ライフサイエンスコーパス: v-Rel

1 reduced association between IkappaBalpha and v-Rel.

2 tein abolish this transactivation ability of v-Rel.

3 he Env aa to influence several properties of v-Rel.

4 bility parallels the transforming ability of v-Rel.

5 alpha is unable to inhibit nuclear import of v-Rel.

6 n of a cis-acting nuclear export signal onto v-Rel.

7 o v-Rel markedly reduced the oncogenicity of v-Rel.

8 n is increased in response to both c-Rel and v-Rel.

9 gnal in v-Rel did not affect oncogenicity by v-Rel.

10 pha in spleen cells transformed by wild-type v-Rel.

11 EST domain are required for association with v-Rel.

12 t essential for the transforming activity of v-Rel.

13 phocytes by the potent NF-kappaB oncoprotein v-Rel.

14 2 contribute to its oncogenicity and that of v-Rel.

15 elomerase (TERT) was directly upregulated by v-Rel.

16 o its weaker oncogenic potential relative to v-Rel.

17 ntributing to the transforming properties of v-Rel.

18 The oncoprotein v-Rel, a member of the Rel/NF-kappaB family of transcrip

19 ian Rev-T retrovirus encodes the oncoprotein v-Rel, a member of the Rel/nuclear factor (NF)-kappaB tr

20 colony numbers comparable to those formed by v-Rel alone.

21 e stronger than c-Rel, and overexpression of v-Rel also resulted in the formation of a v-Rel containi

22 Moreover, the expression of v-Rel altered the ratio of alternatively spliced and ful

23 N-terminus, the center and the C-terminus of v-Rel, altered three different aspects of DNA binding.

24 al transformation of primary spleen cells by v-Rel, although distinct requirements for MAPK activity

25 ifferences in the transactivation domains of v-Rel and c-Rel are responsible for their different abil

26 that p40 regulates cellular localization of v-Rel and c-Rel by distinct mechanisms.

27 that p40 regulates cellular localization of v-Rel and c-Rel by the same mechanism.

28 ic cells and that it responds differently to v-rel and c-rel induction.

29 role of a limited set of alterations between v-Rel and c-Rel located within the Rel homology region (

30 ing genes regulated by NF-kappaB's oncogenic v-Rel and c-Rel proteins uncovered that Rel protein expr

31 mily, is highly elevated in cells expressing v-Rel and contributes to the immortalization of cells tr

32 Moreover, v-Rel and IRF-4 synergistically cooperate in the inducti

33 liminated formation of soft agar colonies by v-Rel and reduced the proliferation of v-Rel-transformed

34 However, the response to v-Rel and the AP-1 factors was not as vigorous as that o

35 ormation we constructed an inducible form of v-rel and used it to identify potential cellular target

36 tion was correlated with the presence of p50/v-Rel and v-Rel/v-Rel nuclear kappaB-binding activity.

37 or an N-terminal transactivation function of v-Rel, and the analysis of several Env mutants demonstra

38 and the expression of IRF-4 is increased in v-Rel- and c-Rel-transformed fibroblasts relative to con

39 tions acquired during c-Rel's evolution into v-Rel are deletion of c-Rel's transactivation domain 2 (

40 n; other sequences in the N-terminal half of v-Rel are needed for full transactivating ability.

41 We find that distinct domains in c-Rel and v-Rel are required for association with p40.

42 (Env) amino acids (aa) at the N-terminus of v-Rel are required for its full oncogenicity.

43 nly a set of six mutations within the RHR of v-Rel are responsible for its ability to bind to a broad

44 v-Rel associated with the imperfect NF-kappa B site stro

45 factor (NF)-kappaB transactivating subunit, v-rel avian reticuloendotheliosis viral oncogene homolog

46 In contrast to v-rel avian reticuloendotheliosis viral oncogene homolog

47 easured, proving a pro-proliferative role of v-rel avian reticuloendotheliosis viral oncogene homolog

48 lear factor kappaB (NF-kappaB) family member v-rel avian reticuloendotheliosis viral oncogene homolog

49 lymphoid cells or alter the distribution of v-Rel between the nucleus and the cytoplasm in v-Rel-tra

50 oprecipitation experiments demonstrated that v-Rel binds to the sh3bgrl promoter in transformed cells

51 Together, these findings demonstrate that v-Rel blocks apoptosis and suggest that this activity ma

52 However, here we demonstrate that v-Rel, but not a truncated c-Rel, expressed under the co

53 associated with a dramatic reduction of p50/v-Rel, but not v-Rel/v-Rel nuclear DNA binding activity

54 their ability to enhance the oncogenicity of v-Rel by increasing its ability to activate transcriptio

55 IkappaBalpha in the transforming activity of v-Rel by overexpressing IkappaBalpha in v-rel transgenic

56 for PEST-dependent cytoplasmic retention of v-Rel by p40.

57 The overexpression of v-Rel, c-Rel, and c-Rel delta resulted in a prolonged el

58 fatal lymphoma/leukemia in young birds, and v-Rel can transform and immortalize a variety of avian c

59 While the Rev-T oncogene v-rel causes tumors in birds, the ability of c-Rel to tr

60 of v-Rel also resulted in the formation of a v-Rel containing complex bound to a consensus AP-1 site.

61 e in transformation and that the capacity of v-Rel-containing complexes to escape the inhibitory effe

62 ults suggest that the oncogenic mutations in v-Rel cooperate and enable v-Rel to form nuclear complex

63 IRF-4 and v-Rel cooperated synergistically to transform fibroblast

64 e (NLS), IkappaB alpha is unable to mask the v-Rel-derived NLS in the context of the v-Rel-IkappaB al

65 third mutation cluster in the C-terminus of v-Rel destabilized the binding of v-Rel to all of the ka

66 Deletion of the NLS of either c-Rel or v-Rel did not abolish association with p40, but did conf

67 letion of the nuclear localization signal in v-Rel did not affect oncogenicity by v-Rel.

68 The highly oncogenic v-Rel differs from c-Rel which has low transforming pote

69 demonstrate that the oncogenic mutations in v-Rel directly alter the ability of this protein to bind

70 However, most models propose that v-rel disrupts the normal transcriptional regulatory net

71 elated with the presence of constitutive p50/v-Rel DNA binding activity and overexpression of several

72 tion of 10 Phe residues at the N terminus of v-Rel does not enable transactivation, indicating that a

73 activities of the Rel/NF-kappaB oncoprotein v-Rel emphasizes the importance of characterizing the de

74 We also show that the addition of the v-Rel Env aa to the N terminus of human c-Rel can enable

75 Using a conditional v-Rel estrogen receptor chimera (v-RelER) which transfor

76 v-Rel exhibited the most pronounced effect, whereas c-Re

77 In v-Rel-transformed cells, v-Rel exists as homodimers or heterodimers with the endo

78 e that the elevated expression of ch-IAP1 in v-Rel-expressing cells is due to an increased rate of tr

79 t example of a gene that is downregulated in v-Rel-expressing cells that also plays a role in v-Rel t

80 assayed in a number of wild-type and mutant v-Rel-expressing fibroblast and hematopoietic cells.

81 ich) family of proteins, is downregulated in v-Rel-expressing fibroblasts, lymphoid cells, and spleni

82 present immature T-lymphocytes, constitutive v-Rel expression appears to be leukemogenic at earlier s

83 and nfkb1, while nontransforming mutants of v-Rel failed to do so, suggesting a role for these two g

84 The relative velocity (v(rel)) for NDTBT with the latter two N-debenzoyl taxane

85 surrounding Phe-3 and Phe-9 is essential for v-Rel function.

86 minal deletion of 118 amino acids present in v-Rel had almost no influence on its DNA binding.

87 The aggressive oncogenic potential of v-Rel has arisen from multiple mutations within the codi

88 v-Rel has multiple changes as compared to the proto-onco

89 s inappropriately activated or suppressed by v-Rel have been identified, their contributions to the v

90 l attempts to transform mammalian cells with v-Rel have failed, suggesting that v-Rel transformation

91 so observe that both v-Rel homodimer and p50/v-Rel heterodimer bind IkappaBalpha weakly compared to o

92 thymocytes lacking p50, indicating that p50/v-Rel heterodimer formation is not essential for the tra

93 -oncoprotein c-Rel, and these changes render v-Rel highly oncogenic in avian lymphoid cells.

94 We also observe that both v-Rel homodimer and p50/v-Rel heterodimer bind IkappaBal

95 We suggest that the ability of v-Rel homodimer to deregulate subunit-specific gene expr

96 Our results indicate that v-Rel homodimers are active in transformation and that t

97 ing that a threshold level of DNA binding by v-Rel homodimers is required for transformation.

98 es examined presumably because it stabilized v-Rel homodimers.

99 . the region immediately following the c-Rel/v-Rel homology domain, appears to play an important role

100 the rapid and complete relocalization of the v-Rel-IkappaB alpha complex from the cytoplasm to the nu

101 is required for cytoplasmic retention of the v-Rel-IkappaB alpha complex.

102 the v-Rel-derived NLS in the context of the v-Rel-IkappaB alpha complex.

103 In summary, these results suggest that v-Rel immortalizes chicken spleen cells through a pathwa

104 The expression of v-Rel in a macrophage cell line resulted in elevated lev

105 also mediates the rapid nuclear shuttling of v-Rel in an interspecies heterokaryon assay.

106 acute oncogenicity of the viral oncoprotein v-Rel in animal models.

107 regulated system to characterize the role of v-Rel in cell transformation.

108 was able to prevent nuclear localization of v-Rel in chicken embryo fibroblasts, coexpression of Ika

109 Expression of v-Rel in fibroblasts, a B-cell line, and spleen cells up

110 The activation of telomerase by v-Rel in lymphocytes was also accompanied by inactivatio

111 The transforming activity of v-Rel in p50 null mice has been identified as v-Rel/v-Re

112 Coexpression of SH3BGRL with v-Rel in primary splenic lymphocytes reduced the number

113 paB) in the GCB-like human BJAB cell line or v-Rel in the chicken DT40 B-lymphoma cell line causes re

114 In agreement with a possible role for v-Rel in the inhibition of programmed cell death, its in

115 These experiments suggest a role for v-rel in the regulation of a unique gene whose protein p

116 roblasts, coexpression of IkappaB-alpha with v-Rel in the target cell for v-Rel mediated transformati

117 To understand the role of v-rel in transformation we constructed an inducible form

118 otent activator of the ch-IAP1 promoter than v-Rel in transient reporter assays, cells stably overexp

119 Overexpression of v-rel in two B-cell lines and in splenic cells induced t

120 y the potent viral Rel/NF-kappaB oncoprotein v-Rel, in contrast to a Pin1 mutant in the WW domain inv

121 to impart a number of unique properties onto v-Rel, including increased transforming and transactivat

122 Although v-Rel increases the expression of these factors, their a

123 een cells approximately as well as wild-type v-Rel, indicating that interaction with I kappa B-alpha

124 In fibroblasts, wild-type v-Rel induced expression of mip-1beta and nfkb1, while n

125 v-rel-induced neoplasias are thought to be caused by the

126 v-Rel induces a rapidly fatal lymphoma/leukemia in young

127 v-Rel induces avian and mammalian lymphoid cell tumors a

128 The mechanism by which v-Rel induces oncogenic transformation remains unclear.

129 The mechanism by which v-Rel induces transformation of avian lymphoid cells and

130 Current models for cell transformation by v-Rel invoke the combined activation of gene expression

131 The retroviral oncoprotein v-Rel is a chimeric protein that has 11 helper virus-der

132 The retroviral oncoprotein v-Rel is a member of the Rel/ NF-kappa B family of trans

133 The retroviral oncoprotein v-Rel is a member of the Rel/ NF-kappaB family of transc

134 The oncogene, v-rel is a member of the rel/NF-kappaB family of transcr

135 v-Rel is a truncated and mutated form of c-Rel and trans

136 paB-alpha to inhibit nuclear localization of v-Rel is affected by cell-type specific differences betw

137 However, v-Rel is also transforming in transgenic thymocytes lack

138 Since v-Rel is an acutely oncogenic member of the Rel/NF-kappa

139 ts show that the transactivation function of v-Rel is necessary but not sufficient for cell transform

140 We show that the continued expression of v-Rel is necessary to maintain the viability of transfor

141 nstrate that a threshold nuclear function of v-Rel is required for manifestation of its oncogenic pro

142 v-Rel is the acutely oncogenic member of the NF-kappaB f

143 The potent oncogenicity of v-Rel is the consequence of a number of mutations that h

144 v-rel is the oncogenic member of the Rel/NF-kappaB famil

145 v-Rel is the oncogenic member of the Rel/NF-kappaB famil

146 been associated with oncogenesis in mammals, v-Rel is the only member of this family that is frankly

147 v-Rel is thus a valuable tool to characterize the role o

148 avian reticuloendotheliosis virus strain T, v-Rel, is a member of the Rel/ NF-kappa B family of tran

149 iptional activator than its viral derivative v-Rel, its oncogenic activity is significantly weaker.

150 uggest that induction of IRF-4 expression by v-Rel likely facilitates transformation of fibroblasts b

151 The mechanism by which v-Rel malignantly transforms chicken spleen cells is not

152 of these two c-Rel-derived amino acids into v-Rel markedly reduced the oncogenicity of v-Rel.

153 suggests that the anti-apoptotic activity of v-Rel may affect other apoptosis inhibitors or other fac

154 Our studies also demonstrate that v-Rel may induce AP-1 members by directly upregulating g

155 The activation of telomerase by v-Rel may, therefore, partially protect the transformed

156 ppaB-alpha with v-Rel in the target cell for v-Rel mediated transformation did not reduce the ability

157 so, suggesting a role for these two genes in v-Rel mediated transformation.

158 v-Rel-mediated activation of telomerase is achieved by m

159 avian IkappaB-alpha protein, contributes to v-Rel-mediated oncogenesis.

160 studies identified Ha-Ras as an effector of v-Rel-mediated transformation and reveal a novel role fo

161 e that elevated TC10 activity contributes to v-Rel-mediated transformation of CEFs and demonstrate fo

162 s suggest that ch-IAP1 is induced during the v-Rel-mediated transformation process and functions as a

163 nts for MAPK activity at different stages of v-Rel-mediated transformation were identified.

164 ated expression of ATF2 is also required for v-Rel-mediated transformation, its ectopic overexpressio

165 amine the contribution of these complexes to v-Rel-mediated transformation, mutations were introduced

166 al in both the initiation and maintenance of v-Rel-mediated transformation, whereas Fra-2 is dispensa

167 evaluated the role of AP-1 family members in v-Rel-mediated transformation.

168 AP-1 transcriptional activity contributes to v-Rel-mediated transformation.

169 mine the role of individual AP-1 proteins in v-Rel-mediated transformation.

170 These v-Rel mice should aid in the study of lymphoma developme

171 This is the first report showing that v-Rel might execute its oncogenic potential through modu

172 A second v-Rel mutant, v-SPW, has been shown to be defective for

173 We have previously characterized two v-Rel mutants (v-G37E and v-R273H) that are temperature-

174 The transforming activity of v-Rel mutants correlated with their ability to inhibit p

175 dimerization interface of v-Rel to generate v-Rel mutants with selective dimerization properties.

176 in cells transformed by weakly transforming v-Rel mutants.

177 the induction of these effects since neither v-Rel nor c-Rel deletion mutants were able to induce sim

178 lta NLS, which has a deletion of the primary v-Rel nuclear localizing sequence, does not interact eff

179 The oncogene v-rel of Reticuloendotheliosis virus, strain T, is deriv

180 The v-rel oncogene encoded by reticuloendotheliosis virus is

181 The v-rel oncogene encoded by reticuloendotheliosis virus st

182 Cell transformation by the v-rel oncogene is mediated by the aberrant expression of

183 The v-rel oncogene is the most efficient transforming member

184 elA and identification of its kinship to the v-Rel oncogene, it was anticipated that NF-kappaB itself

185 NF-kappaB avian reticuloendotheliosis viral (v-rel) oncogene related B (RelB) subunit is not induced

186 The v-Rel oncoprotein belongs to the Rel/NF-kappaB family of

187 The v-Rel oncoprotein belongs to the Rel/NF-kappaB family of

188 imentally manipulate the distribution of the v-Rel oncoprotein between the nucleus and the cytoplasm.

189 In contrast, nuclear export of the v-Rel oncoprotein by IkappaBalpha is disrupted by alanin

190 NF-kappaB in human hematopoietic tumors, the v-Rel oncoprotein induces aggressive leukemia/lymphomas

191 The v-Rel oncoprotein of the avian Rev-T retrovirus is a mem

192 ed the kappaB DNA-binding specificity of the v-Rel oncoprotein relative to c-Rel.

193 The respective abilities of the v-Rel oncoprotein to localize to the nucleus in chicken

194 induction of fatal lymphomas in birds by the v-rel oncoprotein, and the rearrangement and amplificati

195 The avian Rev-T retrovirus encodes the v-Rel oncoprotein, which is a member of the Rel/NF-kappa

196 Removal of the Env aa from v-Rel or site-directed mutations that revert the three m

197 In addition we show that v-rel participates in the transcriptional regulation of

198 ing a transformation-competent chimeric RelA/v-Rel protein, suggesting a correlation with the capacit

199 the co-expression of wild-type or ts mutant v-Rel proteins and the anti-apoptosis proteins Bcl-2 or

200 Analysis of several mutant c-Rel and v-Rel proteins demonstrated that association of Rel prot

201 e now characterized the activities of mutant v-Rel proteins that are defective for specific protein-p

202 Infection with retroviruses expressing v-Rel rapidly induces fatal lymphomas in birds and trans

203 identify potential cellular target genes for v-rel regulation.

204 of fibroblasts with retroviruses expressing v-Rel resulted in an increase in the mRNA levels of IFN1

205 Overexpression of c-Rel or v-Rel resulted in the formation of DNA binding complexes

206 The expression of v-Rel results in the strong and sustained activation of

207 us (P2) private loss-of-function variants of V-Rel Reticuloendotheliosis Viral Oncogene Homolog B (RE

208 HIF1a stabilization decreased the level of v-rel reticuloendotheliosis viral oncogene homolog B pro

209 studies address the difference in c-Rel and v-Rel's ability to synergistically stimulate I kappa B a

210 ely, substitution of vTAD by cTAD1 increased v-Rel's transactivation and transforming efficiencies, w

211 r and gamma delta (gammadelta) T cells in CR vs REL samples.

212 The transactivation domain of v-Rel selectively conferred an oncogenic phenotype upon

213 these cells does not affect ts functions of v-Rel, such as DNA binding and stabilization of I kappa

214 t levels comparable to or slightly less than v-Rel, suggesting that a threshold level of DNA binding

215 ntly reduce the affinity of IkappaBalpha for v-Rel, suggesting that loss of export function for this

216 Two amino acid differences between c-Rel and v-Rel that are principally responsible for PEST-dependen

217 transactivation domain in the C terminus of v-Rel that is necessary for its biological activity.

218 our group identified a serine-rich domain in v-Rel that was required for biological activity.

219 rmation of lymphoid cells and fibroblasts by v-Rel, the oncogenic member of the Rel/NF-kappaB family

220 The ability of v-Rel, the oncogenic viral counterpart of avian c-Rel, t

221 n to enhance the transformation potential of v-Rel, the overexpression of wild-type TC10 or the gain-

222 ression of IRF-10 is induced by the oncogene v-rel, the proto-oncogene c-rel, and IRF-4 in a tissue-s

223 Within these N-terminal Env aa of v-Rel there are three aa substitutions compared to the R

224 either pathway beyond the levels induced by v-Rel through the expression of constitutively active MA

225 e transcription start site were required for v-Rel to activate the ch-IAP1 promoter.

226 o enable sequences in the N-terminal half of v-Rel to activate transcription in yeast and chicken cel

227 erminus of v-Rel destabilized the binding of v-Rel to all of the kappaB sites examined.

228 ter was responsible for increased binding of v-Rel to all the kappaB sites examined presumably becaus

229 The ability of v-Rel to escape IkappaBalpha regulation allows for the g

230 enic mutations in v-Rel cooperate and enable v-Rel to form nuclear complexes with aberrant DNA-bindin

231 ntroduced into the dimerization interface of v-Rel to generate v-Rel mutants with selective dimerizat

232 We also show that the ability of v-Rel to induce MAPK signaling more strongly than c-Rel

233 un-1 strongly interfered with the ability of v-Rel to morphologically transform avian fibroblasts.

234 transformation did not reduce the ability of v-Rel to transform avian lymphoid cells or alter the dis

235 subset of apoptosis inhibitors could rescue v-Rel transactivation mutants suggests that their reduce

236 SH3BGRL abolished the suppressive effect on v-Rel transformation and resulted in colony numbers comp

237 ells with v-Rel have failed, suggesting that v-Rel transformation may be a species-specific event.

238 been identified, their contributions to the v-Rel transformation process have been poorly characteri

239 luate the role of AP-1 family members in the v-Rel transformation process, a supjun-1 transdominant m

240 un heterodimers as major contributors to the v-Rel transformation process.

241 l-expressing cells that also plays a role in v-Rel transformation.

242 L only had a modest effect on suppression of v-Rel transformation.

243 t (TC10Q76L) greatly enhanced the ability of v-Rel transformed CEFs to form colonies in soft agar.

244 4 (HMG 14) is expressed in a wide variety of v-rel transformed cell types.

245 get genes that exhibit altered expression in v-Rel transformed cells.

246 ression of supjun-1 inhibited the ability of v-Rel transformed lymphoid cells and fibroblasts to form

247 f exogenous ch-IAP1 in temperature-sensitive v-Rel transformed spleen cells inhibited apoptosis of th

248 ne expression patterns have been examined in v-Rel-transformed avian bone marrow cells.

249 v-Rel-transformed cell lines have longer telomeres than

250 The inhibition of telomerase activity in v-Rel-transformed cell lines led to apoptosis within 24

251 suppresses apoptosis that is induced when ts v-Rel-transformed cells are shifted to the non-permissiv

252 v-Rel-transformed cells exhibit elevated RNA and protein

253 active, GTP-bound TC10 was also detected in v-Rel-transformed cells relative to control cells.

254 relevance to transformation and apoptosis in v-Rel-transformed cells, mRNA differential display has b

255 In v-Rel-transformed cells, v-Rel exists as homodimers or h

256 es by v-Rel and reduced the proliferation of v-Rel-transformed cells.

257 nd functions as a suppressor of apoptosis in v-Rel-transformed cells.

258 Rel between the nucleus and the cytoplasm in v-Rel-transformed cells.

259 ressed predominantly in the cytoplasm of the v-Rel-transformed cells.

260 decreased the colony formation potential of v-Rel-transformed cells.

261 The expression of TC10 was increased in v-Rel-transformed chicken embryonic fibroblasts (CEFs) 3

262 tibody we detected a 75 kDa-protein (p75) on v-rel-transformed chicken hematopoietic cells.

263 is cleaved in vivo in temperature-sensitive v-Rel-transformed chicken spleen cells undergoing apopto

264 The formation of v-Rel-transformed colonies is enhanced in the presence o

265 The exogenous expression of IRF-4 in v-Rel-transformed fibroblasts decreased the production o

266 v-Rel-transformed fibroblasts produced interferon 1 (IFN

267 ponds to a gene that was highly expressed in v-Rel-transformed fibroblasts.

268 dicated that p75 is ectopically expressed on v-rel-transformed hematopoietic cells and that it respon

269 All v-Rel-transformed hematopoietic cells tested express hig

270 IRF-4 is highly expressed in v-Rel-transformed lymphocytes, and the expression of IRF

271 ing RNA severely impairs colony formation of v-Rel-transformed lymphoid cell lines.

272 This induction is critical for the v-Rel-transformed phenotype, as suppression of MAPK acti

273 ith I kappa B-alpha is not essential for the v-Rel transforming function.

274 and truncated forms of c-Rel, implying that v-Rel transforms, in part, by induction of c-Rel target

275 Overexpression of IkappaBalpha in v-rel transgenic mice resulted in an extended survival,

276 y of v-Rel by overexpressing IkappaBalpha in v-rel transgenic mice.

277 ession of several kappa B-regulated genes in v-rel transgenic thymocytes.

278 t transgenic mice expressing the oncoprotein v-Rel under the control of a T cell-specific promoter de

279 -Rel in p50 null mice has been identified as v-Rel/v-Rel homodimers.

280 h a dramatic reduction of p50/v-Rel, but not v-Rel/v-Rel nuclear DNA binding activity and an increase

281 orrelated with the presence of p50/v-Rel and v-Rel/v-Rel nuclear kappaB-binding activity.

282 While the repression of v-Rel was accompanied by the rapid degradation of Ikappa

283 ransactivation domain substituted by that of v-Rel was potently oncogenic in vitro and in vivo.

284 ng of functions needed for transformation by v-Rel, we have now characterized the activities of mutan

285 transforming and antiapoptotic activities of v-Rel were abolished by defined Ser-to-Ala mutations and

286 ion impaired the transcriptional activity of v-Rel, whereas a double mutant abolished its function.

287 The study of v-Rel will continue to increase our knowledge of how cel

288 n vitro, indicating that the dimerization of v-Rel with endogenously expressed Rel/NF-kappaB proteins

289 esponsible for PEST-dependent association of v-Rel with p40 were identified.

290 contributed to the tumorigenic potential of v-Rel with the relative strength decreasing with their p

291 scuss biological and molecular activities of v-Rel, with particular attention to how these activities

292 two amino acid differences between c-Rel and v-Rel (Y286S and L302P) which link the failure of Ikappa