ライフサイエンスコーパス: LANA

1 LANA acts on the KSHV terminal repeat (TR) elements to m

2 LANA also drives dysregulated cell growth through a mult

3 LANA also induces chromosomal instability, thus promotin

4 LANA also simultaneously binds to TR DNA and mitotic chr

5 LANA binds cooperatively to the terminal repeat (TR) reg

6 LANA binds to KSHV terminal repeat (TR) DNA and tethers

7 LANA bound with high occupancy to the KSHV genome termin

8 LANA has also been suggested to affect host gene express

9 LANA interactions with high-mobility group AT-hook 1 (HM

10 LANA is essential for tethering the Kaposi's sarcoma-ass

11 LANA is known to activate ERK and limit the activity of

12 LANA is required for tethering of the KSHV episome to th

13 LANA mediates KSHV DNA replication and segregates episom

14 LANA recruited PCNA to the KSHV genome via Bub1 to initi

15 LANA recruitment sites on the KSHV genome inversely corr

16 LANA self-associates to bind KSHV terminal-repeat (TR) D

17 LANA-1 and ANG interaction occurred in the absence of th

18 LANA-1 and ANG interaction with one of the proteins, ann

19 LANA-1, ANG, and p53 colocalized in KSHV-infected cells,

20 LANA-associated TIP60 retained acetyltransferase activit

21 h KSHV latency-associated nuclear antigen 1 (LANA-1) and the host transcriptional repressor KAP1, whi

22 g only latency-associated nuclear antigen 1 (LANA-1) protein, and in KSHV latently infected primary e

23 e KSHV latency-associated nuclear antigen 1 (LANA-1; ORF73) and LANA-1 nuclear puncta.

24 We show that KSHV LANA and MHV-68 LANA proteins bind LBS DNA using strikingly different mo

25 ified topoisomerase IIbeta (TopoIIbeta) as a LANA-interacting protein.

26 iched at the KSHV TR during S phase and in a LANA-dependent manner.

27 TR) region of the viral episome via adjacent LANA binding sites (LBS), but the molecular mechanism by

28 ions is a regulated phenomenon, which allows LANA to interact with cellular components in different c

29 Our data further support a role for Bub1 and LANA in PCNA-mediated cellular DNA replication processes

30 Mdm2 in high-molecular-weight fractions, and LANA-1, p53, and Mdm2 also coimmunoprecipitated with ANG

31 he classic histological features of MCD, and LANA-1 immunostaining identified HHV-8-infected plasmabl

32 ciated nuclear antigen 1 (LANA-1; ORF73) and LANA-1 nuclear puncta.

33 nteractions between ANG-LANA-1, ANG-p53, and LANA-1-p53, the induction of p53, p21, and Bax proteins,

34 al cells through the expression of vFLIP and LANA, two KSHV-latent genes that activate the NF-kappaB

35 latent proteins, including vIRF3, vFLIP, and LANA, target the expression, function, and stability of

36 taining analyses, we observed annexin A2-ANG-LANA-1, annexin A2-ANG, and ANG-LANA-1 colocalizations.

37 nexin A2-ANG-LANA-1, annexin A2-ANG, and ANG-LANA-1 colocalizations.

38 G levels, decreased interactions between ANG-LANA-1, ANG-p53, and LANA-1-p53, the induction of p53, p

39 for HHV-8 anti-latent nuclear antigen (anti-LANA) and antilytic antibodies by immunofluorescence ass

40 TIVE-LTC proteins immunoprecipitated by anti-LANA-1 and ANG antibodies identified 28 common cellular

41 ing dependence was derived chiefly from anti-LANA antibodies.

42 -encoded latency-associated nuclear antigen (LANA) disrupts the association of CIITA with the MHC-II

43 of KSHV latency-associated nuclear antigen (LANA) dots, as detected by immunofluorescence microscopy

44 The latency-associated nuclear antigen (LANA) encoded by Kaposi's sarcoma-associated herpesvirus

45 The latency-associated nuclear antigen (LANA) encoded by KSHV plays a key role in regulating a n

46 with the latency-associated nuclear antigen (LANA) encoded by KSHV.

47 inducing latency-associated nuclear antigen (LANA) expression during early stages of infection by tar

48 ing KSHV latency-associated nuclear antigen (LANA) in primary effusion lymphoma (PEL) cell lines and

49 s (KSHV) latency-associated nuclear antigen (LANA) is a 1,162-amino-acid protein that mediates the ma

50 Latency-associated nuclear antigen (LANA) is a conserved gamma-2-herpesvirus protein importa

51 Latency-associated nuclear antigen (LANA) is a conserved Rhadinovirus protein that is necess

52 Latency-associated nuclear antigen (LANA) is a conserved, multifunctional protein encoded by

53 Latency-associated nuclear antigen (LANA) is a multifunctional protein encoded by members of

54 s (KSHV) latency-associated nuclear antigen (LANA) is a multifunctional protein with roles in gene re

55 Latency-associated nuclear antigen (LANA) is central to episomal tethering, replication and

56 Latency-associated nuclear antigen (LANA) is one of the major proteins expressed during late

57 Latency-associated nuclear antigen (LANA) is the most abundantly expressed protein during la

58 KSHV latency-associated nuclear antigen (LANA) mediates persistence of viral episomes in latently

59 The latency-associated nuclear antigen (LANA) of Kaposi sarcoma herpesvirus (KSHV) is mainly loc

60 The latency-associated nuclear antigen (LANA) of the Kaposi's sarcoma-associated herpesvirus (KS

61 xpressed latency-associated nuclear antigen (LANA) of the virus.

62 rescence labeling of latent nuclear antigen (LANA) protein, together with fluorescence in situ RNA hy

63 -encoded latency-associated nuclear antigen (LANA) to repress expression of the major lytic replicati

64 KSHV latency-associated nuclear antigen (LANA) transcription levels rose consistently over the sa

65 pesvirus latency-associated nuclear antigen (LANA)(1-23), human papillomavirus 8 E2, and prototype fo

66 Latency-associated nuclear antigen (LANA), a multifunctional protein expressed by the Kaposi

67 osome by latency associated nuclear antigen (LANA), which binds in the terminal repeat (TR) region of

68 th viral latency-associated nuclear antigen (LANA).

69 pesvirus latency-associated nuclear antigen (LANA).

70 s (KSHV) latency-associated nuclear antigen (LANA).

71 t on the latency-associated nuclear antigen (LANA).

72 CMs, and latency-associated nuclear antigen (LANA).

73 sing its latency-associated nuclear antigen (LANA).

74 tion and latency-associated nuclear antigen (LANA-1) upregulate the multifunctional protein angiogeni

75 ssion of latency-associated nuclear antigen (LANA-1) upregulates the angiogenic multifunctional 123-a

76 abundant latency-associated nuclear antigen, LANA, on the host genome and its impact on host gene exp

77 x vivo responses to the KSHV latent antigens LANA, vFLIP, vCyclin, and Kaposin, with LANA most freque

78 proteins with intrinsic properties, such as LANA, that minimize epitope recognition by CD8(+)T cells

79 ficantly reduced in KSHV-infected as well as LANA-expressing B cells.

80 In addition, authentic LANA binding sites on the KSHV episome in naturally infe

81 es as a scaffold or molecular bridge between LANA and PCNA.

82 es as a scaffold or molecular bridge between LANA and PCNA.

83 ub1 are required for the interaction between LANA and Bub1.

84 hat are required for the interaction between LANA and Bub1.

85 n effect that is exploited during latency by LANA-1-mediated recruitment of the host transcriptional

86 (OR, 11.91, 95% CI: 2.23-63.64) measured by LANA but not lytic antibodies.

87 The downregulation of Bub1 mediated by LANA resulted in chromosomal instability, a hallmark of

88 egulated in latent infection are occupied by LANA at their promoters.

89 erstand the conserved functions performed by LANA homologs, we generated a recombinant MHV68 virus th

90 tein-Barr virus, specific DNA recognition by LANA is highly asymmetric.

91 Candidate cellular LANA binding motifs were identified and assayed for bind

92 By directly binding to cGAS, LANA, and particularly, a cytoplasmic isoform, inhibit t

93 In contrast, LANA rapidly disassociates from episomes during reactiva

94 ized by high-level expression of cytoplasmic LANA and nuclear ORF59, a marker of lytic replication.

95 We confirmed the presence of cytoplasmic LANA in a subset of cells in lytically active multicentr

96 cellular interaction partner of cytoplasmic LANA isoforms.

97 metry analysis demonstrated that cytoplasmic LANA isoforms were full length, containing the N-termina

98 arities in their DNA-binding domains (DBDs), LANA homologs from Kaposi sarcoma-associated herpesvirus

99 nuclear translocation resulted in decreased LANA-1 gene expression and reduced KSHV-infected endothe

100 This suggests that direct LANA binding to promoters is not the prime determinant o

101 lex with its high-affinity viral target DNA, LANA binding site 1 (LBS1), at 2.9 A resolution.

102 The KSHV-encoded LANA protein is multifunctional and promotes both cell g

103 conferred by the binding of the KSHV-encoded LANA protein to the viral terminal repeats (TR).

104 the major viral latency transcripts encoding LANA as well as the viral miRNAs and thus has the potent

105 Here, we have examined LANA interactions with host chromatin on a genome-wide s

106 As expected, LANA mutants with alanine or glutamate substitutions in

107 hyperplasia and lymphoma in mice expressing LANA.

108 HeLa cell nuclear extracts stably expressing LANA and was verified by coimmunoprecipitation analyses

109 h an interaction with LANA which facilitates LANA sequestration away from KSHV episomes during reacti

110 B-cell targets expressing or fed LANA protein were consistently recognized by the clones;

111 in which purified, adenovirus-expressed Flag-LANA protein was incubated with an array displaying 4,19

112 the substitution mutants were deficient for LANA DNA replication and episome maintenance.

113 rf2 association, while Nrf2 is essential for LANA-1 and KAP1 recruitment to the ORF50 promoter and it

114 These studies support a role for LANA in regulating KSHV replication through posttranslat

115 cted B cells with CD4(+)T cells specific for LANA, a protein expressed in all KSHV-infected cells and

116 influenced the expression of the latent gene LANA nor affected KSHV infectivity.

117 substitutions in Kaposi sarcoma herpesvirus LANA and prototype foamy virus chromatin-binding sequenc

118 These host LANA-binding sites are generally found within transcript

119 Understanding how LANA transcription is regulated thus aids our fundamenta

120 However, LANA expression in telomerase immortalized endothelial c

121 o and increased LANA occupancy at identified LANA target promoters in vivo.

122 Since the identified LANA-1- and ANG-interacting common cellular proteins are

123 throughput sequencing (ChIP-Seq) to identify LANA binding sites in the viral and host-cell genomes of

124 In LANA-1-negative TIVE-LTC cells, annexin A2 was detected

125 A significant decrease in LANA-1 expression, an increase in lytic gene expression,

126 exin A2 appeared as punctate nuclear dots in LANA-1-positive TIVE-LTC cells.

127 ion of amino acids 104 to 123 is involved in LANA-1 and p53 interactions.

128 The significance of the methylation in LANA function was examined in both the isolated form and

129 ion between ANG and p53 was also observed in LANA-1-negative cells.

130 the functional role of the positive patch in LANA-mediated episome persistence.

131 TopoIIbeta plays an important role in LANA-dependent latent DNA replication, as addition of el

132 the electrostatic patch exerts a key role in LANA-mediated DNA replication and episome persistence an

133 nternal LANA regions exert critical roles in LANA-mediated DNA replication, segregation, and episome

134 The major arginine methylation site in LANA was mapped to arginine 20.

135 esses multiple viral latent genes, including LANA, vFLIP, vCYC, all viral micro RNAs, and kaposin und

136 ented histone binding in vitro and increased LANA occupancy at identified LANA target promoters in vi

137 Tim depletion inhibited LANA-dependent TR DNA replication and caused the loss of

138 methylation of H3K9 significantly inhibited LANA binding to the histone H3 tail.

139 Our research shows that intact LANA traffics to the cytoplasm of cells undergoing permi

140 This is mediated by two interactions: LANA binds to specific sequences (LBS1 and LBS2) on vira

141 Interestingly, LANA expression ablated RPA1 and RPA2 binding to the cel

142 Interestingly, LANA-1 is crucial for efficient KAP1/Nrf2 association, w

143 ecently showed that deletion of all internal LANA sequences results in highly deficient episome maint

144 Here we assess independent internal LANA regions for effects on episome persistence.

145 These data suggest that internal LANA regions exert critical roles in LANA-mediated DNA r

146 These data indicate that internal LANA sequence exerts a critical effect on its ability to

147 These experiments expand the known LANA-binding proteins to include MHV68 lytic replication

148 ture, we found that apart from the two known LANA binding sites, LBS1 and LBS2, LANA also binds to a

149 KSHV LANA alone can induce the development of B-cell hyperpla

150 EBNA1(ARF) encodes a KSHV LANA-like glutamine- and glutamic acid-rich protein, whe

151 dentifies a novel mechanism utilized by KSHV LANA to deregulate MHC-II gene expression, which is crit

152 its nuclear translocation downregulates KSHV LANA-1 expression and ANG is necessary for KSHV latency,

153 e generated an MHV68 virus that encodes KSHV LANA (kLANA) in place of MHV68 LANA (mLANA) and evaluate

154 19 interactions previously reported in KSHV LANA interaction studies.

155 esulted in no significant difference in KSHV LANA subcellular localization, we found that the methyla

156 Instead, KSHV LANA recruits the host cell DNA replication machinery to

157 While previous studies of KSHV LANA defined interactions with host cell proteins that i

158 We show that KSHV LANA and MHV-68 LANA proteins bind LBS DNA using strikin

159 we report the crystal structure of the KSHV LANA DNA-binding domain (DBD) in complex with its high-a

160 ecombinant MHV68 virus that encodes the KSHV LANA protein in place of the MHV68 LANA homolog.

161 We determined that the KSHV LANA protein is capable of supporting MHV68 latency in a

162 in sequence, structure, and function to KSHV LANA (kLANA), thereby allowing the study of LANA-mediate

163 Similar to KSHV LANA, mLANA broadly associated with mitotic chromosomes

164 posi's sarcoma-associated herpesvirus (KSHV) LANA protein functions in latently infected cells as an

165 posi's sarcoma-associated herpesvirus (KSHV) LANA protein is essential for the replication and mainte

166 Rescue by a larger LANA peptide, LANA(1-32), required second-site mutations

167 During latency, LANA localizes to discrete punctate spots in the nucleus

168 During latency, LANA localizes to the nucleus, where it connects viral a

169 two known LANA binding sites, LBS1 and LBS2, LANA also binds to a novel site, denoted LBS3.

170 ernative mechanism for telomere maintenance, LANA expression had minimal effect on telomere length.

171 We sought to determine if KSHV and MHV68 LANA homologs are functionally interchangeable.

172 encodes KSHV LANA (kLANA) in place of MHV68 LANA (mLANA) and evaluated the virus's capacity to repli

173 We previously demonstrated that MHV68 LANA (mLANA) is required for efficient lytic replication

174 viral proteins that interact with the MHV68 LANA homolog during lytic infection.

175 the KSHV LANA protein in place of the MHV68 LANA homolog.

176 haracteristic subnuclear KSHV microdomains ("LANA speckles"), a hallmark of KSHV latency.

177 ressed viral proteins found in PELs, namely, LANA and viral IRF3 (vIRF3), albeit at lower levels, wit

178 To identify novel LANA protein-cell protein interactions that could contri

179 , these results suggest that activated Nrf2, LANA-1, and KAP1 assemble on the ORF50 promoter in a tem

180 from that of ET domain recognition of NSD3, LANA of herpesvirus, and integrase of MLV, which involve

181 translocation resulted in decreased nuclear LANA-1 and ANG levels, decreased interactions between AN

182 rylation was not dependent on the ability of LANA to drive KSHV-infected cells into S-phase.

183 l sequence exerted effects on the ability of LANA to retain green fluorescent protein (GFP) expressio

184 ression decreased the promoter activities of LANA-regulated genes.

185 r assemblies involve the self-association of LANA into supermolecular spirals.

186 Most surprisingly, the association of LANA to both host and viral DNA is strongly disrupted du

187 s therefore suggests that the association of LANA to chromatin during a productive infection cycle is

188 ur binding assays revealed an association of LANA with NAP1L1 in KSHV-infected cells, which binds thr

189 Thus, H2AX contributes to association of LANA with the TRs, and phosphorylation of H2AX is likely

190 ructure, oligomerization, and DNA binding of LANA have evolved differently to assemble on the TR DNA.

191 n H2AX levels resulted in reduced binding of LANA with KSHV terminal repeats (TRs).

192 enome regulation via a complex consisting of LANA and the H3K9me1/2 histone demethylase JMJD1A/KDM3A.

193 ent sites of the complex, while depletion of LANA expression or overexpression of a KDM3A binding-def

194 D, E, and A proteins, and downregulation of LANA-1 and ANG expression.

195 We show that ectopic expression of LANA can downmodulate IFN-gamma-mediated activation of a

196 Additionally, the expression of LANA in a luciferase promoter reporter assay showed redu

197 We hypothesize that cytoplasmic forms of LANA, whose expression increases during lytic replicatio

198 ytic replication and extends the function of LANA from its role during latency to the lytic replicati

199 onarily conserved and divergent functions of LANA homologs in Rhadinovirus infection and disease.

200 ls and with ANG in 293T cells independent of LANA-1.

201 development of pharmacological inhibitors of LANA E3 ubiquitin ligase activity may allow strategies t

202 ed to the conclusion that the interaction of LANA with RFX proteins interferes with the recruitment o

203 ovel function of the cytoplasmic isoforms of LANA during lytic replication and extends the function o

204 evealed the presence of multiple isoforms of LANA in the cytoplasm of ORF50/RTA-activated Vero cells

205 terminally truncated cytoplasmic isoforms of LANA, resulting from internal translation initiation, ha

206 cell lines and also increases the levels of LANA protein.

207 rnal regions did not reduce the half-life of LANA.

208 or regulation of the nuclear localization of LANA will enhance our understanding of the biology of th

209 Post-translational modification of LANA is important for functional diversification.

210 RFX proteins and that the overexpression of LANA disrupts the association of CIITA with the MHC-II p

211 Further analysis revealed partial overlap of LANA and STAT1 binding sites in several gamma interferon

212 We generated a panel of LANA mutants that included deletions in the large intern

213 The N-terminal region of LANA binds histones H2A and H2B to attach to mitotic chr

214 The specific TopoIIbeta binding region of LANA has been identified to its N terminus and the first

215 Both the N- and C-terminal regions of LANA are essential for episome persistence.

216 N- and C-terminal regions of LANA are sufficient for TR DNA replication.

217 Solution structure of LANA complexes revealed that while kLANA tetramer is int

218 LANA (kLANA), thereby allowing the study of LANA-mediated pathogenesis in mice.

219 0 is important for modulation of a subset of LANA functions and properties of this residue, including

220 Notably, the C terminus of LANA contributed to phosphorylation of H2AX.

221 These results suggest that trafficking of LANA to different subcellular locations is a regulated p

222 program; however, it had a minimal effect on LANA expression and KSHV infectivity.

223 or the controlled nucleation of higher-order LANA oligomers that might contribute to the characterist

224 Rescue by a larger LANA peptide, LANA(1-32), required second-site mutations that are pred

225 We report that PAN RNA promotes LANA-episome disassociation through an interaction with

226 AP1 and the viral latency-associated protein LANA-1 to mediate global lytic gene repression and thus

227 k represents a report of KSHV latent protein LANA and its interactions with AK-B leading to induction

228 an papillomavirus E6 and HIV-1 TAT proteins, LANA did not reduce TIP60 stability.

229 We identified 256 putative LANA binding site peaks with P < 0.01 and overlap in two

230 ed to determine whether they could recognize LANA-expressing cells.

231 assayed for binding to purified recombinant LANA protein in vitro but bound with low affinity compar

232 y-four base pairs are sufficient to regulate LANA transcription in response to the viral RTA protein

233 Annexin A2 colocalized with several LANA-1 punctate spots in KSHV+ body cavity B-cell lympho

234 ion assays from NAP1L1-depleted cells showed LANA-mediated recruitment of NAP1L1 at the terminal repe

235 Presence of NAP1L1 stimulated LANA-mediated DNA replication and persistence of a TR-co

236 ttach to mitotic chromosomes, and C-terminal LANA binds TR DNA and also associates with mitotic chrom

237 o generate a tethering mechanism, N-terminal LANA binds histones H2A/H2B to attach to mitotic chromos

238 These studies confirm that LANA recruits TopoIIbeta at the origins of latent replic

239 These results confirmed that LANA recruitment of NAP1L1 helps in assembling nucleosom

240 Further studies here demonstrate that LANA-1 and ANG colocalize and coimmunoprecipitate in de

241 ammaherpesvirus 68 (MHV68) demonstrated that LANA is important for acute replication, latency establi

242 ide signal amplification, we determined that LANA localizes to the cytoplasm in different cell types

243 lass II-matched CD4(+)T cells and found that LANA-specific T cells restricted to different epitopes r

244 Here, we report that LANA is subject to arginine methylation by protein argin

245 Here we report that LANA promoted the induction of chromosomal instability a

246 Combined, ChIP-seq and RNA-seq reveal that LANA accumulates at active gene promoters that harbor sp

247 nd Gene Ontogeny (GO) analysis revealed that LANA binds to genes within the p53 and tumor necrosis fa

248 Here, we show that LANA blocks MHC-II gene expression to subvert the host i

249 Here, we show that LANA directly interacted with H2AX through domains at bo

250 Here we show that LANA interacts with Aurora kinase B (AK-B) and induces p

251 Here, we show that LANA is able to form a complex with PCNA, a critical pro

252 Our data show that LANA is capable of binding to all three components of th

253 roughput sequencing (ChIP-seq) and show that LANA predominantly targets human genes near their transc

254 Here we show that LANA-1 interacts with ANG and colocalizes in latently in

255 matin immunoprecipitation assays showed that LANA binds to the MHC-II promoter along with RFX protein

256 The studies showed that LANA can also function to regulate viral replication pri

257 Previously, we showed that LANA encoded by KSHV upregulates expression of survivin,

258 Our results showed that LANA interacted physically with the anaphase-promoting c

259 These results suggest that LANA can dysregulate Bub1 activity, which leads to aberr

260 Taken together, our results suggest that LANA may play a role in regulation of epigenetic marks o

261 These studies suggest that LANA-1 association with annexin A2/ANG could be more imp

262 the latently infected cells, suggesting that LANA possesses a novel role in regulating KSHV replicati

263 This suggests that LANA plays important roles in the cytoplasm and nuclear

264 We also report for the first time that LANA's ability to bind host and viral chromatin is highl

265 The LANA-bound PP2A B subunit was associated with the PP2A A

266 roteomics analysis using KSHV TR DNA and the LANA binding site as the affinity column identified topo

267 se chromatin structures were detected at the LANA, RTA and vIL6 promoters.

268 restored recognition but not killing by the LANA-specific clones.

269 As expected, the LANA mutants bound mitotic chromosomes in a wild-type pa

270 ding sites in the KSHV genome, including the LANA promoter region.

271 More than half of the LANA binding sites (170/256) could be mapped to within 2

272 The structure of the LANA DNA binding domain was recently solved, revealing a

273 cells revealed a moderate activation of the LANA promoter region by hypoxia as well as by cotransfec

274 nalysis of a 1.2-kb sequence upstream of the LANA translational start site identified six potential h

275 Moreover, we show that the LANA DBD can coat DNA of arbitrary sequence by virtue of

276 nsus DNA sequence virtually identical to the LANA-binding site 1 (LBS1) motif in KSHV DNA.

277 dy also identified a novel intron within the LANA 5' untranslated region using a splice acceptor at 1

278 a deletion of the RBP-Jkappa site within the LANA promoter to evaluate the function of the RBP-Jkappa

279 mes in cells containing episomes, similar to LANA.

280 CD4(+) T-cell clones specific to LANA, a protein expressed in all KSHV-infected cells and

281 However, the precise mechanism underlying LANA-mediated chromosomal instability remains uncharted.

282 Here, we use LANA-specific chromatin immunoprecipitation coupled with

283 (LBS), but the molecular mechanism by which LANA assembles on the TR remains elusive.

284 hortening may be one more mechanism by which LANA contributes to the development of malignancy.

285 However, the mechanism by which LANA mediates replication is uncertain.

286 we also investigated the mechanism by which LANA promoted Bub1 degradation.

287 sults identifying a novel mechanism by which LANA, a latency-associated antigen encoded by KSHV, can

288 To discover ways in which LANA manipulation of these two kinases might impact PEL

289 provide a potential mechanism through which LANA may regulate several host cell pathways by direct b

290 in 1-like protein 1 (NAP1L1) associates with LANA.

291 me 50 (ORF50) promoter, its association with LANA-1 and KAP1 abrogates this effect.

292 yses of BC-3 cell lysates, ANG coeluted with LANA-1, p53, and Mdm2 in high-molecular-weight fractions

293 Annexin A2 coimmunoprecipitated with LANA-1 and ANG in TIVE-LTC and BCBL-1 cells and with ANG

294 2AX (gammaH2AX) was shown to colocalize with LANA.

295 monstrated that Bub1 can form a complex with LANA and PCNA in KSHV-positive cells.

296 ggested that annexin A2 forms a complex with LANA-1 and ANG as well as a separate complex with ANG.

297 we show that TopoIIbeta forms complexes with LANA that colocalize as punctuate bodies in the nucleus

298 e disassociation through an interaction with LANA which facilitates LANA sequestration away from KSHV

299 gens LANA, vFLIP, vCyclin, and Kaposin, with LANA most frequently recognized.

300 ve to disrupt association of TopoIIbeta with LANA.