ライフサイエンスコーパス: oncoprotein

1 in acute leukemia into the chimeric E2A-PBX1 oncoprotein.

2 r cells, suggesting p27 also functions as an oncoprotein.

3 ion is a major transforming mechanism of Myc oncoprotein.

4 cell proliferation and, therefore, act as an oncoprotein.

5 hat frequently overexpresses the c-Myc (Myc) oncoprotein.

6 associated with directly inhibiting the KRAS oncoprotein.

7 PML-retinoic acid receptor alpha (RARalpha) oncoprotein.

8 us is the smallest known naturally occurring oncoprotein.

9 riven by the activity of the BCR-ABL1 fusion oncoprotein.

10 sses the EWS/FLI fusion transcription factor oncoprotein.

11 ting co-factor in the induction of the c-Myc oncoprotein.

12 ppressor, whereas HIF2alpha is considered an oncoprotein.

13 rkel cell polyomavirus small T antigen viral oncoprotein.

14 nslocation that generates an SS18-SSX fusion oncoprotein.

15 thway leads to aberrant elevation of the ERG oncoprotein.

16 n region 1 (BMI1) has been reported to be an oncoprotein.

17 main-binding protein 2 (WBP2) is an emerging oncoprotein.

18 s and cognate binding-partners of a specific oncoprotein.

19 with polysomes, and translated to produce E7 oncoprotein.

20 ty in the regulation of NF-kappaB by a viral oncoprotein.

21 d to cell death, and a reduction in the same oncoproteins.

22 fferent, clinically relevant ROS1 RTK fusion oncoproteins.

23 nges or translocations that result in fusion oncoproteins.

24 mechanisms and output of certain RTK fusion oncoproteins.

25 use model of carcinogenesis induced by HPV16 oncoproteins.

26 that influence tumor spectra induced by RAS oncoproteins.

27 d from prenylation of the RAS superfamily of oncoproteins.

28 pendent changes produced by HPV16-E6 and -E7 oncoproteins.

29 F4E-dependent export of transcripts encoding oncoproteins.

30 ation and upregulated expression of specific oncoproteins.

31 n of cells with elevated expression of virus oncoproteins.

32 secondary mutations of pathogenic KIT/PDGFRA oncoproteins.

33 numerous client proteins, many of which are oncoproteins.

34 cidic domain sequences homologous to the SET oncoprotein acidic domain reader.

35 proach uncovered key mechanisms by which EBV oncoproteins activate the PI3K/AKT pathway and evade tum

36 PTO (CR-1, TDGF1) is a cell surface/secreted oncoprotein actively involved in development and cancer.

37 ting a possible new avenue in abrogating HPV oncoprotein activity.

38 ty leading to the aberrant activation of the oncoprotein Akt.

39 rs (GPCRs) activate PI3K/v-AKT thymoma viral oncoprotein (AKT) to regulate many cellular functions th

40 izing recent advances that describe how this oncoprotein alters melanocyte proliferation and motility

41 validate GPC2 as a non-mutated neuroblastoma oncoprotein and candidate immunotherapeutic target.

42 st high-risk human papillomavirus type 16 E7 oncoprotein and conferred CD8-mediated protection to a v

43 Finally, we establish that the known oncoprotein and hexose deglycase, fructosamine 3-kinase

44 pn14 encodes a negative regulator of the Yap oncoprotein and is necessary and sufficient for pancreat

45 oach to therapeutically degrade the CIC-DUX4 oncoprotein and provide a precision-based strategy to co

46 cellular localization of the particular ROS1 oncoprotein and the TKI properties such as the preferent

47 e circadian clock on this important oncogene/oncoprotein and tumorigenesis.

48 n for DIF inhibitors, ranging from non-V600E oncoproteins and BRAF fusions to tumors driven by aberra

49 e ubiquitin-proteasome system degrades viral oncoproteins and other microbial virulence factors; howe

50 , ORM repressed the expression of HPV E6/ E7 oncoproteins and restored the expression of their downst

51 erred SigMaps for the ten most mutated human oncoproteins and then for the full repertoire of 715 pro

52 focus on combinatorial targeting of specific oncoproteins and tumour suppressors.

53 etween vFLIP, a Kaposi's sarcoma herpesviral oncoprotein, and NEMO using small molecule screening and

54 However, some GISTs lose expression of KIT oncoproteins, and therefore become KIT-independent and a

55 Many oncoproteins are considered undruggable because they lac

56 It is thought that KRAS oncoproteins are constitutively active because their gua

57 bserved at the cancer stage (SCC), where HPV oncoproteins are highly expressed, supporting the clinic

58 Molecular therapies to directly target these oncoproteins are lacking, and current treatment options

59 Nucleoporin 98 (NUP98) fusion oncoproteins are observed in a spectrum of hematologic m

60 Phosphatase of regenerating liver (PRL) oncoproteins are phosphatases overexpressed in numerous

61 le splicing factors, we identified the SRSF3 oncoprotein as a key enhancer of exon 6 inclusion.

62 Notably, we identify the Pin1 oncoprotein as an upstream Nanog regulator that impairs

63 As an oncoprotein as well as a potential immunomodulator, cont

64 inhibited phosphorylation of all tested RET oncoproteins as well as VEGFR2 and proliferation of cell

65 We show that Erk1(R84S) is an oncoprotein, as NIH3T3 cells that express it form foci i

66 We further show that a PKA fusion oncoprotein associated with an atypical liver cancer pot

67 Protein tyrosine phosphatase SHP2 is an oncoprotein associated with cancer as well as a potentia

68 Because it is an oncoprotein associated with multiple cancer-related dise

69 ously shown that phosphorylation of the Mdm2 oncoprotein at Ser394 by the ATM kinase is required for

70 ovides insight into the biology of the proto-oncoprotein at the physiological level, in both transfor

71 specific regulatory allosteric pocket of the oncoprotein Aurora A (AurA) kinase, thereby offering the

72 Targeting the fusion oncoprotein BCR-ABL with tyrosine kinase inhibitors has

73 TP-competitive tyrosine kinase inhibitors of oncoprotein BCR-ABL1 has enabled durable responses in pa

74 An overlap of NUP98-KDM5A oncoprotein binding sites and H3K4me3-positive loci at t

75 inhibitor 2 of protein phosphatase 2A (PP2A) oncoprotein binds and inhibits PP2A, composed of various

76 re reshaping the fundamental aspects of KRAS oncoprotein biology and the strides being made toward im

77 oncosuppressor by targeting the 3'UTR of two oncoproteins: BRAF and an E3 ubiquitin protein ligase, M

78 nomenon was recently reported for the HPV E6 oncoprotein but has not yet been observed for mammalian

79 Stabilization of the MYC oncoprotein by KRAS signaling critically promotes the gr

80 ing growth dependent on the myelocytomatosis oncoprotein c-Myc.

81 pylori type IV secretion system injects the oncoprotein CagA into epithelial cells to drive carcinog

82 retion system (T4SS), which translocates the oncoprotein CagA into host cells.

83 The ability of H pylori and its oncoprotein CagA to reprogram epithelial cells and activ

84 Bacterial virulence factors, such as the oncoprotein CagA, augment cancer risk.

85 As the first described bacterial oncoprotein, CagA causes gastric epithelial cell transfo

86 riving HA production and demonstrate that an oncoprotein can co-opt HA biosynthesis to drive malignan

87 AML1-ETO is the most common fusion oncoprotein causing acute myeloid leukemia (AML), a dise

88 ed tumorigenic capacity and miR-16-5p target oncoproteins CCND1 and BCL2.

89 n interactions unique to the BRD4-NUT fusion oncoprotein compared with wild-type BRD4.

90 Several human papillomavirus type 16 (HPV16) oncoproteins contribute to cellular transformation in vi

91 CtBP2 is thus a druggable transforming oncoprotein critical for the evolution of neoplasia driv

92 Blockade of DNA damage-induced TMPRSS2-ERG oncoprotein degradation causes chemotherapy-resistant gr

93 ular invasion through the translation of the oncoprotein DEK.

94 T lines in which the parental forms were KIT oncoprotein-dependent, whereas sublines had loss of KIT

95 f tumors with aberrant activity of druggable oncoproteins despite a lack of mutations, and vice versa

96 e strong support for an instructive model of oncoprotein-directed epigenetic silencing.

97 tal models and patient samples, NUP98 fusion oncoprotein-driven leukemogenesis is mediated by changes

98 The RAS oncoprotein drives elevated macropinocytosis, a metaboli

99 otic translation initiation factor eIF4E, an oncoprotein, drives HA biosynthesis.

100 tics, signalling and pathogenesis underlying oncoprotein duality.

101 Oncoprotein E6 of high-risk human papillomavirus (HPV) p

102 d-neck cancers, p53 is degraded by the viral oncoprotein E6.

103 The HPV encoded oncoproteins E6 and E7 (E6/E7), EBV latent membrane prot

104 The expression of the viral oncoproteins E6 and E7 are essential in this process by

105 HPV-related cancers express the viral oncoproteins E6 and E7.

106 14 is significantly downregulated by the HPV oncoprotein E7 during cancer progression.

107 Here, we report that oncoprotein E7 of HPV16 but not HPV18 retards mitotic pr

108 We now show that the HPV oncoprotein E7 of HPV8, HPV11 and HPV16 directly interac

109 heckpoints by the human papillomavirus (HPV) oncoprotein E7 results in replication stress (RS) that l

110 In summary, our results demonstrate that the oncoprotein EGFRvIII sensitizes a fraction of GBM to cur

111 We used immunohistochemistry to assess oncoprotein encoded by the ERG gene as the established s

112 Tumor cells express the chimeric oncoprotein EWS-FLI1 from a specific t(22;11)(q24;12) tr

113 Myc oncoproteins exert tumorigenic effects by regulating exp

114 ROS1 fusion oncoproteins exhibit differential activation of MAPK sig

115 positive for HPV-DNA were screened for viral oncoprotein expression using western blot and dot blot.

116 genetic mechanisms that restrict immunogenic oncoprotein expression, a genome-scale CRISPR-Cas9 scree

117 -dependent, whereas sublines had loss of KIT oncoprotein expression, accompanied by markedly downregu

118 on from the P97 promoter that controls viral oncoprotein expression.

119 tional therapeutic targets to manipulate EBV oncoprotein expression.

120 transcriptionally inactive member of the MYC oncoprotein family, generated by a proteolytic cleavage

121 regulating the levels of the C-MYC and SRC-3 oncoproteins, FBXL16 promoted cancer cell growth and mig

122 age cellular signaling to ablate TMPRSS2-ERG oncoprotein for PCa treatment remains elusive.

123 primary tumor cells are addicted to the MYC oncoprotein for survival.

124 virus (MCV) small T antigen (sT) is the main oncoprotein for the development of Merkel cell carcinoma

125 in-F-box (SCF) ubiquitin ligase that targets oncoproteins for ubiquitination and degradation.

126 compute full protein-peptide kinetics of the oncoprotein fragment (25-109)Mdm2 and the nano-molar inh

127 overy may be able to potentially strike G(q) oncoproteins from the list of undruggable targets, but a

128 n of the mutant Braf but not the mutant Nras oncoprotein further accelerated melanoma progression.

129 nisms of this elimination, we found that the oncoprotein gankyrin (Gank) preferentially binds to and

130 As a novel oncoprotein, gankyrin is expressed aberrantly in cancers

131 o the function of the unique Golgi secretory oncoproteins GOLPH3 and MYO18A.

132 ful targeting of the underlying PML-RARalpha oncoprotein has eliminated the need for chemotherapy for

133 Direct inhibition of KRAS oncoproteins has been a long-standing pursuit in precisi

134 The direct targeting of KRAS oncoproteins has been a longstanding objective in precis

135 RIT1 oncoproteins have emerged as an etiologic factor in Noon

136 eric antigen receptor (CAR) specific for the oncoprotein HER-2 increased the activation of the Src fa

137 The manner how viral oncoproteins hijack the host cell metabolism to meet the

138 l, Ge et al. show that overexpression of the oncoprotein iASPP in cancer cells provokes NRF2-mediated

139 coupled with reduced expression of c-MYC, an oncoprotein implicated in tumor progression and therapeu

140 -eleven translocation 1 (TET1) is a critical oncoprotein in AML.

141 that may be exploited for modulating the YAP oncoprotein in cancer and regenerative medicine.

142 K-Ras is the most frequently mutated oncoprotein in human cancers, and G12D is its most preva

143 nce has shown that Jab1/CSN5 functions as an oncoprotein in human cancers, its regulation through miR

144 gests that the selective expression of viral oncoprotein in invasive cases may propose a role for HR-

145 degradation, whereas it might function as an oncoprotein in kidney cancer, for example, by targeting

146 a prototype receptor tyrosine kinase and an oncoprotein in many solid tumors.

147 ection, we expressed the high-risk HPV-16 E6 oncoprotein in primary human keratinocytes and measured

148 antly activated, Gfi1 may function as a weak oncoprotein in the lymphoid system, but collaborates str

149 previously unknown function of the HPV16 E5 oncoprotein in the suppression of interferon (IFN) respo

150 ding proteins (RBPs) have important roles as oncoproteins in an array of tumor types, including leuke

151 essor" protein in normal T and B cells, and "oncoprotein" in a subset of established T and B cell mal

152 enin, and abrogating expression of E6/E7 HPV oncoproteins including smoking compound benzo[a]pyrene (

153 n HPV16 E7-expressing cells.IMPORTANCE Viral oncoproteins, including HPV16 E6 and E7, have been instr

154 affect host pathways already targeted by HPV oncoproteins, including the p53 and pRB pathways, or dis

155 Overall, our results suggest that HPV16 oncoproteins induce a reorganization of the local epithe

156 HPV16 oncoproteins induced a decrease in epidermal Skint1 expr

157 ta T cells promoted the development of HPV16 oncoprotein-induced lesions.

158 Merkel cell polyomavirus (MCV) small T (sT) oncoprotein induces centrosome overduplication, aneuploi

159 y-relevant human papilloma virus (HPV) 16 E7 oncoprotein induces cytotoxicity against peptide-express

160 Accordingly, many oncoproteins inhibit, and several oncosuppressor protein

161 gadomains" are formed by the BRD4-NUT fusion oncoprotein, interact both within and between chromosome

162 cific elucidation of physical and functional oncoprotein interactions could improve tumorigenic mecha

163 SP27-regulated survival signaling and client-oncoprotein interactions.

164 Whether or not these oncoproteins interfere with other DNA-dependent processe

165 tion system (cagT4SS), which translocates an oncoprotein into host cells.

166 ecretion system (T4SS) that injects the CagA oncoprotein into host cells.

167 lori Cag T4SS translocates CagA, a bacterial oncoprotein, into gastric cells, contributing to gastric

168 EVI1 is a zinc finger oncoprotein involved in the development of acute myeloid

169 It is characterized by fusion oncoproteins involving EWSR1 and variable members of the

170 MYC oncoprotein is a multifunctional transcription factor th

171 its carcinogenic activity.IMPORTANCE The E7 oncoprotein is a primary driver of HPV-mediated carcinog

172 The human papillomavirus (HPV) E7 oncoprotein is a primary driver of HPV-mediated carcinog

173 The Muc-1 oncoprotein is a tumor-associated mucin often overexpres

174 Overexpression of the MYC oncoprotein is an initiating step in the formation of se

175 he SUMO ligase activity of the E1B-55K viral oncoprotein is intimately linked to its growth-promoting

176 The c-MYC (MYC) oncoprotein is often overexpressed in human breast cance

177 These data suggest that the E7 oncoprotein is the fundamental contributor to in vivo ca

178 Since the KRAS oncoprotein is, as yet, not directly druggable, efforts

179 lation of nuclear-cytoplasmic trafficking of oncoproteins is critical for growth homeostasis.

180 the N-terminal fusion partner in RTK fusion oncoproteins is poorly understood.

181 , a chaperone protein that regulates several oncoproteins, is upregulated in EAC, and may be a novel

182 f lung cancer, expression of the BRAF(V600E) oncoprotein kinase initiates the growth of benign tumors

183 er driven by a pharmacologically intractable oncoprotein, KRAS(1-4).

184 ivated following overexpression of the viral oncoprotein KSHV vFLIP (ks-vFLIP).

185 Inactive EGFR interacts with the oncoprotein LAPTM4B that is required for the endosomal a

186 ll-defined epitopes of a clinically relevant oncoprotein, large T Ag.

187 The EBV oncoprotein latent membrane protein 1 (LMP1) functions t

188 The Mdm4 (alias MdmX) oncoprotein, like its paralogue and interaction partner

189 The EBV oncoprotein LMP1 constitutively activates NFkappaB and i

190 ing by secreting viral components such as an oncoprotein, LMP1, into host cell membrane-bound EVs.

191 Here, we demonstrate that the candidate oncoprotein, LYAR, enhances ribosomal DNA (rDNA) transcr

192 that a positive serologic response to HPV16 oncoproteins may be the best approach to assess HPV-dise

193 that a positive serologic response to HPV16 oncoproteins may be the best approach to assess HPV-dise

194 Here, we report that FKBP12 interacts with oncoprotein MDM2 and induces MDM2 degradation.

195 Here, we report that the oncoprotein Mdm2 can bind directly to the tumor suppress

196 y overexpression of its negative regulators, oncoproteins MDM2/MDMX.

197 inhibits nuclear factor kappaB, and reduces oncoprotein messenger RNA translation, is a potential no

198 The proto-oncoprotein MET is a receptor tyrosine kinase that plays

199 anscription-associated methyltransferase and oncoprotein MLL1 to the DDR, leading us to investigate t

200 a is initiated and exacerbated by a chimeric oncoprotein, most commonly, EWS-FLI1.

201 gned as dimerization inhibitors of prominent oncoprotein mucin 1.

202 ficacious in silencing the signaling of G(q) oncoproteins, mutant G(q) variants that mostly exist in

203 e ubiquitin-dependent transactivation of the oncoprotein Myc by other E3s.

204 the anti-apoptotic protein Bcl2, but not the oncoprotein Myc, or loss of the tumor suppressor protein

205 is in cells stimulated to proliferate by the oncoprotein MYC.

206 imilar to other members of the MYC family of oncoproteins, MYCN (also known as N-Myc) is a transcript

207 on via its post-translational control of the oncoprotein N-myc (encoded by Mycn).

208 hin the histone lysine methyltransferase and oncoprotein NSD2 that preferentially binds to nucleosome

209 Hijacking of E6AP by the E6 oncoprotein of distinct human papillomaviruses (HPV) con

210 d a transgenic mouse model expressing the E7 oncoprotein of HPV8 in the murine epidermis under the co

211 Middle T antigen (MT), the principal oncoprotein of murine polyomavirus, transforms by associ

212 The E7 oncoprotein of the high-risk human papillomavirus (HPV)

213 used for protein prenylation, including the oncoproteins of the RAS superfamily.

214 oma pathogenesis is driven by EWS/Ets fusion oncoproteins, of which EWS/Fli1 is the most common.

215 These chimeric oncoproteins often contain the C-terminal kinase domain

216 es to bind to Fcgamma receptor IIIa and HER2 oncoprotein on the cell surface, a proliferation inhibit

217 Blockage of more than one oncoprotein or pathway is now a standard approach in mod

218 n how these mechanisms may be deregulated by oncoproteins or mutations/variants in CEBPA enhancers ar

219 oncogene amplification and consequent N-Myc oncoprotein over-expression die of the disease.

220 lead probe termed ADAPT6 that binds HER2, an oncoprotein overexpressed in many breast cancers that se

221 Focusing on C-MYC, a well-known oncoprotein overexpressed in most human cancers, we show

222 and their response to short-term c-Myc (Myc) oncoprotein overexpression.

223 Our results therefore suggest that the oncoprotein p27 reorganizes the effects of TGF-beta in t

224 approaches that primarily suppress the BRAF oncoprotein pathway have a high predictability of effica

225 childhood soft tissue tumor, which exists in oncoprotein PAX-FOXO1 fusion positive and fusion negativ

226 E6 oncoprotein plays a crucial role in cervical carcinogene

227 Human oncoproteins promote transformation of cells into tumour

228 n the recent paradigm shift in regard to how oncoproteins promote transformation, we review the funda

229 d genes colocalized with Meq (an MDV-encoded oncoprotein) recruitment sites.

230 rpins single-cell protein analysis, here for oncoprotein-related signaling in human breast biopsy.

231 SDC4-ROS1 and SLC34A2-ROS1 fusion oncoproteins resided on endosomes and activated the MAPK

232 is through specific interactions between the oncoprotein's DNA-binding domain, which may be targeted

233 EBP2's affinity for c-Myc and prolonged the oncoprotein's half-life.

234 We show that the HPV16 E6/E7 oncoproteins sensitize HNSCC cells to single-agent WEE1i

235 re we use a proteomic screen to identify the oncoprotein SET as a major cellular factor whose binding

236 The oncoprotein SET was recently suggested to modulate the D

237 EGFL6 signaled at least in part via the oncoprotein SHP2 with concomitant activation of ERK.

238 ic, orally bioavailable inhibitor of the PTP oncoprotein SHP2 with in vivo activity, suggests that al

239 insights into the mechanism of CysLTR2-L129Q oncoprotein signaling and suggest CYSLTR2 as a promising

240 hese syndromes offer an opportunity to study oncoprotein signalling and its biology in the absence of

241 TCH1) protein releases its inhibition of the oncoprotein Smoothened (SMO) after binding the HH ligand

242 The oncoprotein Smoothened (SMO), a G-protein-coupled recept

243 l structures of the Hh signal transducer and oncoprotein Smoothened, a GPCR that contains two distinc

244 Since MYC is a ubiquitous oncoprotein, some of these lncRNAs probably play a signi

245 owever, lack context specificity and are not oncoprotein specific.

246 important molecular chaperone that regulates oncoprotein stability and tumorigenesis.

247 eted demethylation of transcripts coding for oncoproteins such as epidermal growth factor receptor (E

248 by the E3 ligase targeting capacity of viral oncoproteins such as MCV sT, which may contribute to Mer

249 Transforming viral oncoproteins, such as adenovirus E1A and papillomavirus

250 nt T cell-amplified sequence 1 (MCT-1/MCTS1) oncoprotein support noncanonical translation initiation,

251 However, the HPV E5 oncoprotein suppressed immune responses by downregulatin

252 cell lines, we demonstrate that the HPV16 E7 oncoprotein suppresses canonical nonhomologous end-joini

253 -peptidase complex ClpXP associates with the oncoprotein survivin and the respiratory chain Complex I

254 that acts by inhibiting dimerization of the oncoprotein survivin, thereby promoting its degradation

255 ational treatments of multivalent DLL-1 with oncoprotein targeting drugs in preclinical mouse models

256 The retroviral oncoprotein Tax from human T-cell leukemia virus type 1

257 by the human T-lymphotropic virus 1 (HTLV-1) oncoprotein Tax immediately triggers a host senescence r

258 human T-cell leukemia virus type 1 (HTLV-1) oncoprotein Tax induces an epigenetic-dependent global m

259 tabolism, represents a particularly powerful oncoprotein that affects cancer cells at several levels,

260 these data identified PAX5-ETV6 as a potent oncoprotein that drives B-cell leukemia development.

261 Y box protein 1 (YBX1) is a well known oncoprotein that has tumor-promoting functions.

262 Mucin 1 (MUC1) is a heterodimeric oncoprotein that is aberrantly overexpressed in most TNB

263 ErbB2, an oncoprotein that is often overproduced in breast tumors,

264 LMP1) is an Epstein-Barr virus (EBV)-encoded oncoprotein that is packaged into small extracellular ve

265 MUC1-C is an oncoprotein that is similarly overexpressed in carcinoma

266 ence of proteasomal degradation of the c-Myc oncoprotein that led to glutathione depletion.

267 Our study identifies WDR4 as an oncoprotein that negatively regulates PML via ubiquitina

268 ypes induce cervical cancer and encode an E7 oncoprotein that plays a major role in HPV-induced carci

269 regulators converged on Smoothened (SMO), an oncoprotein that transduces the Hh signal across the mem

270 ROS1 fusion oncoproteins that better activate MAPK formed more aggre

271 Identifying the multiple dysregulated oncoproteins that contribute to tumorigenesis in a given

272 omal fusions involving ROS1 produce chimeric oncoproteins that drive a diverse range of cancers in ad

273 findings of Ben Shlomo et al. indicate that oncoproteins that drive constitutively high cAMP signali

274 minimal region of the human SS18-SSX fusion oncoprotein (the hallmark driver of synovial sarcoma) th

275 we describe that by stabilizing key melanoma oncoproteins, the ubiquitin ligase RNF4 promotes tumorig

276 l-length MAGI3 from interacting with the YAP oncoprotein, thereby relieving YAP inhibition and promot

277 nistic insight into how Bcl3 functions as an oncoprotein through collaboration with IKK1/2, Akt, and

278 degradation of wild-type ERG and TMPRSS2-ERG oncoprotein through ERG threonine-187 and tyrosine-190 p

279 UL97, which functionally mimics these viral oncoproteins through phosphorylation of Rb, fails to ind

280 fted adaptor protein binding from the fusion oncoprotein to EGFR.

281 on also cooperates with the AML-ETO9a fusion oncoprotein to impair myeloid differentiation and enhanc

282 ltiple cofactors associate with NUP98 fusion oncoproteins to mediate transcriptional changes possibly

283 SNF5 also interacts with the oncoprotein transcription factor MYC and is proposed to

284 The oncoprotein transcription factor MYC is overexpressed in

285 h a sT domain that also inhibits MCV large T oncoprotein turnover.

286 The oncoprotein tyrosine kinase MET, which is the receptor f

287 The MDM2 oncoprotein ubiquitinates and antagonizes p53 but may al

288 Because intratumoral HPV oncoproteins upregulate immune checkpoint proteins such

289 The MUC1 oncoprotein was subsequently identified as the critical

290 Although oncoproteins were discovered many years ago and have bee

291 A prime example is the CIC-DUX4 oncoprotein, which fuses Capicua (CIC) to the double hom

292 e, we demonstrate that the ETO2-GLIS2 fusion oncoprotein, which is found in aggressive acute megakary

293 romising the N-terminal half of the chimeric oncoprotein, which is known to be similarly redistribute

294 ral cancers show oncogene addiction to viral oncoproteins, which are required for survival and prolif

295 Cancer-specific fusion oncoproteins, which display unique chromatin localizatio

296 , persistent HPV infections induce E6 and E7 oncoproteins, which promote cell proliferation and carci

297 Gankyrin is an ankyrin-repeat oncoprotein whose overexpression has been implicated in

298 One mechanism by which oncoproteins work is through perturbation of cellular ma

299 F peptide from the intracellular Wilms tumor oncoprotein WT1 in complex with HLA-A*02:01.

300 of the transcriptional regulators and potent oncoproteins, YAP/TAZ, is considered necessary for adult