ライフサイエンスコーパス: oncoprotein

1 ppressor, whereas HIF2alpha is considered an oncoprotein.

2 rkel cell polyomavirus small T antigen viral oncoprotein.

3 nslocation that generates an SS18-SSX fusion oncoprotein.

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

5 thway leads to aberrant elevation of the ERG oncoprotein.

6 ic expression of an activated NPM-ALK fusion oncoprotein.

7 part, through expression of its small T (sT) oncoprotein.

8 op carcinoma, confirming that cyclin E is an oncoprotein.

9 and allosteric activators such as the HPV E6 oncoprotein.

10 somal degradation of the PAX3-FOXO1 chimeric oncoprotein.

11 ults in the formation of the BRD4-NUT fusion oncoprotein.

12 The function of p53 is inhibited by the MDM2 oncoprotein.

13 s ATO-induced degradation of the NPM1 mutant oncoprotein.

14 fferences in the cytotoxin-associated gene A oncoprotein.

15 d human cancer virus encoding a small T (sT) oncoprotein.

16 T cell responses by targeting the HPV-16 E7 oncoprotein.

17 ribed antibodies directed against the HPV E6 oncoprotein.

18 modulate the expression of the B-Raf(V600E) oncoprotein.

19 POP-mediated degradation function on the ERG oncoprotein.

20 n the pleckstrin homology domain of the Akt1 oncoprotein.

21 lly through a mechanism involving the HPV E7 oncoprotein.

22 associated with directly inhibiting the KRAS oncoprotein.

23 ormed into a significantly more leukemogenic oncoprotein.

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

25 he proinvasive Fos-related antigen 1 (FRA-1) oncoprotein.

26 us is the smallest known naturally occurring oncoprotein.

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

28 sses the EWS/FLI fusion transcription factor oncoprotein.

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

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

31 ation and upregulated expression of specific oncoproteins.

32 use model of carcinogenesis induced by HPV16 oncoproteins.

33 n of cells with elevated expression of virus oncoproteins.

34 ex and how the complex is disrupted by viral oncoproteins.

35 inhibited phosphorylation of all tested RET oncoproteins.

36 from upstream cues, including those from Ras oncoproteins.

37 t promotes the stabilization of key lymphoma oncoproteins.

38 hat SCF(Fbw7) regulates a network of crucial oncoproteins.

39 that influence tumor spectra induced by RAS oncoproteins.

40 d from prenylation of the RAS superfamily of oncoproteins.

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

42 F4E-dependent export of transcripts encoding oncoproteins.

43 Viral oncoprotein action on RBs results in the release of acti

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

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

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

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

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

49 cuss the influence of cancer stem cells, HPV oncoproteins, altered molecular pathways, and mutations

50 n the steady-state levels of Hsp70-sheltered oncoproteins, an effect associated with inhibition of ca

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

52 prevented MAGE-A11 interaction with the E2F1 oncoprotein and inhibited the MAGE-A11-induced increase

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

54 must be inactivated by E1B-55K/E4-ORF3 viral oncoproteins and a global MRN-independent ATM DDR to vir

55 Viral oncoproteins and cellular mutations drive the transforma

56 id cell lines (LCLs), we identified four EBV oncoproteins and five EBV-activated NF-kappaB subunits c

57 important for translation of mRNAs encoding oncoproteins and growth-promoting factors, which often h

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

59 cell proliferation through depleting client oncoproteins and shutting down multiple oncogenic pathwa

60 the human genome beyond expression of viral oncoproteins and suggest that specific integration event

61 rs of PP2A, I2PP2A, Inhibitor-2 of PP2A (SET oncoprotein) and cancerous inhibitor of PP2A (CIP2A), in

62 tor tyrosine kinase were first identified as oncoproteins, and both can induce tumorigenesis when ove

63 demonstrated that the cancer-causing HPV E6 oncoproteins are all subject to posttranslational modifi

64 orylation, degradation, and binding by viral oncoproteins are also codified.

65 Many oncoproteins are considered undruggable because they lac

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

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

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

69 ity purification, we have identified the DEK oncoprotein as a critical factor that interacts with an

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

71 L6, a transcriptional repressor and lymphoma oncoprotein, as a pivotal factor required for neurogenes

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

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

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

75 ylation of the ETS1 and ETS2 transcriptional oncoproteins at specific serine or threonine residues cr

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

77 lated tyrosine kinase activity of the fusion oncoprotein BCR-ABL.

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

79 is driven by the creation of a translocation oncoprotein, BRD4-NUT, which blocks differentiation and

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

81 show that KIT D816V is a disease-propagating oncoprotein, but it does not activate MCs to release pro

82 drive cancer by the actions of the E6 and E7 oncoproteins, but the molecular architecture of HPV infe

83 K17 functions specially among keratins as an oncoprotein by controlling the ability of p27(KIP1) to i

84 ally, we determined that K17 functions as an oncoprotein by regulating the subcellular localization a

85 Moreover, the proto-oncoprotein c-Fos has an emerging role in glycerolipid s

86 A high expression of the oncoprotein c-Met in primary uveal melanoma is associate

87 proteome revealed the presence of the proto-oncoprotein c-MYC and of ENY2.

88 gion also interacted with the cellular proto-oncoprotein c-MYC and the homolog of enhancer of yellow

89 ational design of inhibitors of the bHLH-ZIP oncoprotein c-Myc is hampered by a lack of structure in

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

91 Helicobacter pylori strains that harbor the oncoprotein CagA increase gastric cancer risk, and this

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

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

94 uired for the translocation of the bacterial oncoprotein CagA.

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

96 ern HK2 sequences, which encode two putative oncoproteins, can lead to disease remains to be studied.

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

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

99 ) diminishes endosomal targeting of the EGFR oncoprotein, consequently enhancing EGFR signaling durin

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

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

102 ular invasion through the translation of the oncoprotein DEK.

103 cancer progression, likely through an HPV E7 oncoprotein-dependent mechanism.

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

105 KRAS-positive CRCs indicates that different oncoproteins direct the assembly of distinct repressor c

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

107 In addition, NUP98 oncoproteins displayed a prolonged half-life in cells.

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

109 Recently, the human papillomavirus (HPV) oncoprotein E6 has been identified as a potent activator

110 cancer and oral cancer as well, and the HPV oncoprotein E6 may induce the degradation of p53 functio

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

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

113 g site increases the expression of the viral oncoproteins E6 and E7 and promotes host cell proliferat

114 HPV expresses the oncoproteins E6 and E7, both of which play key roles in

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

116 HPV oncogenesis is driven by two viral oncoproteins, E6 and E7, which are expressed through alt

117 Expression of the HPV16 oncoproteins E7 and E6 drives HPV-associated tumor forma

118 over 70% of cervical cancers and produce the oncoprotein, early protein 6 (E6), which binds to p53 an

119 Ls) requires four EBV nuclear antigen (EBNA) oncoproteins: EBNA2, EBNALP, EBNA3A, and EBNA3C.

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

121 ogene RUNX1-RUNX1T1) and PML-RARalpha fusion oncoproteins (encoded by PML-RARA) are extremely sensiti

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

123 Myc oncoproteins exert tumorigenic effects by regulating exp

124 Cdc20) activity via expressing the Tax viral oncoprotein exhibit reduced Bim levels and resistance to

125 show that SRSF2 is a key regulator of HPV16 oncoprotein expression and cervical tumor maintenance.

126 The translational control of oncoprotein expression is implicated in many cancers.

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

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

129 d whether these proteins could control HPV16 oncoprotein expression.

130 exity of splicing events that regulate viral oncoprotein expression.

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

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

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

134 bunit complexes, which also protect the LMO2 oncoprotein from degradation.

135 The HPV E6 oncoprotein from HPV degrades p53 and abrogates cell cyc

136 s have failed to reproduce MCC in mice using oncoproteins from this polyomavirus.

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

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

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

140 The mucin 1 (MUC1) oncoprotein has been linked to the inflammatory response

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

142 d activates telomerase, but the multifaceted oncoprotein has numerous other functions that are highli

143 Animal polyomavirus sT oncoproteins have been found to cause experimental tumor

144 The E6 and E7 oncoproteins have emerged as key players in the deregula

145 sing high-risk human papillomavirus (HPV) E6 oncoproteins have PDZ binding potential, an activity whi

146 inued cellular propagation, HPVs express two oncoproteins, HPV E6 and E7.

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

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

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

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

151 negatively regulate the stability of the ERG oncoprotein in prostate cancer.

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

153 geneity among the different high-risk HPV E6 oncoproteins in how they are regulated by different cell

154 We tested the papillomavirus E6 and E7 oncoproteins in three functional assays and found that E

155 small T antigen, another well-characterized oncoprotein, in two of these assays.

156 ssense mutations in several previously known oncoproteins including HRAS, EGFR, and PIK3CA.

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

158 The stability of several oncoproteins, including c-Myc, is regulated by ubiquitin

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

160 HPV16 oncoproteins induced a decrease in epidermal Skint1 expr

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

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

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

164 Accordingly, many oncoproteins inhibit, and several oncosuppressor protein

165 , we identified that YAP/TAZ, two homologous oncoproteins inhibited by the Hippo tumor suppressor pat

166 how that LAPTM4B, an endosomal transmembrane oncoprotein, inhibits EGF-induced EGFR intraluminal sort

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

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

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

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

171 The Ras oncoprotein is a key driver of cancer.

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

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

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

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

176 ng the effector pathways downstream of these oncoproteins is important to identify opportunities for

177 mbrane protein-1 (LMP1), the principal viral oncoprotein, is a latency-associated protein implicated

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

179 vels of the E6-regulated p53 proteins and E7 oncoprotein itself.

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

181 complex and define a mechanism by which the oncoprotein LAPTM4B can transform cells and promote tumo

182 Thus, the oncoprotein LAPTM4B facilitates the role of inactive EGF

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

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

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

186 The major EBV oncoprotein, latent membrane protein 1 (LMP1), mimics co

187 MYC master oncoprotein levels were markedly decreased.

188 The EBV oncoprotein LMP1 constitutively activates NFkappaB and i

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

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

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

192 y as the concomitant degradation of multiple oncoproteins may lead to effective antineoplastic agents

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

194 d lid region of the N-terminal domain of the oncoprotein MDM2 in the presence of different ligands we

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

196 anslation during mitosis revealed by a viral oncoprotein, Merkel cell polyomavirus small T (MCV sT).

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

198 the cell proliferative function of the human oncoprotein mouse double minute2 (MDM2) primarily to its

199 gned as dimerization inhibitors of prominent oncoprotein mucin 1.

200 domain (p53 DBD), and the N-terminus of the oncoprotein murine double minute 2 (NT-MDM2)-have been s

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

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

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

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

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

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

207 e protein 1 (LMP1) is considered the primary oncoprotein of EBV, and in epithelial cells it induces t

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

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

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

211 The E6 and E7 oncoproteins of human papilloma virus (HPV) drive the ma

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

213 T antigens (ST) are shared by the E6 and E7 oncoproteins of two oncogenic papillomaviruses.

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

215 tor JQ1 or conditionally inactivating an EBV oncoprotein or NF-kappaB decreased MYC or BCL2 expressio

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

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

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

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

220 cal relevance and position KSR1 in the major oncoprotein pathways in breast tumorigenesis.

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

222 The mucin 1 C-terminal subunit (MUC1-C) oncoprotein plays a critical role in regulating cell pro

223 and AF6 co-silencing confirmed that MLL-AF6 oncoprotein potentiates the activity of the RAS pathway

224 Together, our findings suggest that NUP98 oncoproteins predispose myeloid cells to oncogenic trans

225 ctivating protein (GAP) that inactivates the oncoprotein Ras and plays important roles in nervous sys

226 DNA tumor virus oncoproteins reduce Rb function by either inducing Rb de

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

228 exhibits a 10:1 in vitro selectivity for the oncoprotein relative to the WT, with a similar selectivi

229 haracterized by the expression of PAX3-FOXO1 oncoprotein, remains unknown.

230 Furthermore, we show that the HPV E6 oncoprotein rescues the disability of full-length E6AP t

231 viral transactivator Tax is regarded as the oncoprotein responsible for contributing toward the tran

232 he idea that it should also be considered an oncoprotein, responsible for cyclin D-cdk4 activity.

233 periments revealed that SRSF1 did not affect oncoprotein RNA levels.

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

235 ation, which triggers degradation of the Tax oncoprotein, selectively induces apoptosis of ATL cell l

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

237 The oncoprotein SET was recently suggested to modulate the D

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

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

240 ility of siRNAs designed to target the CIP2A oncoprotein (siCIP2A) into oral cancer cells and consequ

241 CC tumor cells express putative polyomavirus oncoprotein small T antigen (sTAg) and truncated large T

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

243 -associated protein 1 (YY1AP1) is a critical oncoprotein specifically activated in EpCAM(+) AFP(+) HC

244 and experimentally validate PPIs between the oncoprotein SRSF1 and members of the anti-tumor drug tar

245 istance, often involving upregulation of the oncoprotein STAT3 (signal transducer and activator of tr

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

247 Transforming viral oncoproteins, such as adenovirus E1A and papillomavirus

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

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

250 targeted CAR T cells thus represent a potent oncoprotein-targeted immunotherapy for high-risk ALL.

251 Oncoprotein targeting can be a successful strategy to tr

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

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

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

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

256 The viral oncoprotein Tax, which is rarely expressed in ATLL cells

257 f adult T-cell leukemia, expresses the viral oncoprotein Tax1.

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

259 HPV encodes an E6 oncoprotein that degrades the tumor suppressor p53 and a

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

261 r RNA (mRNA) cap-binding protein eIF4E is an oncoprotein that has an important role in cancer initiat

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

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

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

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

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

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 Thus, GWL is a human oncoprotein that promotes the hyperactivation of AKT via

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

271 atic breast cancer typically feature mutated oncoproteins that activate PI3K, Stat3, and Ras signalin

272 ot require immune suppression, and the viral oncoproteins that are frequent targets for an immunologi

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

274 or genes can lead to the formation of fusion oncoproteins that directly modify chromatin as their mec

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

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

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

278 ntly favors the expression of 2 key lymphoma oncoproteins, thus confirming its candidacy as a valuabl

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

280 nveying tumorigenic signals from the BCR-ABL oncoprotein to ribosome biogenesis, affecting cellular g

281 esponse and reinforce the ability of the HPV oncoproteins to disrupt the innate immune response, whic

282 MYC is an oncoprotein transcription factor that is overexpressed i

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

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

285 The MDM2 oncoprotein ubiquitinates and antagonizes p53 but may al

286 Because intratumoral HPV oncoproteins upregulate immune checkpoint proteins such

287 (ALK), causing expression of several fusion oncoprotein variants.

288 The MUC1 oncoprotein was subsequently identified as the critical

289 gain-of-function mutations are expected for oncoproteins, we found that tumor suppressor proteins al

290 mutations is often regarded as a hallmark of oncoproteins, we observed that a number of tumor suppres

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

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

293 We show that the LXCXE motif of these oncoproteins, which is essential for blockade of the ret

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

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

296 EWS-FLI1 is an Ewing sarcoma (ES) oncoprotein with an interactome that we demonstrate to h

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

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

299 nds a peptide derived from the intracellular oncoprotein WT1 presented on HLA-A*02:01.

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