation-induced RAD51 foci
82  the BLM helicase activity but abolished BLM nuclear foci and the association of BLM with condensed D
83 onstrate that Sall1 is localized to discrete nuclear foci and this localization depends on the N-term
84 R clones could form DNA-damage-induced RAD51 nuclear foci and were able to limit genotoxin-induced ge
85 east cancer susceptibility protein 1 (BRCA1) nuclear foci, and a C-terminal domain is required for Vp
86 ation during the cell cycle, localization to nuclear foci, and interaction with Brca1 and Rad51.
87  stress, Mex67 does not localize to the Mlp1 nuclear foci, and its association with Nab2 complexes is
88                  Most Hd protein is found in nuclear foci, and some may traverse the nuclear envelope
89 scle nucleoplasm because of sequestration in nuclear foci, and the associated splicing defects are re
90 lar proteins are present in E1-E2-containing nuclear foci, and the viral origin of replication is req
91 d protein RAP80 recruits BRCA1 to postdamage nuclear foci, and these chromatin structures then restri
92 gamma-H2AX and 53BP1 (p53 binding protein 1) nuclear foci, and this induction was heightened in FA-de
93 tion is a critical event required for Fancd2 nuclear foci assembly, release from chromatin, and funct
94 5) phospho-p53, BLM, and RAD51 colocalize in nuclear foci at sites likely to contain DNA replication
95    Chk2 phosphorylated at Thr-68 is found in nuclear foci at sites of DNA damage (1).
96 lation on Ser(139) (gamma-H2AX), which forms nuclear foci at sites of DNA damage.
97 tributes in cells from cytoplasm to discrete nuclear foci at sites of DNA double-strand breaks.
98 horylated histone H2AX (gamma-H2AX) in large nuclear foci at sites of stalled replication forks.
99 e DNA double-strand break (DSB) repair, form nuclear foci at the Ch region in the G1 phase of the cel
100 reatment and co-localizes with H2AX, forming nuclear foci at the site of DNA damage.
101 response to DNA damage, BRCA1 relocalizes to nuclear foci at the sites of DNA lesions.
102 lized with RNA polymerase II (RNA Pol II) in nuclear foci, bound to histone H2B, and deubiquitylated
103 ted ATM, hypoxia-activated ATM does not form nuclear foci but is instead diffuse throughout the nucle
104 CA1 interact and co-localize within discrete nuclear foci but separate after gamma irradiation.
105  finger (UBZ) domain directs human WRNIP1 to nuclear foci, but the functional significance of its pre
106           A significant fraction of the hTDG nuclear foci co-localize with hRad9 foci in cells treate
107         A significant fraction of the hNEIL1 nuclear foci co-localize with hRad9 foci in hydrogen per
108                          We find that FANCD2 nuclear foci colocalize with telomeres and PML bodies in
109 f the FANCD2 protein and formation of FANCD2 nuclear foci confirmed the activation of the pathway by
110 lectrophoresis or by formation of gamma-H2AX nuclear foci, considered the most sensitive assay for DN
111 2 to 1%) contained large, intensely staining nuclear foci consistent with productive, replicative inf
112 lowed us to visualize replication factories, nuclear foci consisting of replication proteins where th
113                     MCPyV sT translocates to nuclear foci containing actively replicating viral DNA,
114 resulting in the redistribution of FANCD2 to nuclear foci containing BRCA1.
115 e downstream FANCD2 protein and targeting to nuclear foci containing BRCA1.
116  1 (HSV-1) induces the formation of discrete nuclear foci containing cellular chaperone proteins, pro
117 ) cell cycle arrest through the induction of nuclear foci containing gamma-H2AX and BRCA1.
118  Finally, we find that c-Jun associates with nuclear foci containing gammaH2AX and ATM following irra
119 histone 2A variant X (H2AX) and formation of nuclear foci containing H2AX and breast cancer susceptib
120 ells assemble the amyloid bodies (A-bodies), nuclear foci containing heterogeneous proteins with amyl
121 or mitomycin C (MMC) led to the formation of nuclear foci containing phosphorylated Nbs1.
122 f activated forms of ATM and Chk2 as well as nuclear foci containing phosphorylated substrates of ATM
123 uorescent protein-polkappa fusion protein to nuclear foci containing sites of active DNA synthesis in
124 xogenous pri-miRNAs unexpectedly localize to nuclear foci containing splicing factor SC35; yet these
125                                              Nuclear foci corresponding to epigenetic marks as well a
126 ly expressed RGS12TS-S localized to discrete nuclear foci (dots), a characteristic of various tumor s
127 in response to DNA damage and is targeted to nuclear foci (dots).
128 nally, ATR activation and its recruitment to nuclear foci during cisplatin treatment were attenuated,
129 d that DHX9 partially colocalized with SM in nuclear foci during EBV lytic replication.
130  DNA processes, Mms22p localizes to discrete nuclear foci, even in the absence of etoposide or its bi
131 quitination of FANCD2 or its localization to nuclear foci following DNA damage.
132 CA1 function, such as BRCA1 association with nuclear foci following DNA damage.
133 is domain of ATM is required for ATM to form nuclear foci following exposure to ionizing radiation.
134 endent BRCA2 S3291 phosphorylation and MRE11 nuclear foci formation and can be rescued by inhibition
135     Disruption of BTB dimerization abrogates nuclear foci formation and telomeric localization of not
136  to repair double strand breaks is inducible nuclear foci formation at the sites of damage.
137 placed by phenylalanine, exhibit compromised nuclear foci formation in response to IR.
138                Furthermore, IR-induced Rad52 nuclear foci formation is markedly suppressed by the exp
139                       Monoubiquitination and nuclear foci formation of FANCD2 are critical steps of t
140                   The monoubiquitination and nuclear foci formation of FANCD2 are essential for the f
141 CC complex formation, monoubiquitination and nuclear foci formation of FANCD2, and mitomycin C resist
142 d PSMB3) inhibited monoubiquitination and/or nuclear foci formation of FANCD2, whereas depletion of D
143 ibitors, whereas ATM autophosphorylation and nuclear foci formation of gammaH2AX, MDC1, and RPA were
144 e show that RNF8 controls DNA damage-induced nuclear foci formation of PTIP, which in turn regulates
145 (IR) induces the phosphorylation of NBS1 and nuclear foci formation of the complex.
146 evec, radiation-induced Rad51 expression and nuclear foci formation were reduced.
147 romosomal aberrations and elevated gammaH2AX nuclear foci formation.
148 ge-inducible FANCD2/I monoubiquitination and nuclear foci formation.
149 rthermore, ATR nuclear foci overlap with the nuclear foci formed by BRCA1.
150 t also resulted in the colocalization of the nuclear foci formed with RecQ4 and xeroderma pigmentosum
151 s also resulted in the colocalization of the nuclear foci formed with the two complexes.
152      Two compounds that reduce and/or remove nuclear foci have been identified, Ro 31-8220 and chromo
153 oteins at the nuclear periphery, or in other nuclear foci, have also been identified.
154    We found that UBR5 forms damage-inducible nuclear foci in a manner dependent on the PRC1 component
155 ow that UvsC(RAD51) forms DNA-damage-induced nuclear foci in a manner that requires SepB function.
156 anded CUG repeats in vitro, localized to the nuclear foci in both DM1 and DM2.
157 C (G2C4) repeat-expansion RNAs accumulate in nuclear foci in brain.
158 localization of PALB2 and BRCA2 to RPA-bound nuclear foci in cells experiencing replication stress.
159 ulate in MCPyV large T antigen (LT)-positive nuclear foci in cells infected with native MCPyV virions
160  of the complex and induces the formation of nuclear foci in cells on DNA damage.
161 A, is mounted upon the nuclear matrix in sub-nuclear foci in differentiated vertebrate cells, but not
162 otypic assay, based on the identification of nuclear foci in DM patient cell lines using in situ hybr
163 ions of MBNL, MBLL and MBXL co-localize with nuclear foci in DM1 and DM2 cells, suggesting that all t
164 ntiation, but the EXP proteins accumulate in nuclear foci in DM1 cells.
165 e-labeled CAG-repeat oligonucleotides showed nuclear foci in DM2 similar to those seen in DM1.
166  We show that ATR is recruited to IR-induced nuclear foci in G(1) and S phase of the cell cycle, supp
167 e its fly counterpart, hp53 formed prominent nuclear foci in germline cells but cancer-associated p53
168 e also demonstrate that FANCI forms discrete nuclear foci in HeLa cells in the absence or presence of
169  binds BRC repeats and forms BRCA2-dependent nuclear foci in human cells in response to gamma-irradia
170 w that TRIP promotes hPoleta localization to nuclear foci in human cells.
171 related with a significant increase in yH2AX nuclear foci in Mof-deficient MLL-AF9 tumor cells.
172                   BRD4-NUT forms distinctive nuclear foci in patient tumors, which we found correlate
173 36 depletion prevents the formation of BRCA1 nuclear foci in response to DNA damage in breast cancer
174 comes hyperphosphorylated and forms discrete nuclear foci in response to DNA damage.
175         The rapid accumulation of BRCA1 into nuclear foci in response to induction of DNA breaks sugg
176 t phosphorylate p53 in vivo and did not form nuclear foci in response to ionizing radiation.
177 )-phosphorylated form of Chk2 forms distinct nuclear foci in response to ionizing radiation.
178 ernal repeats and is an early participant in nuclear foci in response to IR.
179 cells leads to loss of Rad51 localization to nuclear foci in response to replication arrest, cells la
180 nctionally in human cells and co-localize to nuclear foci in response to replication stress.
181       We found that senataxin forms distinct nuclear foci in S/G(2)-phase human cells and that the nu
182 ed most drastic changes, accumulating in two nuclear foci in the 64- to 1k-cell-stage embryos.
183 mplex chromosome aberrations, and lack Rad51 nuclear foci in the presence of DNA-damaging agents, suc
184 raction enhances the recruitment of 53BP1 to nuclear foci in the S phase, resulting in impaired HR an
185         Moreover, BLM and WRN colocalized to nuclear foci in three human cell lines.
186 localization pattern but also forms distinct nuclear foci in unperturbed growing and G(2)/M-arrested
187 alization of endogenous CBP/p300 proteins to nuclear foci in vivo.
188   Immunostaining shows that RPA localizes to nuclear foci in Vpr-expressing cells.
189                              Fluorescence of nuclear foci increased during the first hour of stimulat
190 processing redistributes GANP from NPCs into nuclear foci indicating that mammalian TREX-2 is associa
191 o the nucleus, and enhances formation of the nuclear foci indicative of recombination sites.
192 dogenous Brca1-Delta11 localizes to discrete nuclear foci indistinguishable from those found in wild-
193  G1, ectopically expressed HDHB localizes in nuclear foci induced by DNA damaging agents and that thi
194 pathways and that ionizing radiation-induced nuclear foci (IRIF) of NFBD1 colocalize with several DNA
195 lian 53BP1, forms ionizing radiation-induced nuclear foci (IRIF).
196  Rad3(ATR), forms ionizing radiation-induced nuclear foci (IRIF).
197            RAD51 and BRCA2 colocalization in nuclear foci is a hallmark of HRR.
198    Accumulation of expanded poly(CUG) RNA in nuclear foci is associated with sequestration of muscleb
199 active tuning of BRCA1 activity, executed in nuclear foci, is important to genome integrity maintenan
200 n that colocalizes with cellular proteins in nuclear foci known as Tax speckled structures (TSS).
201 tein kinase (DMPK) transcripts accumulate in nuclear foci, leading to abnormal regulation of RNA proc
202  completion because these markers persist as nuclear foci long after drug removal.
203 Immunofluorescence staining reveals discrete nuclear foci of ANCO-1 that are distinct from known nucl
204                              CAG25 disperses nuclear foci of CUGexp RNA and reduces the overall burde
205 lve sequestration of RNA binding proteins in nuclear foci of expanded poly(CUG) RNA.
206                                 Formation of nuclear foci of FANCD2 was normal in the BRCA2 mutant CA
207 hat calcitriol induces formation of multiple nuclear foci of heterodimers.
208 nhibitors and ionomycin caused appearance of nuclear foci of NFATc-GFP without electrical stimulation
209        Moreover, we quantified cardiomyocyte nuclear foci of phosphorylated ataxia telangiectasia mut
210                        These markers include nuclear foci of phosphorylated histone H2AX and their co
211 with an increased number of cells exhibiting nuclear foci of phosphorylated histone H2AX as well as a
212                      In addition, UV-induced nuclear foci of the recombination proteins, RAD51 and BR
213       These effects correlate with increased nuclear foci of the single-stranded DNA binding protein
214 o found that these progeroid cells exhibited nuclear foci of xeroderma pigmentosum group A (XPA), a u
215 ey affect neither the assembly of Rad51 into nuclear foci on damaged DNA nor DNA repair by HR.
216      UV-exposed cells did not exhibit FANCD2 nuclear foci once they entered mitosis or when growth-ar
217 ique pattern of subnuclear organization into nuclear foci or dots when expressed endogenously or ecto
218 efects cause mRNAs to accumulate in discrete nuclear foci or dots, in mammalian cells as well as yeas
219 sociation and did not redistribute Poleta to nuclear foci or promote Poleta-PCNA interaction efficien
220  of the expanded repeat (r(GGGGCC)exp) forms nuclear foci or undergoes repeat-associated non-ATG (RAN
221 ll showed diffuse nuclear staining, multiple nuclear foci, or one or two larger bodies confined to th
222 r the initial disruption of ND10 and display nuclear foci, or prereplicative sites, containing the vi
223 cells is a defect in the targeting of SMN to nuclear foci; our results uncover a role for coilin in t
224                             Furthermore, ATR nuclear foci overlap with the nuclear foci formed by BRC
225 produced a large increase of CUG(exp) RNA in nuclear foci, owing to reduced turnover of the CUG(exp)
226 ed by phosphorylation, displays a BRCA1-like nuclear foci pattern and colocalizes with gamma-H2AX.
227 e gamma-H2AX apoptotic ring differs from the nuclear foci patterns observed in response to DNA-damagi
228 ins ZNF423, CEP164, and NPHP10 colocalize to nuclear foci positive for TIP60, known to activate ATM a
229 GGGGCC)n-containing transcripts aggregate in nuclear foci possibly sequestering repeat-binding protei
230 GGCCCC)n-containing transcripts aggregate in nuclear foci, possibly sequestering repeat-binding prote
231              PALB2 colocalizes with BRCA2 in nuclear foci, promotes its localization and stability in
232 romote HR concentrate together with BRCA1 in nuclear foci, RAP80/BRCA1 complexes suppress excessive D
233    We show that the same compound eliminates nuclear foci, reduces MBNL1 protein in the nucleus, affe
234  the removal of DNA damage-induced gammaH2AX nuclear foci, reduces RAD51 nuclear focus formation and
235                             BLM localizes to nuclear foci referred to as PML nuclear bodies (NBs).
236 repeats are more prone to localize to static nuclear foci separate from the chromosomes.
237          We found that RecQ4 formed discrete nuclear foci specifically in response to UV irradiation
238 ointegrator complex) relocalizes to distinct nuclear foci specifically upon exposure of cells to alky
239 lators accomplish this task by forming dense nuclear foci termed insulator bodies that result from th
240  stimulates p53 activity by recruiting it to nuclear foci termed PML nuclear bodies.
241 at endogenous ataxin-7 localizes to discrete nuclear foci that also contain additional components of
242 ion of FANCD2, resulting in its targeting to nuclear foci that also contain BRCA1 and BRCA2/FANCD1, p
243 dependent manner, and rapidly relocalizes to nuclear foci that also contain the MRE11 complex, phosph
244 hat BRD4-NUT and BRD4 colocalize in discrete nuclear foci that are hyperacetylated but transcriptiona
245 radiation, CENP-A is found in multiple small nuclear foci that are mutually exclusive to gammaH2AX as
246   Unmodified forms of Hsp27 are localized in nuclear foci that are outside of replication compartment
247 ure to ionizing radiation, PTIP localizes to nuclear foci that are sites of DNA damage and repair.
248                    Phosphorylated TDP1 forms nuclear foci that co-localize with those of phosphorylat
249 iated protein that forms irradiation-induced nuclear foci that colocalize with gamma-H2AX foci.
250 induced stalled replication forks by forming nuclear foci that colocalize with gamma-H2AX within 2 ho
251 totic cells, detects Cyclin E/Cdk2-dependent nuclear foci that colocalize with nascent histone transc
252 eloping thymocytes, NBS1 and gamma-H2AX form nuclear foci that colocalize with the T cell receptor al
253 aging agents, RAP80 translocates to discrete nuclear foci that colocalize with those of gamma-H2AX.
254 uorescence, pol epsilon appeared in discrete nuclear foci that colocalized with proliferating cell nu
255 inutes after gamma-irradiation, NFBD1 formed nuclear foci that colocalized with the phosphorylated fo
256 ion of BRCA1 and causes its recruitment into nuclear foci that contain DNA repair proteins.
257 microscopy that Tax forms damage-independent nuclear foci that contain DNA-PK, BRCA1, and MDC1.
258  in homologous DNA recombination to distinct nuclear foci that contain HPV genomes and cellular repli
259 RAD50-MRE11-NBS1 complex colocalize to large nuclear foci that contain PCNA when cells are treated wi
260 HR)-type DSB repair, concentrate at distinct nuclear foci that demarcate sites of genome breakage.
261 ospho-ser15-p53 in hydroxyurea-induced RAD51 nuclear foci that may correspond to the sites of presume
262 nd piRNA clusters and colocalize in distinct nuclear foci that overlap with sites of piRNA transcript
263  in Tax that targets the protein to discrete nuclear foci that we have previously termed Tax speckled
264               Unexpectedly, Mlh1-Pms1 formed nuclear foci that, although dependent on Msh2-Msh6 for f
265 ntranuclear relocalization, translocating to nuclear foci thought to represent sites of DNA damage an
266 calization patterns, ranging from bright sub-nuclear foci to almost exclusively cytoplasmic localizat
267 The repeat-bearing transcripts accumulate in nuclear foci, together with proteins in the muscleblind
268                 We show that RAD52 NTD forms nuclear foci upon DNA damage in BRCA-deficient human cel
269 erved that the FBL17 protein is recruited at nuclear foci upon double-strand break induction and colo
270         Anumber of proteins are recruited to nuclear foci upon exposure to double-strand DNA damage,
271 ncy of cells with detectable NR2F2 and NR2C2 nuclear foci varies considerably between ALT+ cell lines
272 RNA polymerase II nor the formation of Hsc70 nuclear foci was observed during infection with the phos
273 mation of green fluorescent protein-polkappa nuclear foci was temporally coincident with checkpoint-m
274   ATM and H2AX phosphorylation and gammaH2AX nuclear foci were also induced by UV-inactivated KSHV, w
275        Furthermore, DNA damage-induced Rad17 nuclear foci were dramatically reduced in Ppp5-deficient
276                                              Nuclear foci were present in all patients with symptomat
277                            HomeoRR and RAD51 nuclear foci were strongly reduced by RAD51(Y315F) phosp
278 ation of the FANCD2 protein, targeting it to nuclear foci where it co-localizes with FANCD1/BRCA2, RA
279 n coincides with PGC-1beta redistribution to nuclear foci where it co-localizes with GCN5.
280 d in response to DNA damage, targeting it to nuclear foci where it preserves chromosomal integrity.
281             This expanded RNA is retained in nuclear foci where it sequesters and induces alterations
282 TR and RPA translocate to punctate, abundant nuclear foci where they continue to colocalize.
283 oteins, targeting these proteins to discrete nuclear foci where they function in DNA repair.
284 2 and FANCI localize in chromatin-associated nuclear foci where they interact with several well-chara
285 ssociated with C/EBPdelta translocation from nuclear foci, where C/EBPdelta co-localizes with p300, t
286 se nuclear distribution to discrete punctate nuclear foci, where E2F1 colocalized with TopBP1 and BRC
287 Ub), signaling its translocation to discrete nuclear foci, where it co-localizes with the central DNA
288 ax with Mxi1, Mad3, or Mad4 were enriched in nuclear foci, whereas complexes formed with Myc were mor
289 ontaining expanded CUG repeats (CUG(exp)) in nuclear foci which sequester several factors regulating
290 ve BPLF1 caused relocalization of Rad18 into nuclear foci, which is consistent with sites of cellular
291 Nbs1 (MRN) complex were found in distinct E2 nuclear foci, which peaked during mid-S phase, indicatin
292 se to DNA damage, Crb2 localizes to distinct nuclear foci, which represent sites of DNA double-strand
293                     GANT61 induced gammaH2AX nuclear foci, while transient transfection of Gli3R show
294  from human cells, and FANCG co-localized in nuclear foci with both BRCA2 and RAD51 following DNA dam
295 phosphorylation, Nab2 and Yra1 colocalize in nuclear foci with Mlp1, a protein involved in mRNA reten
296                Rhino colocalizes to germline nuclear foci with Rai1/DXO-related protein Cuff and the
297           The FANCD2 protein co-localizes in nuclear foci with the BRCA1 protein following DNA damage
298 axia syndrome, and show that these RNAs form nuclear foci with unexpected morphological plasticity th
299                        NFBD1 associates with nuclear foci within minutes following IR, a property sim
300 are identified that reduce GGGGCC-containing nuclear foci without altering overall C9orf72 RNA levels

 
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