ライフサイエンスコーパス: DDR2

1 discoidin domain receptor tyrosine kinase 2 (DDR2).

2 sion proteins, which contain only the ECD of DDR2.

3 eakened and nearly absent in the presence of DDR2.

4 We examined signal transduction pathways of DDR2.

5 se of Flt-1, Flk-1, c-met, PDGFR, and Tyro10/DDR2.

6 uration and mineralization in the absence of Ddr2.

7 e SFK inhibitor dasatinib than those with WT DDR2.

8 ction of type II and III DFG-out binders for DDR2.

9 with total brain volume at rs10494373 within DDR2 (1q23.3; N = 6,500; P = 5.81 x 10(-7)).

10 , we identified discoidin domain receptor 2 (DDR2), a cell surface receptor for fibrillar collagen, a

11 Discoidin domain receptor 2 (DDR2), a collagen receptor preferentially activated by t

12 agen receptors, discoidin domain receptor 2 (DDR2), a collagen-specific receptor tyrosine kinase, and

13 titutively active chimeric DDR2 receptor (Fc-DDR2), a truncated receptor expressing the extracellular

14 lines stably overexpressing either wild-type DDR2, a constitutively active chimeric DDR2 receptor (Fc

15 Further, DDR2 acted via integrin-beta1 to regulate alpha-smooth m

16 In this context, we show that DDR2 activation specifically regulates the directional m

17 DDR2 activation was found to be noticeably more effectiv

18 progression to OA, which was associated with DDR2 activation.

19 obility shift assays, and ChIP revealed that DDR2 acts via extracellular signal-regulated kinase 1/2

20 tion and phosphorylation status of DDR1b and DDR2 after collagen stimulation.

21 oma overexpress discoidin domain receptor 2 (DDR2) after treatment.

22 2 knockdown or pharmacological inhibition of DDR2 also inhibited the MT1-MMP-dependent cellular degra

23 that binding of the GVMGFO motif to VWF and DDR2 also results in structural changes and the formatio

24 Discoidin domain receptor 2 (DDR2), an understudied collagen receptor, plays an impor

25 -146 were associated with down-regulation of DDR2 and IGFBP6, which are genes involved in the recover

26 The expression of both DDR2 and MMP-13 was increased in chondrocytes cultured o

27 bservations extend the functional roles that DDR2 and possibly other membrane-anchored, collagen-bind

28 lities and spatial distribution of DDR1b and DDR2 and their impact on receptor phosphorylation.

29 2 signaling in skin fibroblasts derived from DDR2(-/-) and DDR2(+/-) mice.

30 d factor (VWF), discoidin domain receptor 2 (DDR2), and the extracellular matrix protein SPARC/osteon

31 ations and less likely to have PIK3CA, CDH1, DDR2, and GATA3 mutations than non-Black participants.

32 chemistry and demonstrate that both DDR1 and DDR2 are up-regulated in nodules of LAM as compared to n

33 Discoidin domain receptors (DDR1 and DDR2) are receptor tyrosine kinases that bind to and are

34 Discoidin domain receptors (DDR1 and DDR2) are receptor tyrosine kinases that signal in respo

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

36 Discoidin domain receptors (DDR1 and DDR2) are widely expressed cell-surface receptors, which

37 ses of the discoidin domain family, DDR1 and DDR2, are activated by different types of collagen and p

38 discoidin domain receptors (DDRs), DDR1 and DDR2, are expressed widely and, uniquely among receptor

39 The discoidin domain receptors, DDR1 and DDR2, are nonintegrin collagen receptors and tyrosine ki

40 The discoidin domain receptors, DDR1 and DDR2, are receptor tyrosine kinases that are activated b

41 discoidin domain receptors (DDRs), DDR1 and DDR2, are unique among receptor tyrosine kinases in that

42 , we identified discoidin domain receptor 2 (DDR2) as a crucial receptor that mediates this process i

43 Collagen II served as a potent stimulator of DDR2 autophosphorylation, the first step in transmembran

44 onstruct, but not the D4 construct, mediated DDR2 binding and receptor autophosphorylation, demonstra

45 e D2 period of collagen II was essential for DDR2 binding and receptor autophosphorylation, whereas t

46 The DDR2 binding site on collagen II was further defined by

47 Here, we localised a specific DDR2 binding site on the triple-helical region of collag

48 To map the DDR2 binding site(s) on collagen II, we used recombinant

49 e collagen molecule and there were preferred DDR2 binding sites on the collagen I triple helix.

50 As expected, DDR2 binding to collagen II was dependent on triple-heli

51 hemical responsive) or the collagen receptor DDR2 (biomechanical responsive) abrogated polarization o

52 omains, and the isolated discoidin domain of DDR2 bound collagen I with high affinity.

53 en but not on gelatin, and overexpression of DDR2, but not of a truncated form, was found to induce t

54 Furthermore, the discoidin domain of DDR2, but not of DDR1, was sufficient for transmembrane

55 Knocking down DDR2, but not the beta1 integrin subunit, a common subun

56 g the extracellular domain, or a kinase-dead DDR2 Cells overexpressing DDR2 showed enhanced prolifera

57 ts was significantly decreased compared with DDR2(+/-) cells.

58 R2 or constitutively active chimeric DDR2 in DDR2(-/-) cells by retroviral infection restored cell pr

59 on of type I collagen was greatly reduced in DDR2(-/-) cells.

60 esis, (ii) the effect of collagen binding on DDR2 clustering, and (iii) the spatial distribution and

61 the filamentous structures of both DDR1b and DDR2 co-localized with antibodies directed against tyros

62 Interestingly, DDR1b, but not DDR2, completely hindered the ability of HT1080 cells to

63 we characterized the surface topographies of DDR2 complexes and collagen I, and investigated binding

64 e were able to image and identify binding of DDR2 complexes onto individual molecules of triple-helic

65 Binding of DDR2 complexes to collagen I coated on plastic plates wa

66 (multimerized) by use of antibodies to form DDR2 complexes.

67 gnments and homology modeling, we designed a DDR2 construct appropriate for fluorescent labeling.

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

69 phenotype switching context, we report that DDR2 control cell and tumor proliferation through the MA

70 results suggest that inhibition of DDR1 and DDR2 controls pancreatic inflammation and fibrosis, whic

71 Therefore, inhibition of DDR2 could be a new and promising strategy for counterin

72 orresponding expansion of DDR2(+) CSCs, with DDR2(+) CSC expansion being a direct maladaptive respons

73 taining receptor 2 (DDR2) lineage stem cell (DDR2(+) CSC) that we identified in this study.

74 Finally, the human counterparts of DDR2(+) CSCs and CTSK(+) CSCs display conserved function

75 DDR2(+) CSCs display full stemness features, and our res

76 Implantation of DDR2(+) CSCs into suture sites is sufficient to induce f

77 DDR2(+) CSCs mediate a distinct form of endochondral oss

78 TSK(+) CSCs and a corresponding expansion of DDR2(+) CSCs, with DDR2(+) CSC expansion being a direct

79 the known or suspected STRE-regulated genes DDR2, CTT1, HSP12, and TPS2, transcript induction was im

80 The impaired bone healing associated with Ddr2 deficiency may be related to reduced osteoprogenito

81 ype XI collagen-deficient [Col11a1(+/-)] and Ddr2-deficient [Ddr2(+/-)]) mutant mice were generated.

82 rols at 4 wk postsurgery was not observed in Ddr2-deficient mice even after 12 wk.

83 As will be shown, Ddr2-deficient mice exhibit defects in craniofacial bone

84 A similar phenotype was observed in Ddr2-deficient mice, which exhibit dwarfism and defectiv

85 vealed a 50% reduction in new bone volume in Ddr2-deficient mice.

86 defects were generated in wild-type (WT) and Ddr2-deficient mice.

87 ements and biochemical assays indicated that DDR2 delays the formation of collagen fibrils.

88 , through either constitutive or conditional Ddr2 deletion or pharmaceutical inhibition, reduced HO f

89 Discoipyrroles A-D potently inhibit DDR2 dependent migration of BR5 fibroblasts and show sel

90 might be a potential strategy for inhibiting DDR2-dependent cancer progression.

91 No DDR2-dependent degenerative changes were seen in knees.

92 Furthermore, DDR2-dependent MT1-MMP activation by cartilage was found

93 promoter region of the arginase-1 gene, and DDR2-depleted CAFs had decreased levels of SNAI1 protein

94 In addition, DDR2-depleted CAFs had decreased ornithine levels leadin

95 addition of exogenous polyamines to CM from DDR2-depleted CAFs led to increased tumor cell invasion.

96 efect was rescued in the presence of CM from DDR2-depleted CAFs that constitutively overexpressed arg

97 Patients with loss of function mutations in DDR2 develop spondylo-meta-epiphyseal dysplasia (SMED),

98 However, the increased DDR2 did not induce MMP-13 expression.

99 site to the polypeptide chain termini of the DDR2 discoidin domain constitutes the collagen recogniti

100 spatially adjacent surface loops within the DDR2 discoidin domain were found to be critically involv

101 ple-helical collagen and was mediated by the DDR2 discoidin domain.

102 We first defined the expression pattern of Ddr2 during tooth formation using Ddr2-LacZ knock-in mic

103 icroscopy, we demonstrate that unlike DDR1b, DDR2 ECD and DDR2-GFP do not undergo collagen-induced re

104 teoblast cell lines stably secreting DDR1 or DDR2 ECD as soluble proteins.

105 We show that the oligomeric form of DDR2 ECD displayed enhanced binding to collagen and inhi

106 ed (i) the impact of the oligomeric state of DDR2 ECD on collagen binding and fibrillogenesis, (ii) t

107 es were conducted using purified recombinant DDR2 ECD proteins in monomeric, dimeric or oligomeric st

108 a novel and important functional role of the DDR2 ECD that may contribute to collagen regulation via

109 esults led to a novel functional role of the DDR2 ECD.

110 tion, the current study investigates how the DDR2-ECD, when expressed as a membrane-anchored, cell-su

111 ion results revealed that HSP47 binds to the DDR2 ectodomain.

112 1 at both mRNA and protein levels, but only DDR2 enhances MMP2 activation.

113 e phosphorylated tyrosine kinases, including DDR2, EphB4, TYR2, AXL, SRC, LYN, and FAK.

114 amplicons in total; KRAS, NRAS, HRAS, BRAF, DDR2, ERBB2, KEAP1, NFE2L2, PIK3CA, PTEN, RHOA, BRCA1, B

115 However, implantation of DDR1b- or DDR2-expressing HT1080 cells with collagen I significant

116 Neither DDR1b nor DDR2 expression altered tumour growth at the primary sit

117 Ddr2 expression during calvarial bone regeneration was m

118 r, type I collagen-dependent upregulation of DDR2 expression establishes a positive feedback loop in

119 DDR2 expression increased in the knee joints of transgen

120 This Ddr2 expression pattern suggests a potential role in the

121 Ddr2 expression was detected in the dental follicle/sac

122 with IMT effectively downregulated DDR1 and DDR2 expression.

123 involved in collagen binding of the isolated DDR2 extracellular domain.

124 we confirmed that further oligomerization of DDR2-Fc (by means of anti-Fc antibody) greatly enhances

125 Our in vitro binding assay utilizes DDR2-Fc fusion proteins, which can be clustered (multime

126 Our in vitro assays utilized DDR2-Fc fusion proteins, which contain only the ECD of D

127 Clustering of the DDR2-Fc with antibody was found to be requisite for bind

128 M in cases with targetable mutations in SMO, DDR2, FGFR1, PTCH1, FGFR2, and MET Our results indicate

129 ane (Matrigel), and MMP-2 levels to those of DDR2(+/-) fibroblasts.

130 DDR2(-/-) fibroblasts exhibited markedly impaired capaci

131 Proliferation of DDR2(-/-) fibroblasts was significantly decreased compar

132 localized with non-fibrillar collagen, DDR1b/DDR2 filamentous structures associated with collagen fib

133 discoidin domain receptors (DDRs), DDR1 and DDR2, form a unique subfamily of receptor tyrosine kinas

134 e development and homeostasis and that these DDR2 functions are restricted to TMJ fibrocartilage and

135 rapeutic target genes, for example, EGFR and DDR2 gene mutations, ALK gene fusions, or FGFR1 gene amp

136 nds for discoidin domain receptors (DDR1 and DDR2), generating an interest in studying the properties

137 Activation of the CUP1, CYC1, GAL1, and DDR2 genes was decreased or abolished completely in the

138 demonstrate that unlike DDR1b, DDR2 ECD and DDR2-GFP do not undergo collagen-induced receptor cluste

139 ged collagen stimulation, both DDR1b-YFP and DDR2-GFP formed filamentous structures consistent with s

140 e, and MC3T3-E1 cells expressing full-length DDR2-GFP or DDR1b-YFP.

141 In contrast, a lack of DDR2 had no effect on cell motility or alpha-smooth musc

142 Given that DDR2 has a crucial role in the epithelial-to-mesenchymal

143 However, it is not known if Ddr2 has a role in tooth formation.

144 Excessive signaling by DDR1 and DDR2 has been linked to the progression of various human

145 llagen receptor discoidin domain receptor 2 (DDR2) has no impact on human primary neutrophil migratio

146 differentiation since knockdown/knockout of Ddr2 in a mesenchymal cell line and primary calvarial os

147 ors that the action of the collagen receptor DDR2 in CAFs controls tumor stiffness by reorganizing co

148 mouse model with inducible overexpression of DDR2 in cartilage.

149 o/+) permits activation and up-regulation of DDR2 in chondrocytes.

150 y, we have investigated the role of DDR1 and DDR2 in CP.

151 These data establish a role for DDR2 in critical events during wound repair.

152 -type DDR2 or constitutively active chimeric DDR2 in DDR2(-/-) cells by retroviral infection restored

153 outs further established the requirement for Ddr2 in GLI +skeletal progenitors and chondrocytes.

154 vitro, retroviral overexpression of DDR1 or DDR2 in human SMCs cultured on polymerized collagen gels

155 odontoblast- and PDL-specific expression of Ddr2 in mature and immature teeth, as well as indicate t

156 Conditional overexpression of DDR2 in mature mouse articular cartilage was controlled

157 The action of DDR2 in mouse and human CAFs, and tumors in vivo, was fo

158 s from Ddr2(slie/slie) mice, and deletion of Ddr2 in primary cell cultures from dental pulp and PDL i

159 The specific induction of MMP-13 by DDR2 in response to its cartilage-specific ligand, type

160 Therefore, conditionally overexpressing DDR2 in the mature articular cartilage of mouse knee joi

161 evidence for the potential roles of DDR1 and DDR2 in the regulation of collagen turnover mediated by

162 To assess the requirement for Ddr2 in TMJ development, studies were undertaken to comp

163 The action of DDR2 in tumor CAFs is thus critical for remodeling colla

164 n of discoidin domain-containing receptor 2 (DDR2) in breast cancer tissues.

165 ese results suggest that binding of HSP47 to DDR2 increases DDR2 stability and regulates its membrane

166 The DDR2-induced expression of MMP-13 appears to be specific

167 We demonstrate that DDR2 inhibition induces a decrease in AXL expression and

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

169 collagen, the extracellular domain (ECD) of DDR2 inhibits collagen fibrillogenesis and alters the mo

170 monstrate that overexpression of full length DDR2 inhibits fibrillogenesis of collagen type 1.

171 llagen receptor discoidin domain receptor 2 (DDR2) inhibits fibrillogenesis of collagen endogenously

172 Downstream of the DDR2-integrin-beta1 axis, alpha-SMA was found to regulat

173 Here, we probed the role of DDR2-integrin-beta1 cross-talk in the regulation of coll

174 The DDR2-integrin-beta1 link was also evident in spontaneous

175 and cancer progression, targeting the HSP47-DDR2 interaction might be a potential strategy for inhib

176 Hence, ECM-DDR2 interactions are critical in driving HO and could s

177 These data suggest that DDR2 is a microenvironment sensor that regulates fibrobl

178 Here we show that DDR2 is also unusual in that it requires Src activity to

179 by localization and lineage-tracing studies, Ddr2 is expressed in progenitor cell-enriched craniofaci

180 These data show that DDR2 is induced during stellate cell activation and impl

181 These studies demonstrate that DDR2 is necessary for normal TMJ condyle development and

182 erstudied collagen receptor and suggest that DDR2 is necessary for proper collagen organization, chon

183 mice and immunohistochemistry, we found that DDR2 is preferentially expressed and activated in the ar

184 In conclusion, Ddr2 is required for cranial bone regeneration and may b

185 Discoidin domain receptor 2 (DDR2) is a collagen-activated tyrosine kinase receptor s

186 Discoidin domain receptor 2 (DDR2) is a receptor tyrosine kinase involved in a variet

187 Discoidin domain receptor 2 (DDR2) is a tyrosine kinase receptor expressed in mesench

188 Discoidin domain receptor 2 (DDR2) is an unusual receptor tyrosine kinase in that its

189 lagen receptor, discoidin domain receptor 2 (DDR2), is increased in chondrocytes of the articular car

190 e assays demonstrated that the expression of DDR2/-KD reduced the rate and abundance of collagen depo

191 sses a kinase-deficient form of DDR2, termed DDR2/-KD, on its cell surface.

192 Interestingly, DDR2 knockdown or pharmacological inhibition of DDR2 als

193 ident in spontaneously hypertensive rats and DDR2-knockout mice.

194 Using Ddr2 LacZ-tagged mice and immunohistochemistry, we found

195 pattern of Ddr2 during tooth formation using Ddr2-LacZ knock-in mice.

196 lvarial bone regeneration was measured using Ddr2-LacZ knock-in mice.

197 ve compound library identified high-affinity DDR2 ligands validated by orthogonal activity-based assa

198 rate discoidin domain-containing receptor 2 (DDR2) lineage stem cell (DDR2(+) CSC) that we identified

199 contain a spontaneous 150-kb deletion in the Ddr2 locus to produce an effective null.

200 Ddr2 loss-of-function mutations in humans and mice cause

201 ace collagen degradation by MT1-MMP involves DDR2-mediated collagen signaling.

202 This DDR2-mediated mechanism is only present in non-transform

203 Furthermore, Src is required for DDR2-mediated transactivation of the matrix metalloprote

204 on toward OA was dramatically delayed in the Ddr2(+/-) mice compared with that in their wild-type lit

205 Knee joints of Ddr2(+/-) mice were subjected to microsurgical destabili

206 skin fibroblasts derived from DDR2(-/-) and DDR2(+/-) mice.

207 DDR2 mRNA and protein are induced in stellate cells acti

208 broblasts and show selective cytotoxicity to DDR2 mutant lung cancer cell lines (IC50 120-400 nM).

209 deficient [Col11a1(+/-)] and Ddr2-deficient [Ddr2(+/-)]) mutant mice were generated.

210 binding site within the discoidin domain of DDR2, mutant constructs were created, in which potential

211 d ligand stimulation of EGFR and MET rescued DDR2-mutant lung SCC cells from dasatinib-induced loss o

212 ylation was weakly inhibited by dasatinib in DDR2-mutant lung SCC cells, suggesting that dasatinib in

213 st new, rationale cotargeting strategies for DDR2-mutant lung SCC.

214 Select DDR2 mutations have been shown to confer enhanced sensit

215 DDR2 mutations occur in approximately 4% of lung squamou

216 ll lines harboring endogenous and engineered DDR2 mutations were more sensitive to the SFK inhibitor

217 ons, PIK3CA mutations, FGFR1 amplifications, DDR2 mutations, ROS1 rearrangements, and RET rearrangeme

218 3K pathway changes, FGFR1 amplification, and DDR2 mutations.

219 a panel of human lung SCC tissues harboring DDR2 mutations.

220 The PDGFRA(pos):Lin(neg):THY1(neg):DDR2(neg) cells were bipotential as the majority express

221 tified by the PDGFRA(pos):Lin(neg):THY1(neg):DDR2(neg) signature, expresses desmosome proteins and di

222 cells, we investigated the role of DDR1b and DDR2 on primary tumour growth and experimental lung meta

223 CAFs with high DDR2 or arginase promote tumor colonization in the oment

224 sence CAF conditioned media (CM) depleted of DDR2 or arginase-1, and this invasion defect was rescued

225 Stable reconstitution of either wild-type DDR2 or constitutively active chimeric DDR2 in DDR2(-/-)

226 Moreover, DDR2 overexpression increases SMC-mediated collagen and

227 ications in clinical indications of DDR1 and DDR2 overexpression or mutation, including lung cancer.

228 res reduced osteoblast differentiation while Ddr2 overexpression was stimulatory.

229 Mechanistically, DDR2 perturbation alters focal adhesion orientation and

230 llagen receptor Discoidin domain receptor 2 (DDR2) promotes neutrophil chemotaxis in 3D by triggering

231 lagen receptor, Discoidin Domain Receptor 2 (DDR2), promotes collagen production in human and mouse o

232 HSP47 silencing reduced DDR2 protein stability, accompanied by suppressed cell m

233 ly sustains the membrane localization of the DDR2 protein.

234 -type DDR2, a constitutively active chimeric DDR2 receptor (Fc-DDR2), a truncated receptor expressing

235 he data support a model in which Src and the DDR2 receptor cooperate in a regulated fashion to direct

236 D2 period of collagen II harbours a specific DDR2 recognition site.

237 These findings highlight how DDR2 regulates collagen production by CAFs in the tumor

238 We further demonstrate that DDR2 regulates directionality through its ability to inc

239 pression of the discoidin domain receptor 2 (DDR2) results from its interaction with collagen type II

240 , or a kinase-dead DDR2 Cells overexpressing DDR2 showed enhanced proliferation and invasion through

241 rotein Shc as key signaling intermediates in DDR2 signal transduction.

242 We have compared DDR2 signaling in skin fibroblasts derived from DDR2(-/-

243 and immature teeth, as well as indicate that DDR2 signaling is important for normal tooth formation a

244 ), from Bacillus hunanensis that inhibit the DDR2 signaling pathway.

245 Inhibition of DDR2 signaling, through either constitutive or condition

246 Analysis of older Ddr2(slie/slie) mice (3 and 10 mo) revealed that the ear

247 Ddr2(slie/slie) mice also had abnormal collagen content

248 tive changes in the TMJs of 3- and 10-mo-old Ddr2(slie/slie) mice as compared with wild-type controls

249 In comparison with wild-type littermates, Ddr2(slie/slie) mice displayed disproportional tooth siz

250 Analysis of TMJs from newborn Ddr2(slie/slie) mice revealed a developmental delay in c

251 MJ articular chondrocytes from wild-type and Ddr2(slie/slie) mice showed defects in chondrocyte matur

252 In marked contrast, knee joints of Ddr2(slie/slie) mice were normal.

253 lasts; RUNX2-S319-P was reduced in PDLs from Ddr2(slie/slie) mice, and deletion of Ddr2 in primary ce

254 To uncover the function of Ddr2, we used Ddr2(slie/slie) mice, which contain a spontaneous 150-kb

255 gest that binding of HSP47 to DDR2 increases DDR2 stability and regulates its membrane dynamics and t

256 We prioritize DDR2, STOM, and KANK2 as promising therapeutic targets i

257 TK-driven adaptive-resistant mechanisms upon DDR2 targeting, and they suggest new, rationale cotarget

258 stably expresses a kinase-deficient form of DDR2, termed DDR2/-KD, on its cell surface.

259 II was found to be a much better ligand for DDR2 than for DDR1.

260 n 3-month-old transgenic mice overexpressing DDR2 to destabilize the medial meniscus, and serial para

261 within primary tumor organoids use CXCR4 and DDR2 to polarize to the leading edge and direct migratio

262 ice, which contain a spontaneous deletion in Ddr2 to produce an effective null allele.

263 The induced expression of DDR1 and DDR2 was observed in primary pancreatic stellate cells (

264 f the pericellular matrix of chondrocytes on DDR2, we generated a mouse model with inducible overexpr

265 To uncover the function of Ddr2, we used Ddr2(slie/slie) mice, which contain a spon

266 in which potential surface-exposed loops in DDR2 were exchanged for the corresponding loops of funct

267 ecombinant extracellular domains of DDR1 and DDR2 were produced to explore DDR-collagen binding in de

268 ; that is, the extracellular domain (ECD) of DDR2, when used as a purified, soluble protein, inhibits

269 ons in the discoidin domain receptor 2 gene (DDR2), which encodes a non-integrin collagen receptor, a

270 discoidin domain tyrosine kinase receptor 2 (DDR2), which signals in response to type I collagen, in

271 monomeric state of collagen was present with DDR2, while control solutions had an abundance of polyme

272 ore potent molecule, which inhibits DDR1 and DDR2 with an IC50 of 9nM.

273 We are interested in the interaction of DDR2 with collagen I because of its potential role in li

274 discovery of a site-specific interaction of DDR2 with collagen II gives novel insight into the natur

275 at Src activity also promotes association of DDR2 with Shc.