ライフサイエンスコーパス: ErbB receptor

1 CF-10A, without interference from endogenous ErbB receptors.

2 neuregulin (NRG-1), that binds to different ErbB receptors.

3 ites of tyrosine phosphorylation on the four ErbB receptors.

4 ilarly coexpress multiple NRG-1 isoforms and erbB receptors.

5 segregate from their basolaterally localized erbB receptors.

6 radial glia and that it acts via one or more erbB receptors.

7 where it immediately binds to and activates erbB receptors.

8 t of sequential signaling through Notch1 and erbB receptors.

9 ream pathways, including, e.g., signaling by ErbB receptors.

10 wth factor (EGF) family and their astrocytic erbB receptors.

11 induced interactions of erbB3 with different erbB receptors.

12 s transfected with different combinations of erbB receptors.

13 (s) of hetero- and homodimerization of the c-erbB receptors.

14 sitive autocrine/paracrine feedback loop via ErbB receptors.

15 ll lines expressing different complements of ErbB receptors.

16 ions figure prominently in signaling through ErbB receptors.

17 ve modifier of breast cancer in concert with ErbB receptors.

18 where it was in a position to signal through erbB receptors.

19 ave been shown to interact with and activate erbB receptors.

20 s activity may rely on signals transduced by erbB receptors.

21 ns in advanced human malignancies expressing erbB receptors.

22 utonomous fashion and independently of known erbB receptors.

23 negative regulatory activity and stabilizes ErbB receptors.

24 mal trafficking and signaling attenuation of ErbB receptors.

25 ctivity through interaction with its cognate ErbB receptors.

26 aptic signaling pathways, (1) neuregulin and erbB receptors 2, 3, and 4 and (2) agrin, MuSK, and raps

27 , we show that heregulin (HRG), a ligand for ErbB receptors, activates c-Src and, in turn, stimulates

28 eas PE01 cells were growth stimulated by the erbB receptor-activating ligands, such as transforming g

29 Mutation of this amino acid led to increased ERBB receptor activation and upregulation of the ERBB3/P

30 ely blocks N-sulfation significantly reduced erbB receptor activation by neuregulin-1 but had no effe

31 Further, erbB receptor activation by neuregulin-1 enhances cell m

32 between extracellular matrix-hyaluronan and ErbB receptor activation during development of early hea

33 ntial mechanisms of p85-sErbB3 inhibition of ErbB receptor activation exist, our results suggest that

34 protein levels are suppressed in response to ErbB receptor activation in breast tumor cells but are u

35 The need for sustained erbB receptor activation may be the reason why neureguli

36 nic secretion and if differential effects on ErbB receptor activation may explain the ability of the

37 ediates the stimulatory effect of astroglial erbB receptor activation on neuronal LHRH release.

38 Fbeta-specific signals are also required for ErbB receptor activation.

39 se mammary tumor cells derived from aberrant ErbB receptors activation, but does not interfere with t

40 ErbB receptors also form higher order oligomers, but the

41 The neuregulin/erbB receptor and agrin/MuSK pathways are critical for c

42 ligand deprivation Mig6 dissociates from the ErbB receptor and binds to and activates the tyrosine ki

43 , by activating Src-FAK, TGF-beta integrates ErbB receptor and integrin signaling to induce cell migr

44 totally within the cytoplasmic domain of an ErbB receptor and suggests that the s80 ICD may function

45 ells requires the convergence of inputs from ErbB receptors and a Gbetagamma- and PI3Kgamma-dependent

46 nsory neurons and supporting cells involving erbB receptors and BDNF.

47 her oncogenic proteins such as beta-catenin, erbB receptors and c-Src, but a functional role for MUC1

48 tructure completes the gallery of unliganded ErbB receptors and demonstrates that all human ligand-bi

49 receptor-receptor interaction sites for the erbB receptors and demonstrates the possibility of disab

50 HRG/M was unable to autophosphorylate the erbB receptors and did not affect the level of MAPK phos

51 Expression of the four ERBB receptors and downstream signaling elements in tumo

52 ely by the presence or absence of particular ErbB receptors and emphasizes the dynamic nature of the

53 ng analysis to analyze the expression of the ErbB receptors and neuregulin (NRG) 1-alpha and NRG1-bet

54 er in a single pathway, which is mediated by ErbB receptors and PI3K/Akt.

55 t Kek1 may be used experimentally to inhibit ErbB receptors and point to the possibility that, as yet

56 es (c-Abl, Arg) are activated by deregulated ErbB receptors and Src kinases, and drive invasion of ag

57 cancer cell lines, downstream of deregulated ErbB receptors and Src kinases.

58 unction of the AR and provide a link between ErbB receptors and the AR.

59 Vascular endothelial cells (ECs) express erbB receptors and their ligand, neuregulin-1, and can r

60 ability of Muc4 to segregate ErbB2 and other ErbB receptors and to alter downstream signaling cascade

61 k in a novel signaling pathway downstream of ErbB receptors and upstream of Rac, p38 MAPK, and ERK5 a

62 nic MUC1 physically associates with all four erbB receptors, and co-localizes with erbB1 in the lacta

63 Heregulin binds erbB receptors, and in our studies, primary cultures of

64 ms and suggests new approaches for designing ErbB receptor antagonists.

65 ErbB receptors are a family of ligand-activated tyrosine

66 ErbB receptors are activated by ligand-induced formation

67 However, ErbB receptors are also expressed in several healthy tis

68 , higher order complexes of nonoverexpressed ERBB receptors are an integral and qualitatively distinc

69 When the glial erbB receptors are blocked, neurons fail to induce radia

70 ErbB3 therapeutically in parallel with other ErbB receptors are challenging because its intracellular

71 isms for homo- and hetero-oligomerization of erbB receptors are different, and contradicts the simple

72 ErbB receptors are essential mediators of cell prolifera

73 These results showed that erbB receptors are expressed widely in adult rat brain a

74 In CCA, ErbB receptors are frequently overexpressed, leading to

75 ErbB receptors are key regulators of cell survival and g

76 heterodimerization (oligomerization) of the erbB receptors are known to be critical events for recep

77 We have found that ErbB receptors are present in brain subcellular fraction

78 ErbB receptors are required for Schwann cell migration,

79 Neuregulin (Nrg) ligands and their ErbB receptors are required for the development of Schwa

80 Chimera analyses indicate that ErbB receptors are required in all migrating Schwann cel

81 mechanisms that regulate the localization of ErbB receptors are unknown.

82 1-ntfbeta, which could similarly activate an ErbB receptor as evidenced by increased phosphorylation

83 odomains to heterodimerize, thereby creating erbB receptor assemblies which are defective in signalin

84 ErbB receptors associate in a ligand-dependent or -indep

85 At interneuronal synapses, neuregulin ErbB receptors associate with PDZ-domain proteins at pos

86 naling pathways argue against neuregulin and erbB receptors being localized to the NMJ via direct int

87 s, whereas other neurons expressed all three erbB receptors but sequestered each of these polypeptide

88 for inducing homo- or heterodimerization of ErbB receptors by using synthetic ligands without interf

89 s is not generic and suggest that individual ErbB receptors can discriminate between different EGF-li

90 mechanism by which targeting both IGF-1R and ErbB receptors causes synergistic effects on cell growth

91 ErbB receptor chimeras containing synthetic ligand bindi

92 The extracellular, ligand binding regions of ErbB receptors consist of four domains that can assume a

93 growth and differentiation factors and their erbB receptors contribute importantly to the development

94 lin 1 (Nrg1) type III, which signals through ErbB receptors, controls Schwann cell migration in addit

95 effect of NRG-1beta on cardiac function via ErbB receptor coupling and expression.

96 ighlight additional levels of complexity for ErbB receptor coupling to downstream effectors that cont

97 es to pathological activation of Galphaq and ErbB receptor-dependent pathways in the heart.

98 on status of the enzyme mediated by Src- and ErbB receptor-dependent PI 3-K activation.

99 To test whether an ErbB receptor dimer is capable of discriminating among l

100 A dose-dependent inhibition of native erbB receptor dimerization by the erbB peptides has been

101 for Nrg-1 back signaling include binding of erbB receptor dimers to the extracellular domain of Nrg-

102 ered for ligand discrimination by individual ErbB receptor dimers; receptors appear to realize which

103 has emerged as a physiological mechanism of ErbB receptor down-regulation, and this mechanism appear

104 exogenous NRG1 or antibodies that stimulate erbB receptors dramatically improve the morphology of di

105 s have been shown to selectively bind to the erbB receptor ectodomains and isolated subdomain IV of e

106 some phenotypic similarities with mutants in ErbB receptors, EGFR homologs that are implicated in div

107 nal through distinct combinations of dimeric ErbB receptors - elicits its multitude of biological eff

108 t NMDA receptor functions via actions on its ErbB receptors enriched in postsynaptic densities, hence

109 ces in the extracellular subdomain IV of the erbB receptors (erbB peptides).

110 h factor, which mediates its effects through erbB receptors, erbB1 and erbB2/C-neu.

111 Recently, the interaction between ErbB receptors (ErbB2 and ErbB3) on the surface of Schwa

112 Lrig3 was recently reported to increase ErbB receptor expression suggesting that it may function

113 Pharmacokinetic studies and ERBB-receptor expression and signaling studies were perf

114 In contrast, ligand-induced erbB receptor extracellular domain hetero-oligomers did

115 Our findings argue that erbB receptor extracellular domains do not recapitulate

116 homo- and hetero-oligomerization of purified erbB receptor extracellular domains.

117 Given the similarities in the mechanism of ErbB receptor family activation, these findings could fa

118 lls do not detectably express members of the ErbB receptor family and do not proliferate in response

119 h each of the known members of the mammalian ErbB receptor family and that the Kek1/EGFR interaction

120 ed the role of the tumor microenvironment on ErbB receptor family expression and found that the statu

121 Mutations within members of the EGF/ErbB receptor family frequently release the oncogenic po

122 ed with the ability to bias signaling in the ErbB receptor family in a cell motility assay.

123 The ErbB receptor family is dysregulated in many cancers, an

124 The ErbB receptor family is implicated in the malignant tran

125 Neuregulin-1beta is an ErbB receptor family ligand that is effective against DO

126 The ErbB receptor family member ErbB3 has been implicated in

127 Although ErbB receptor family members are expressed in pituitary

128 n the context of the DNA damage response and ErbB receptor family signaling and offer a perspective o

129 conserved in any of the other members of the ErbB receptor family suggesting its physiological functi

130 amined whether disabling oncoproteins of the erbB receptor family would sensitize transformed human g

131 d by selective inhibitors of Src kinase, the ErbB receptor family, and phosphoinositide 3-kinase (PI

132 1 and erbB-2, two of the four members of the erbB receptor family, and respond to TGFalpha with recep

133 ltered cell responsiveness to ligands of the erbB receptor family.

134 transmembrane tyrosine kinases, such as the ErbB receptor family.

135 hat bind and activate several members of the ErbB receptor family.

136 ransmembrane tyrosine kinases constitute the ErbB receptor family: the epidermal growth factor (EGF)

137 Mitogen-inducible gene 6 [Mig-6; Errfi1 (ErbB receptor feedback inhibitor 1); RALT (receptor-asso

138 GEO cells depend on multiple ErbB receptors for aberrant growth.

139 suggest a role for TM domain interactions in ErbB receptor function, possibly in stabilizing inactive

140 adation may contribute to the suppression of ErbB receptor function.

141 ating erbB-dependent signaling and promoting erbB receptor gene expression in astrocytes, a neuron-to

142 ng metalloproteinase activity, and increased erbB receptor gene expression.

143 a by a mechanism involving activation of the ErbB receptor-->c-Src pathway and transport by the molec

144 of cancer-associated genetic alterations in ERBB receptors has also been identified.

145 eraction between neuregulin 1 (Nrg1) and its ErbB receptors has been implicated in the pathological m

146 Higher order complexes of ERBB receptors have been observed biophysically and offe

147 Although ErbB receptors have been shown to crosscommunicate with

148 mbinations of agents that inhibit IGF-1R and ErbB receptors have been shown to synergistically block

149 Although ErbB receptors have been widely studied in cholangiocarc

150 Anticancer therapies targeting ErbB receptors have shown promise, and a monoclonal anti

151 lthough ErbB2 is unique among the four human ErbB receptors, here we show that it is the closest stru

152 One model proposed for ligand-induced erbB receptor hetero-oligomerization involves simple het

153 r aim has been to understand the features of erbB receptor homo- and heterodimer assembly to develop

154 n receptor kinase activation, ligand-induced ErbB receptor homo- and heterodimerization is thought to

155 nal changes may determine the specificity of ErbB receptor homo- versus heterodimerization.

156 that postnatally express a dominant-negative ErbB receptor in non-myelinating but not in myelinating

157 ansgenic mice expressing a dominant-negative erbB receptor in these glial cells.

158 positive bands were also identified for each ErbB receptor in whole brain homogenates and separate cy

159 y NRG-1beta and that it interacts with other ErbB receptors in a distinctly hierarchical fashion.

160 t can be used for further studies of NRG and ErbB receptors in brain circuits and demonstrate the fea

161 ious studies established that stimulation of ErbB receptors in breast cancer cells activates Rac1 and

162 ty, cell growth, and tumorigenesis driven by ErbB receptors in breast cancer cells.

163 cal modeling to quantify phospho-turnover at ErbB receptors in human cells and to determine the conse

164 erent sensory neurons, and signaling through ErbB receptors in intrafusal muscle fibers.

165 The continued expression of NRGs and their erbB receptors in mature brain also implies that these m

166 ons between the transmembrane domains of the erbB receptors in micellar solutions.

167 The differential distributions of erbB receptors in neurons and glia and the known functio

168 le the current knowledge on the functions of ErbB receptors in physiology and physiopathology of the

169 and show HER2 poised to interact with other ErbB receptors in the absence of direct ligand binding.

170 focused on neuregulin (NRG1), acting through erbB receptors, in maintaining their morphology.

171 yrosine kinase signaling that directly links ErbB receptor inactivation to the induction of apoptosis

172 soforms of neuregulin-1 (Nrg-1), ligands for erbB receptors, include an extracellular domain with an

173 ellular region that autoinhibits other human ErbB receptors, including the epidermal growth factor (E

174 ErbB receptors, including the epidermal growth factor re

175 ells, LRIG1 forms a complex with each of the ErbB receptors independent of growth factor binding.

176 The ubiquitous expression of ErbB receptors indicates that many cell populations thro

177 lated phosphorylation of ErbB4 but not other ErbB receptors, indicating that this is a specific respo

178 Moreover, ErbB receptor inhibition increases LTP at potentiated sy

179 this report, we show that dacomitinib, a pan-ErbB receptor inhibitor, diminished growth, clonogenic p

180 Using specific ErbB receptor inhibitors and depletion of receptors by R

181 ozen tumor sections after treatment with the erbB receptor inhibitors OSI-774 and Herceptin.

182 We describe a new approach that directs ErbB receptor interactions, resulting in biased signalin

183 n different responses observed when the same ErbB receptor is stimulated by different ligands.

184 Degradation of activated ERBB receptors is an important mechanism for signal atte

185 Although coexpression of ErbB receptors is associated with poor patient prognosis

186 growth factors whose signalling through the ErbB receptors is essential to the growth and differenti

187 Neuregulin signaling through ErbB receptors is known to play an essential role in Sch

188 istance, ERBB1, the most extensively studied ERBB receptor, is examined as a target for tumor cell ra

189 Inhibition of ErbB receptor kinase in adult Tg2576 restores LTP but im

190 utant-specific intermolecular regulation for ErbB receptors, knowledge of which could potentially be

191 gulin (NRG) signaling proteins interact with ErbB receptors leading to the proliferation, differentia

192 like growth factor (HB-EGF), a member of the ErbB receptor ligand family, exists in distinct molecula

193 In addition, not all of the expected ErbB receptor ligand-induced dimerization events can be

194 uced activation of CDK2 also depended on the ErbB receptor, MAPK, and PI3K, all of which have previou

195 sm by which HRG-beta1-activated signaling of erbB receptors may affect invasive/metastatic properties

196 Disabling erbB receptors may improve the response to gamma-irradia

197 r ATF approach has elucidated differences in ErbB receptor-mediated proliferation, migration, and int

198 ed several molecular mechanisms required for ErbB receptor-mediated proliferation.

199 plex, not TRAF6, is a critical E3 ligase for ErbB-receptor-mediated Akt ubiquitination and membrane r

200 expression of ErbB2 in cells devoid of other ErbB receptor members is sufficient to promote ERK activ

201 Proximal receptor interactions between erbB receptor members thus influence cell cycle checkpoi

202 inoma cells depleted of ErbB2, but not other ErbB receptor members, to specifically examine the role

203 holine receptor gene expression and that the erbB receptors need to be kept phosphorylated during thi

204 In this study we have used the ErbB receptor network to explore the relationship betwee

205 sponse and resistance to therapies targeting ErbB receptors occur and are often associated with activ

206 These growth factors induce erbB receptor oligomerization, and their biological spec

207 response initiated by HRGbeta1 binding to c-erbB receptors on the cell surface and which leads to th

208 antibodies that either blocked or stimulated erbB receptors, or a soluble erbB subtype that binds to

209 Here, we have examined if ErbB receptors, other than the EGFR, have a role in regu

210 ese cell lines express only two of the known ErbB receptors, our results imply that EGF-like ligands

211 ally enhance the dimerization of the various ErbB receptor pairings, with the EGFR/ErbB3 heterodimer

212 through Galphaq in NRVMs and via the Galphaq/ErbB receptor pathways in cardiac fibroblasts.

213 bility of specific oligosaccharides to block erbB receptor phosphorylation in L6 muscle cells.

214 ure media, resulting in high basal levels of erbB receptor phosphorylation.

215 Neuregulin signaling through the ErbB receptor regulates Schwann cell development; howeve

216 This suggests that downstream effectors of ErbB receptors represent good therapeutic targets for br

217 the exchange factors (Rac-GEFs) that mediate ErbB receptor responses.

218 named TOXCAT, we find that the TM domains of ErbB receptors self-associate strongly in the absence of

219 srupted by expression of a dominant-negative erbB receptor show severe hearing loss and 80% postnatal

220 omprehensive, multi-scale dynamical model of ErbB receptor signal transduction in human mammary epith

221 t tumors examined, and it has been linked to ErbB receptor signaling and AKT activation.

222 ent contacted myotubes by Neuregulin1 (Nrg1)/ErbB receptor signaling and it has an essential role in

223 Furthermore, tumors that depend on ErbB receptor signaling for survival and exhibit activat

224 These data suggest a role for disabled erbB receptor signaling in the transition from compensat

225 e examine the potential for the neuregulin-1/erbB receptor signaling network to contribute to this pr

226 de evidence implicating the neuregulin (NRG)-erbB receptor signaling pathway in this process.

227 In this report, we show that neuregulin-erbB receptor signaling plays a crucial role in the migr

228 hese results suggest that the attenuation of erbB receptor signaling seems to be associated with acti

229 oresistant human glioblastoma cells in which erbB receptor signaling was inhibited exhibited increase

230 G2-dependent effects on tumor progression to ErbB receptor signaling, and raise the possibility that

231 has been linked to alpha6beta1 integrin and ErbB receptor signaling, and we show that myelination by

232 rlying the dependence of cancers on aberrant ERBB receptor signaling.

233 eved in transformed glial cells by disabling erbB receptor signaling.

234 ragment that in turn binds to and stimulates ErbB receptor signaling.

235 show that ESX transcription is regulated by ErbB receptor signalling.

236 Thus, targeting both IGF-1R and ErbB receptors simultaneously results in cell cycle arre

237 e have developed a general approach to cause erbB receptor-specific trans inhibition of human neoplas

238 nown about the neuroanatomical expression of ErbB receptors specifically in primates.

239 shown that MUC1 interacts with beta-catenin, erbB receptors, src, GSK-3beta and protein kinase Cdelta

240 ssed widely in adult rat brain and that each erbB receptor subtype has a distinct distribution.

241 tor and/or a monoclonal antibody against the ErbB receptor subtype HER-2/neu on carcinoma cell growth

242 one step in the signaling events mediated by erbB receptors such as p185neu and EGFR.

243 The ErbB receptors, such as EGFR, have been intensely pursue

244 In addition, comparison of the vertebrate ErbB receptors suggest that a gene duplication event gen

245 f the sequences for the known ligands of the ErbB receptors suggests that the vertebrate ligands segr

246 on and a variety of stimulating ligands, the ErbB receptor system is both diverse and flexible, which

247 f transformed cells overexpressing different erbB receptors, T6-17 and 32D, in standard MTT (3-(4,5-d

248 restingly, the expression of ErbB4, the only ErbB receptor that EGFR co-precipitates in wild-type cel

249 re upregulated by heregulin, an activator of ErbB receptors that are known to be important in mammary

250 pment of mechanism-based therapies targeting ERBB receptors that have improved outcome for many cance

251 triggered cell proliferation by induction of ErbB receptors through the proteolytic shedding of an Er

252 s; (ii) potentiation of signaling downstream ErbB receptors, thus contributing to tumor progression a

253 ver, it has proven difficult to link a given ErbB receptor to a specific biological process since mos

254 (Nrg1-ntfbeta), which can bind to a cognate ErbB receptor to activate the specific signaling cascade

255 eptor-ligand affinities and the necessity of ErbB receptors to dimerize to signal, bivalent ligands,

256 The capacity of ErbB receptors to interact with PDZ-domain proteins at c

257 t is obliged to form heterodimers with other ErbB receptors to signal.

258 irreversible pharmacologic antagonists of c-erbB receptor tyrosine kinase activity.

259 In contrast, the c-erbB receptor tyrosine kinase antagonists and the neutra

260 n gene family, down-regulates members of the ErbB receptor tyrosine kinase family and attenuates thei

261 th factor receptor (EGFR), a member of the c-ErbB receptor tyrosine kinase family, is involved in reg

262 respond to NRGs by activating members of the erbB receptor tyrosine kinase family.

263 idermal growth factor receptor (EGFR/HER) or ErbB receptor tyrosine kinase family.

264 lin was mainly blocked by application of the ErbB receptor tyrosine kinase inhibitor, phospholipase C

265 Neratinib is an oral, irreversible pan-ErbB receptor tyrosine kinase inhibitor.

266 sphorylation were inhibited by two different ErbB receptor tyrosine kinase inhibitors, by the ErbB1-s

267 d by two structurally distinct and selective ErbB receptor tyrosine kinase inhibitors.

268 The erbB receptor tyrosine kinase-activated phosphatidylinos

269 that act through activation of cell-surface erbB receptor tyrosine kinases and have essential functi

270 ErbB receptor tyrosine kinases can transit to nuclei in

271 imultaneously targeting the entire family of ErbB receptor tyrosine kinases for ubiquitination and de

272 ing the activation, uptake, and signaling of ErbB receptor tyrosine kinases in human tumor cell lines

273 Dysregulation of ErbB receptor tyrosine kinases is thought to promote mam

274 previous studies reveal that signals through ErbB receptor tyrosine kinases modulate Xenopus gastrula

275 The epidermal growth factor receptor (EGFR)/ErbB receptor tyrosine kinases regulate several aspects

276 exhibited an upregulation of ErbB2 and other ErbB receptor tyrosine kinases that may supersede the fu

277 serves as a critical component that couples ErbB receptor tyrosine kinases to the migration/invasion

278 Its receptors, ErbB receptor tyrosine kinases, are localized at the pos

279 s, alternatively spliced ligands for several erbB receptor tyrosine kinases, are thought to play impo

280 and differentiation factor that signals via erbB receptor tyrosine kinases, has been shown to have b

281 arge family of growth factors that stimulate ERBB receptor tyrosine kinases.

282 u differentiation factor (NDF), a ligand for erbB receptor tyrosine kinases.

283 erodimerization with and activation by other ErbB receptor tyrosine kinases.

284 However, NRG-2 stimulates different ErbB-receptor tyrosine-phosphorylation profiles from NRG

285 Deregulation of ErbB receptor-tyrosine kinases is a hallmark of many hum

286 quitination is also induced by activation of ErbB receptors; unexpectedly, and in contrast to IGF-1 i

287 ese data suggest that increased signaling by ErbB receptors up-regulates MAPK activity, which, in tur

288 rred by mutations such as those in oncogenic ErbB receptor variants or by treatment with drugs such a

289 the glial cell membrane, transactivation of erbB receptors via a mechanism requiring metalloproteina

290 Tyrosine phosphorylation of ErbB receptors was not observed after treatment of cells

291 Abs specific for the extracellular domain of ErbB receptors was the first implementation of rational

292 een shown to be functionally associated with ErbB receptors, we asked if this pathway could mediate P

293 e protein expression and interactions of the ErbB receptors were examined in different liver prolifer

294 ERBB receptors were linked to human cancer pathogenesis

295 neuregulin-3 as well, binds to Schwann cell ErbB receptors, which in turn regulate remyelination.

296 We postulated that broader inhibition of ErbB receptors with afatinib would improve clinical outc

297 e, we discuss current paradigms of targeting ERBB receptors with cancer therapeutics and our understa

298 throblastic leukemia viral oncogene homolog (erbB) receptors with mAbs promoted erbB tetrameric assem

299 omplex and independent programs regulate the ErbB receptors, with implications for differential cell

300 itulate most heteromeric interactions of the erbB receptors, yet reproduce their ligand-induced homo-