ライフサイエンスコーパス: DDR1

1 DDR1 (discoidin domain receptor tyrosine kinase 1) kinas

2 DDR1 activation appears to be mediated by its ligand, co

3 DDR1 activation suppressed genotoxic-mediated cell death

4 DDR1 also has a major splice form, which has a 37 amino

5 DDR1 and ADAM10 were found to be in a complex on the cel

6 DDR1 dimerization precedes receptor activation suggestin

7 DDR1 does not affect JE permeability but may play a role

8 DDR1 expression in wound healing was confirmed by histol

9 DDR1 is a receptor tyrosine kinase (RTK).

10 DDR1 is constitutively expressed in a variety of normal

11 DDR1 is functionally activated as determined by its tyro

12 DDR1 knockdown and DDR1 pharmacological inhibitor decrea

13 DDR1 knockdown decreased melanocyte adhesion to collagen

14 DDR1 promotes adhesion, proliferation, differentiation,

15 DDR1 recognized collagen I only as a dimeric and not as

16 DDR1 shedding is not a result of an activation of its si

17 DDR1 transmembrane signaling thus appears to occur witho

18 DDR1 undergoes autophosphorylation in response to collag

19 DDR1, discoidin domain receptor 1, belongs to a subfamil

20 DDR1-specific siRNA and a highly selective DDR1 inhibito

21 , including the discoidin domain receptor 1 (DDR1) and E-Cadherin (E-Cad), which interact with COLXV

22 lysis identifies Discodin Domain Receptor 1 (DDR1) as a uniquely upregulated and patient-relevant gen

23 Discoidin domain receptor 1 (DDR1) belongs to a unique family of receptor tyrosine ki

24 llagen receptor discoidin domain receptor 1 (DDR1) by human MKs at both mRNA and protein levels and p

25 tyrosine kinase discoidin domain receptor 1 (DDR1) expressed in granule cells throughout their develo

26 Discoidin domain receptor 1 (DDR1) is a collagen receptor expressed at the epithelium

27 Discoidin domain receptor 1 (DDR1) is a collagen receptor expressed in epithelium.

28 Discoidin domain receptor 1 (DDR1) is a collagen-activated receptor tyrosine kinase w

29 Discoidin domain receptor 1 (DDR1) is a key sensor of COL fiber state and composition

30 Discoidin domain receptor 1 (DDR1) is a nonintegrin collagen receptor constitutively

31 Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase activated by collage

32 Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase activated by collage

33 Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase that binds and trans

34 Discoidin domain receptor 1 (DDR1) is a unique collagen-activated tyrosine kinase tha

35 Discoidin domain receptor 1 (DDR1) is a widely expressed tyrosine kinase receptor whi

36 The discoidin domain receptor 1 (DDR1) is activated by collagens, upregulated in injured

37 A encoding anti-discoidin domain receptor 1 (DDR1) single-chain variable fragments (mscFv) and siRNA

38 e, we show that Discoidin Domain Receptor 1 (DDR1), a collagen receptor overexpressed in cancer, colo

39 re we show that discoidin domain receptor 1 (DDR1), a collagen receptor with tyrosine kinase activity

40 hich identified discoidin domain receptor 1 (DDR1), a collagen-activated tyrosine kinase, as a potent

41 y, knockdown of discoidin domain receptor 1 (DDR1), a collagen-binding protein that also co-localizes

42 y reported that discoidin domain receptor 1 (DDR1), a nonintegrin collagen receptor, is expressed dur

43 Discoidin domain receptor 1 (DDR1), a receptor tyrosine kinase (RTK), has been shown

44 ls, upregulates discoidin domain receptor 1 (DDR1), a receptor tyrosine kinase activated by collagen.

45 , we identified discoidin domain receptor 1 (DDR1), a receptor tyrosine kinase that acts as a collage

46 in 1 (LMP1) and discoidin domain receptor 1 (DDR1), which is activated by collagen(s) and contributes

47 Discoidin domain receptors 1 and 2 (DDR1/2) play a central role in fibrotic disorders, such

48 hoGTPase Cdc42 is activated on collagen in a DDR1-dependent manner.

49 Aberrant DDR1 activity contributes to the progression of human di

50 posure to collagen is sufficient to activate DDR1 in Hodgkin lymphoma-derived cell lines.

51 nse to exogenous overexpression of activated DDR1, dominant-negative DDR1 inhibited irradiation-induc

52 s reveal a novel mechanism whereby activated DDR1 translates to the nucleus to regulate synthesis of

53 insights may be used to develop allosteric, DDR1-specific, kinase inhibitors.

54 We show that although DDR1 and its natural ligand, collagen, lack an NLS, DDR1

55 n, recurrent mutations in ARID1A, ARID1B and DDR1.

56 ortical contractility through E-cadherin and DDR1 proteins.

57 ) cells in the evolution of liver cancer and DDR1 as a potential driver of this process.

58 Overall, we show that Galpha13 and DDR1-Par3 differentially regulate cell-cell junctions an

59 1 human kinases, particularly ABL1, KIT, and DDR1, all of which are known drug targets in other cance

60 DDR1 knockdown and DDR1 pharmacological inhibitor decreased cell growth and

61 phoserine-15 p53, as well as induced p21 and DDR1 levels, suggesting that DDR1 functions in a feedfor

62 ated tyrosine kinases such as PDGFRalpha and DDR1 not previously implicated in the genesis of NSCLC a

63 DR1 tagged with cyan fluorescent protein and DDR1 tagged with yellow fluorescent protein in live cell

64 Moreover, the combination of RG7787 and DDR1 inhibitor caused greater shrinkage of tumor xenogra

65 The AH18.2 was highly conserved between DDR1 and HLA-DQA1 genes; therefore most probably the sec

66 The correlation between DDR1 expression in tumor tissues and clinicopathological

67 oscopy, we monitored the interaction between DDR1 tagged with cyan fluorescent protein and DDR1 tagge

68 suggest that the 1.65 Mb MHC region between DDR1 and HLA-DRA genes is likely to carry additional sus

69 Nonetheless, both DDR1 JM regions contain potentially usable signaling sit

70 munohistochemistry and demonstrate that both DDR1 and DDR2 are up-regulated in nodules of LAM as comp

71 a novel mechanism of collagen regulation by DDR1.

72 of the ABL P-loop appear poorly satisfied by DDR1-IN-1 suggesting a structural basis for its DDR1 sel

73 Excessive signaling by DDR1 and DDR2 has been linked to the progression of vari

74 sm to explain these findings is signaling by DDR1 clusters.

75 We conclude that non-canonical DDR1 signaling enables breast cancer cells to exploit th

76 These collagenases cleave DDR1 and attenuate collagen I- and IV-induced receptor p

77 Our results therefore indicate that collagen-DDR1 signaling is essential for granule neuron axon form

78 The collagen/DDR1 axis is implicated in tumor-stromal interactions an

79 ctivated EMT, is inhibited and concurrently, DDR1 signaling is suppressed.

80 Making use of enforced covalent DDR1 dimerisation, which does not affect receptor functi

81 reaction (qPCR) were employed to assess Ddr1/DDR1 messenger RNA expression in mouse and human tissues

82 The human discoidin domain receptors (DDRs), DDR1 and DDR2, are expressed widely and, uniquely among

83 mammalian discoidin domain receptors (DDRs), DDR1 and DDR2, are unique among receptor tyrosine kinase

84 The discoidin domain receptors (DDRs), DDR1 and DDR2, form a unique subfamily of receptor tyros

85 DDR1 mutant, we found that ADAM10-dependent DDR1 shedding regulates the half-life of collagen-induce

86 We report here that collagen-dependent DDR1 activation is partly regulated by the proteolytic a

87 and that DNA damage induced a p53-dependent DDR1 response associated with activation of its tyrosine

88 The DDR1 extracellular domain (DDR1-ECD), but not its intracellular kinase domain, is r

89 te phosphorylation of receiver DDR1 by donor DDR1 in response to collagen.

90 ervention with IMT effectively downregulated DDR1 and DDR2 expression.

91 ion (K562), both of which express endogenous DDR1.

92 how that constitutive shedding of endogenous DDR1 in breast cancer HCC1806 cells is partly mediated b

93 We confirm that endogenous DDR1 is phosphorylated slowly by collagen in adherent T4

94 onuclear neutrophils were induced to express DDR1 after incubation in RPMI 1640.

95 sine kinases of the discoidin domain family, DDR1 and DDR2, are activated by different types of colla

96 Finally, DDR1 depletion blocked cell invasion in a collagen gel.

97 mic domains are individually dispensable for DDR1 dimerization.

98 lusion, this study has elucidated a role for DDR1 in epithelial cell migration during skin wound heal

99 ther, our data uncover an important role for DDR1, acting through Tuba and Cdc42, in proteolysis-base

100 to be a much better ligand for DDR2 than for DDR1.

101 f combinations of intracellular regions from DDR1 and TrkA (with the extracellular domain of hPDGFRbe

102 nt DDR1 mutants ('receiver') with functional DDR1 ('donor') and demonstrate phosphorylation of receiv

103 the association signal spans several genes (DDR1, GTF2H4, VARS2, SFTA2 and DPCR1) with expression le

104 In human gingiva, DDR1 was expressed at the epithelial front, migrating to

105 The results demonstrate that higher DDR1 expression significantly correlates with recurrence

106 How DDR1 activity is regulated is poorly understood.

107 ing extracellular matrix production, but how DDR1 controls fibrosis is poorly understood.

108 However, how DDR1-dependent signaling is regulated has not been under

109 sulted in their partial maturation; however, DDR1 activation markedly amplified TNF-alpha- and LPS-in

110 acellular juxtamembrane (JM) region of human DDR1 and found that the kinase-proximal segment, JM4, is

111 Co-crystal structures of human DDR1 reveal a DFG-out conformation (DFG, Asp-Phe-Gly) of

112 se whose tumours have high levels of cCol I, DDR1 and NRF2.

113 l of patients are mediated through the Col I-DDR1-NF-kappaB-NRF2 mitochondrial biogenesis pathway, an

114 1 in tumorigenesis, we previously identified DDR1 kinase as a transcriptional target of tumor suppres

115 hey apparently are not activated directly in DDR1 (or DDR1 chimeras) in a ligand-dependent fashion.

116 orescence, we analyzed the steps involved in DDR1 nuclear translocation.

117 P-loop residues in DDR1 that confer drug resistance in ABL are therefore ac

118 ed different types of signalling-incompetent DDR1 mutants ('receiver') with functional DDR1 ('donor')

119 of JM4 tyrosines abolished collagen-induced DDR1 activation in cells.

120 r this event is mediated by collagen-induced DDR1 activation, we generated renal cells expressing wil

121 Here we demonstrate ligand-induced DDR1 clustering by widefield and super-resolution imagin

122 Ligand-induced DDR1 clustering was abolished by transmembrane mutations

123 molecular events underpinning ligand-induced DDR1 kinase activity and provide an explanation for the

124 We previously reported that collagen induces DDR1 activation through lateral dimer association and ph

125 , as well as the selective type II inhibitor DDR1-IN-1.

126 as the more potent molecule, which inhibits DDR1 and DDR2 with an IC50 of 9nM.

127 Ligand binding resulted in initial DDR1 reorganisation into morphologically distinct cluste

128 that cannot bind collagen is recruited into DDR1 signalling clusters.

129 1-IN-1 suggesting a structural basis for its DDR1 selectivity.

130 he collagen-binding receptor tyrosine kinase DDR1 (discoidin domain receptor 1) is a drug target for

131 ouples the collagen receptor tyrosine kinase DDR1 to the cortical adaptor syntenin 2 and, hence, to P

132 int-1, the collagen receptor tyrosine kinase DDR1, N-Cadherin, CLCP1/DCBLD2, KIRREL, BCAM and others.

133 Discoidin domain receptor 1 tyrosine kinase (DDR1) and the ErbB1 receptor of amphiregulin are, for ex

134 ibition of one of these upregulated kinases, DDR1, suppressed PDAC growth.

135 Upon ligand-mediated DDR1 kinase activation, Notch1 was activated, bound to D

136 nd a 3D cell culture model was used to mimic DDR1 effects in an in vivo environment.

137 Moreover, DDR1 ligand (collagen I) treatment significantly increas

138 Finally, we show that mutant DDR1 that cannot bind collagen is recruited into DDR1 si

139 transmembrane signaling, although the mutant DDR1 proteins were still able to dimerize, whereas mutat

140 ression of activated DDR1, dominant-negative DDR1 inhibited irradiation-induced MAPK activation and p

141 d its natural ligand, collagen, lack an NLS, DDR1 is present in the nucleus of injured human and mous

142 Once in the nucleus, DDR1 binds to chromatin to increase the transcription of

143 periodontal homeostasis and that absence of DDR1 predisposes mice to periodontal breakdown.

144 igate epithelial responses in the absence of DDR1.

145 Activation of DDR1 endogenously expressed on macrophages also up-regul

146 Activation of DDR1 on immature DCs resulted in their partial maturatio

147 Collagen stimulation induced aggregation of DDR1, followed by a sharp increase in FRET signal, local

148 PC12 cells, which express modest amounts of DDR1, nor transfected PC12 cells, which express much lar

149 cells, which express much larger amounts of DDR1, respond to this ligand.

150 Further analysis of DDR1 aggregation revealed that DDR1 undergoes cytoplasmi

151 reby collagen induces lateral association of DDR1 dimers and phosphorylation between dimers.

152 Mechanistically, the binding of DDR1-ECD to collagen enforces aligned collagen fibres an

153 nd mutational analyses show that cleavage of DDR1 takes place within the extracellular juxtamembrane

154 Here, we evaluated the contribution of DDR1 in the differentiation of the human monocytic THP-1

155 esidue plays a unique role in the control of DDR1 dimerization and autophosphorylation.

156 study, recombinant extracellular domains of DDR1 and DDR2 were produced to explore DDR-collagen bind

157 otein Par3, which can function downstream of DDR1, also reversed the effects of Galpha13 knockdown on

158 tein tyrosine kinase (Pyk2) is downstream of DDR1, whereas FAK is downstream of alpha2beta1 integrin.

159 sion proteins, which contain only the ECD of DDR1.

160 Furthermore, the effect of DDR1 inhibition on clonogenicity was evaluated using a c

161 Therefore, we investigated the effects of DDR1 on RIT.

162 Subsequently, the protective effects of DDR1/DDR2 inhibitor, imatinib (IMT) were investigated.

163 A and protein levels and provide evidence of DDR1 involvement in the regulation of MK motility on typ

164 The induced expression of DDR1 and DDR2 was observed in primary pancreatic stellat

165 previously reported inducible expression of DDR1 in human leukocytes and suggested a role for the DD

166 The expression of DDR1 is also inversely correlated to the response to neo

167 his finding, in human TNBC the expression of DDR1 negatively correlates with the intratumoral abundan

168 The ectopic expression of DDR1 significantly increased the survival of collagen-tr

169 verexpression of a dominant-negative form of DDR1 in immature granule cells results in severe reducti

170 However, since soluble forms of DDR1 and DDR2 containing its ECD are known to naturally

171 ells expressing wild-type or mutant forms of DDR1 no longer able to bind collagen.

172 7rh, were applied to determine the impact of DDR1 expression on osteosarcoma cell growth and prolifer

173 have applications in clinical indications of DDR1 and DDR2 overexpression or mutation, including lung

174 Conversely, induction of DDR1 expression or collagen-stimulated DDR1 activity pro

175 er, these results suggest that inhibition of DDR1 and DDR2 controls pancreatic inflammation and fibro

176 ifically, we demonstrated that inhibition of DDR1 binding to type I collagen, preserving the engageme

177 Nonetheless, inhibition of DDR1 function resulted in strikingly increased apoptosis

178 artial or complete deletion or inhibition of DDR1 in a mouse model challenged with alpha-synuclein in

179 Interaction of DDR1 oligomers with collagen was found to modulate colla

180 ittle is understood about the interaction of DDR1 with collagen and its possible functional implicati

181 iated receptor activation and interaction of DDR1 with SEC61B, a component of the Sec61 translocon, a

182 duces the aggregation and internalization of DDR1 dimers at timescales much before receptor activatio

183 occurs naturally in kinase-dead isoforms of DDR1 and as a shedded soluble protein.

184 We found the kinetics of DDR1 internalization to be fast, with a significant perc

185 Knockdown of DDR1 by siRNA or treatment with inhibitor, 7rh, greatly

186 Conversely, knockdown of DDR1 significantly decreased the survival of collagen-tr

187 The expression level of DDR1 in PBMC was increased further by stimulation with t

188 nriched for iCol I and express low levels of DDR1 and NRF2 have improved median survival compared to

189 man diseases, but the molecular mechanism of DDR1 activation is poorly defined.

190 re, the discoidin domain of DDR2, but not of DDR1, was sufficient for transmembrane receptor signalin

191 we confirmed that further oligomerization of DDR1-Fc (by means of anti-Fc antibody) greatly enhances

192 In vitro, retroviral overexpression of DDR1 or DDR2 in human SMCs cultured on polymerized colla

193 Notch1 protein as an interacting partner of DDR1 receptor, as determined by tandem affinity protein

194 downstream signals after phosphorylation of DDR1 by collagen were not transmitted through the classi

195 s, collagen induced rapid phosphorylation of DDR1.

196 may inhibit or delay the phosphorylation of DDR1.

197 The presence of DDR1 ECD resulted in "locking" of collagen molecules in

198 Collagen fibers formed in the presence of DDR1 had a larger average diameter, were more cross-link

199 insights into the cellular redistribution of DDR1 following its interaction with collagen type I.

200 contacts within the extracellular region of DDR1 by using cysteine-scanning mutagenesis.

201 at the extracellular juxtamembrane region of DDR1 is exceptionally flexible and does not constrain th

202 e, the extracellular juxtamembrane region of DDR1 tolerated large deletions as well as insertions of

203 e transmembrane and intracellular regions of DDR1, also fails to mediate neuronal-like differentiatio

204 Elucidating the regulation of DDR1 activity and expression under different pathophysio

205 enase of membrane-type MMPs in regulation of DDR1 cleavage and activation at the cell-matrix interfac

206 Translational relevance of DDR1 is supported by its marked elevation in HCC which i

207 if evolved to act as a negative repressor of DDR1 phosphorylation in the absence of ligand.

208 sent study, we have investigated the role of DDR1 and DDR2 in CP.

209 olecular mechanism(s) underlying the role of DDR1 in cancer.

210 In this study, we evaluated the role of DDR1 in DC maturation using human monocyte-derived DCs.

211 To address the role of DDR1 in PDA, Ddr1-null (Ddr(-/-)) mice were crossed with

212 Besides the role of DDR1 in tumorigenesis, we previously identified DDR1 kin

213 Finally, we investigated the role of DDR1 in wound healing in human sections and in a live an

214 provide evidence for the potential roles of DDR1 and DDR2 in the regulation of collagen turnover med

215 gnostic relationship and functional roles of DDR1 in osteosarcoma.

216 uces ADAM10-dependent ectodomain shedding of DDR1.

217 While the oligomeric state of DDR1 is reported to play a significant role in collagen

218 nown about the effect of collagen binding on DDR1 oligomerization and cellular distribution.

219 pe MMPs (MT4- and MT6-MMP) have no effect on DDR1 cleavage or activation.

220 entiated DDR1b-overexpressing THP-1 cells or DDR1 on mature DCs induced the formation of TNFR associa

221 ently are not activated directly in DDR1 (or DDR1 chimeras) in a ligand-dependent fashion.

222 ociated with collagen frequently overexpress DDR1 and that short-term exposure to collagen is suffici

223 itro and on surfaces of cells overexpressing DDR1.

224 rs with highly aggregated and phosphorylated DDR1.

225 Here we show that potent and preferential DDR1 inhibitors reduce neurotoxic protein levels in vitr

226 and demonstrate phosphorylation of receiver DDR1 by donor DDR1 in response to collagen.

227 The collagen receptor DDR1 is a receptor tyrosine kinase that promotes progres

228 r beta (PDGFRbeta) and the collagen receptor DDR1.

229 The discoidin domain receptor (DDR1) is characterized by a discoidin I motif in the ext

230 Discoidin domain receptors (DDR1 and DDR2) are receptor tyrosine kinases that bind t

231 Discoidin domain receptors (DDR1 and DDR2) are receptor tyrosine kinases that signal

232 Discoidin domain receptors (DDR1 and DDR2) are the collagen receptors of the family

233 Discoidin domain receptors (DDR1 and DDR2) are widely expressed cell-surface recepto

234 d as ligands for discoidin domain receptors (DDR1 and DDR2), generating an interest in studying the p

235 The discoidin domain receptors, DDR1 and DDR2, are nonintegrin collagen receptors and ty

236 The discoidin domain receptors, DDR1 and DDR2, are receptor tyrosine kinases that are ac

237 ADAM10 plays an important role in regulating DDR1-mediated cell adhesion to achieve efficient cell mi

238 Using a shedding-resistant DDR1 mutant, we found that ADAM10-dependent DDR1 sheddin

239 mouse osteoblast cell lines stably secreting DDR1 or DDR2 ECD as soluble proteins.

240 DDR1-specific siRNA and a highly selective DDR1 inhibitor, 7rh, were applied to determine the impac

241 tigation into the mechanism of action showed DDR1 silencing was associated with decreased expression

242 n activation of its signaling pathway, since DDR1 mutants defective in signaling were shed in an effi

243 rovide an explanation for the unusually slow DDR1 activation kinetics.

244 sm (ECM and adhesion-related pathways, SPP1, DDR1), B-cell migration (CXCL13, SPP1), activated B-cell

245 on of DDR1 expression or collagen-stimulated DDR1 activity protected cancer cells from RG7787 killing

246 bsence of collagen was able to induce strong DDR1 phosphorylation, indicating that a phosphatase may

247 robe compounds, have been developed to study DDR1/2 kinase signaling.

248 In conclusion, our study supports DDR1 expression as an independent predictor of poor prog

249 somatic mutations, JAK1(V623A), JAK1(T478S), DDR1(A803V), and NTRK1(S677N), once each in 4 respective

250 These data demonstrate that DDR1 is a key modulator of RIT activity and represents a

251 Collectively, these data demonstrate that DDR1 regulates autophagy and reduces neurotoxic proteins

252 We further demonstrated that DDR1 activated the MAPK cascade in a Ras-dependent manne

253 dentoalveolar tissues, we hypothesized that DDR1 plays an important role in dentoalveolar developmen

254 Our data indicates that DDR1 inhibition can augment cell cycle suppressive effec

255 We propose that DDR1 plays an important role in periodontal homeostasis

256 ans of atomic force microscopy revealed that DDR1 oligomers bound at overlapping or adjacent collagen

257 r analysis of DDR1 aggregation revealed that DDR1 undergoes cytoplasmic internalization and incorpora

258 We show that DDR1 nuclear translocation requires collagen-mediated re

259 We showed that DDR1 is a direct p53 transcriptional target, and that DN

260 The results suggest that DDR1 exerts prosurvival effect, at least in part, throug

261 Overall, these data suggest that DDR1 regulates tissue homeostasis in the neoplastic and

262 specific apoptotic stimulus, suggesting that DDR1 also influences baseline survival.

263 induced p21 and DDR1 levels, suggesting that DDR1 functions in a feedforward loop to increase p53 lev

264 The DDR1 extracellular domain (DDR1-ECD), but not its intrac

265 The DDR1 transmembrane domain contains two putative dimeriza

266 Those with the TrkA kinase domain and the DDR1 JM regions were able to produce differentiation to

267 odulation of collagen fibrillogenesis by the DDR1 ECD elucidates a novel mechanism of collagen regula

268 to Abelson kinase (ABL) are observed in the DDR1 P-loop, where a beta-hairpin replaces the cage-like

269 er cryptic binding sites for PLCgamma in the DDR1 sequences) and markedly reduced the differentiative

270 requirement for receptor dimerization in the DDR1-collagen interaction.

271 leading to MAPK activation) is weaker in the DDR1/TrkA chimeras than in TrkA alone, and the PLCgamma

272 Moreover, the DDR1 knockdown cancer cells showed the reduced transform

273 at maintains the autoinhibitory state of the DDR1 dimers is unknown.

274 signify an important functional role of the DDR1 ECD, which occurs naturally in kinase-dead isoforms

275 ere, we elucidate the binding pattern of the DDR1 extracellular domain (ECD) to collagen type 1 and i

276 Then, we determined the location of the DDR1 upon collagen stimulation.

277 Inhibition of the DDR1-stimulated expression of NF-kappaB or mitochondrial

278 These findings suggest that the DDR1 receptors do have signaling capacity but may requir

279 eporter assay (named TOXCAT) showed that the DDR1 transmembrane domain has a strong potential for sel

280 ow clear that aberrant signaling through the DDR1 receptor is closely associated with various steps o

281 enuated or reversed after treatment with the DDR1 inhibitor, nilotinib.

282 Among three DDR1 isoforms, DDR1alpha was the major transcript in leu

283 ivation of wild-type Notch signaling through DDR1.

284 e activation, Notch1 was activated, bound to DDR1, and activated canonical Notch1 targets, including

285 dding did not occur unless collagen bound to DDR1.

286 nds was further investigated with respect to DDR1 inhibition.

287 centromeric to HLA-DRA gene and telomeric to DDR1 gene.

288 e is known about how ligand binding triggers DDR1 kinase activity.

289 In addition, a chimeric TrkA-DDR1 receptor failed to become phosphorylated on stimula

290 Two DDR1 isoforms, DDR1a and DDR1b, were expressed in both i

291 an affinity similar to that of the wild-type DDR1 ectodomain.

292 Unexpectedly, DDR1 kinase activity is not required for invadosome form

293 ally distinct clusters with unphosphorylated DDR1.

294 Membrane-untethered DDR1-ECD is sufficient to rescue the growth of Ddr1-knoc

295 Our in vitro assays utilized DDR1-Fc fusion proteins, which contain only the ECD of D

296 In vivo, DDR1 mRNA was detectable in mononuclear leukocytes infil

297 h1 receptor in the nuclear fraction, whereas DDR1 knockdown cells show little or no increase of the a

298 and provide evidence for a mechanism whereby DDR1 kinase activity is determined by its molecular dens

299 To determine whether DDR1 translocates to the nucleus and whether this event

300 signaling responses of the two chimeras with DDR1 JM sequences (with and without the insert) indicate