ライフサイエンスコーパス: S100A4

1 to expression of a canonical EMT biomarker (S100A4).

2 ) of RPE cells was assessed by expression of S100A4.

3 rker p21(WAF1/Cip) or the mesenchymal marker S100A4.

4 homologue of the metastasis-promoting human S100A4.

5 even more extensive than, that reported for S100A4.

6 sess myosin fragment filament disassembly by S100A4.

7 is-inducing proteins osteopontin, S100P, and S100A4.

8 r residues in the hydrophobic pocket of Ca2+-S100A4.

9 he 1.7 A crystal structure of the human Ca2+-S100A4.

10 ers vimentin, alpha-smooth muscle actin, and S100A4.

11 ression of the small calcium-binding protein S100A4.

12 xpressing Ki67 and the MPC markers SSEA4 and S100A4.

13 ic mediator S100 Calcium-binding protein A4 (S100A4) (1.78-fold, P<0.05).

14 found that S100 calcium-binding protein A4 (S100A4), a major metastasis-promoting protein, confers m

15 eased expression of S100 calcium-binding A4 (S100A4), a protein linked to cancer cell proliferation a

16 ctional demonstration that overexpression of S100A4, a calcium-binding protein that is frequently ove

17 ity, it significantly reduced SUMOylation of S100A4, a critical posttranslational modification that d

18 ssing cancer cells responded by upregulating S100A4, a marker of cancer-associated fibroblasts (CAFs)

19 Overexpression of S100A4, a member of the S100 family of Ca(2+)-binding pr

20 S100A4, a member of the S100 family of Ca(2+)-binding pr

21 S100A4, a member of the S100 family of Ca(2+)-binding pr

22 S100A4, a member of the S100 family of Ca(2+)-binding pr

23 S100A4, a member of the S100 family of proteins, plays a

24 S100A4, a specific protein-binding partner for CD16A-CY

25 Biochemical assays revealed that S100A4 activates Src and focal adhesion kinase (FAK) sig

26 a activation of JAK/STAT signaling, and then S100A4 acts in an autocrine manner to stimulate MMP-13 p

27 h levels of the S100 calcium binding protein S100A4 also called fibroblast specific protein 1 (FSP1)

28 S100A4, also known as mts1, is a member of the S100 fami

29 BEC expression of S100A4 (an early fibroblast lineage marker established a

30 ased while expression of mesenchymal markers S100A4 and alpha-smooth muscle actin increased.

31 ost of these residues are not exposed in apo-S100A4 and explain the Ca2+ dependence of formation of t

32 Targeting S100A4 and GRM3 may help prevent bone metastasis.

33 art to the post-metastatic downregulation of S100A4 and GRM3.

34 han two other markers of cancer progression, S100A4 and MACC1, and clustering of all GEFs together im

35 d STAT-3, leading to increased production of S100A4 and MMP-13.

36 lated in an S100A4-dependent manner and that S100A4 and NDUFS2 exhibit co-occurrence at significant l

37 ted the formation of a complex between RhoA, S100A4 and NM myosin II.

38 Interestingly, we found that S100A4 and Rhotekin can form a complex with active RhoA.

39 ence, we determined that suppression of both S100A4 and Rhotekin leads to loss of Rho-dependent membr

40 dingly, our data suggest that interaction of S100A4 and Rhotekin permits S100A4 to complex with RhoA

41 s and primary human glioma tissues show that S100A4 and S100A6 are expressed in a small subset of can

42 the expression of two genes from this list (S100a4 and S100a6) in primary mouse gliomas and human gl

43 Furthermore, coordinate expression of S100A4 and SAA in tumor samples from colorectal carcinom

44 ression of prometastatic proteins S100A2 and S100A4 and survival was assessed.

45 eraction between the calcium-binding protein S100A4 and the C-terminal fragments of nonmuscle myosin

46 We have thus demonstrated that both S100A4 and UA act as DAMPs and, as such, may play a crit

47 Similar to necrotic tumor material, S100A4 and UA both dose-dependently induced chemotaxis o

48 With regard to MSC proliferation, both S100A4 and UA inhibited MSCs without altering survival o

49 es, such as S100 calcium-binding protein A4 (S100A4) and miR-181b, after SCF plus GM-CSF administrati

50 with growth or local invasion such as Ki67, S100A4, and MMP2, 9, and 13.

51 h mobility group box (HMGB)-1, B7 Homolog 1, S100A4, and resistin have been detected in tissues of de

52 rs for the metastasis-promoting functions of S100A4, and serve as a link between inflammation and tum

53 in, and the mesenchymal markers fibronectin, s100A4, and vimentin were evaluated.

54 Since both IL-7 and S100A4 are up-regulated in OA cartilage and can stimulat

55 he well-characterized myofibroblastic marker S100A4, are functionally relevant.

56 Overall, our findings highlight nuclear S100A4 as a candidate therapeutic target in cholangiocar

57 stemness and EMT in glioblastoma, suggesting S100A4 as a candidate therapeutic target.

58 Overall, our results establish S100A4 as a central node in a molecular network that con

59 owth in vitro and in vivo We also identified S100A4 as a critical regulator of GSC self-renewal in mo

60 Our studies point to S100A4 as a critical regulator of matrix degradation, wh

61 ibitors and in vitro studies we have defined S100a4 as a novel, promising therapeutic candidate to im

62 vide evidence that supports a novel role for S100A4 as a prosurvival factor in pancreatic cancer.

63 demonstrate a novel mechanism for sumoylated S100A4 as a regulator of expression of the MMP-13 gene.

64 These studies establish S100A4 as a regulator of physiological macrophage motili

65 In contrast with previous reports of S100A4 as a reporter of EMT, we discovered that S100A4 i

66 S100A4 binding to Rhotekin is calcium-dependent and uses

67 that the coiled-coil partially unwinds upon S100A4 binding.

68 Interestingly, we also find that S100A4 binds as strongly to a homologous heavy chain fra

69 The latter assay demonstrated that S100A4 binds to the filaments and actively promotes disa

70 S100A4 binds to the heavy chain of non-muscle (NM) myosi

71 Human S100A4 binds two Ca2+ ions with the typical EF-hand exhi

72 S100A4(-/-) BMMs form unstable protrusions, overassemble

73 the 2.3 A crystal structure of human Ca(2+)-S100A4 bound to TFP.

74 imide blocked the IL-7-mediated secretion of S100A4, but pretreatment with brefeldin A did not.

75 Downregulation of nuclear S100A4 by low-dose paclitaxel was associated with a stro

76 Suppression of S100A4 by small interference RNA resulted in a reduced c

77 required post-translational modification of S100A4 by the sumo-1 protein.

78 Although the metastatic capabilities of S100A4(+) cancer cells have been examined, the functiona

79 Increased numbers of S100A4(+) cells are associated with poor prognosis in pa

80 S100A4(+) cells in gliomas are enriched with cancer cell

81 ttributable to local non-bone marrow-derived S100A4(+) cells, which are likely fibroblasts in this se

82 Knockdown of S100A4 clearly induced apoptosis with increased fragment

83 delling of these in vitro data suggests that S100A4 concentrations in the micromolar region could dis

84 F MPCs are intrinsically fibrogenic and that S100A4 confers MPCs with fibrogenicity.

85 We hypothesized that S100A4 contributes to the regulation of contraction in a

86 g cancer cells showed a dramatic increase in S100A4, COX-2 and the alteration of 30 tumor-related gen

87 ls (Sharpin(cpdm)), and mice with a stromal (S100a4-Cre) deletion of Sharpin, have reduced mammary du

88 S100a4-Cre; EP4 (flox/flox) (EP4cKO(S100a4)) repairs hea

89 S100A4 to normal physiology, we established S100A4-deficient mice by gene targeting.

90 emarkably decreased in animals injected with S100A4-deficient pancreatic tumor cells.

91 , while cyclin E expression is decreased, in S100A4-deficient pancreatic tumors in vivo.

92 S100A4-deficient tumors have lower expression of vascula

93 Here we establish an S100A4-dependent link between inflammation and metastati

94 ) Fe-S protein 2 (NDUFS2) is regulated in an S100A4-dependent manner and that S100A4 and NDUFS2 exhib

95 osis to a model of persistent fibrosis in an S100A4-dependent manner.

96 w S100A4 regulates metabolism, we found that S100A4 depletion decreases oxygen consumption rates, mit

97 S100A4 depletion did not affect ACh-stimulated SM myosin

98 S100P, like S100A4, differentially interacts with the isoforms of no

99 ues of the coiled-coil are wrapped around an S100A4 dimer disrupting the ACD and resulting in filamen

100 sin chain is wrapped around the Ca(2+)-bound S100A4 dimer occupying both hydrophobic binding pockets.

101 n each pentamer most of the contacts between S100A4 dimers occurs through the TFP moieties.

102 S100A4 downregulation remarkably reduces cell migration

103 S100A4 downregulation results in significant cell growth

104 We demonstrate that S100a4 drives fibrotic tendon healing primarily through

105 etic studies in a Drosophila model to define S100A4 effector functions that mediate metastatic dissem

106 sed metastatic dissemination associated with S100A4 elevation, defining required signaling pathway(s)

107 Selective ablation of S100A4-expressing cells was sufficient to block tumor gr

108 In the tumor mass, nuclear S100A4 expression by cholangiocarcinoma cells was signif

109 S100A4 expression correlated well with integrin alpha6be

110 S100A4 expression is associated with poor clinical outco

111 eoperative nomogram incorporating S100A2 and S100A4 expression predicted survival and nomograms deriv

112 ibodies, there was a significant decrease in S100A4 expression.

113 ome alpha-SMA(+) myofibroblasts, via loss of S100a4 expression.

114 ctional importance of stromal Tenascin-C and S100A4(+) fibroblast-derived VEGF-A in metastasis was es

115 In particular, S100A4(+) fibroblast-derived VEGF-A plays an important r

116 Reduction in metastasis due to the loss of S100A4(+) fibroblasts correlated with a concomitant decr

117 study demonstrates a crucial role for local S100A4(+) fibroblasts in providing the permissive "soil"

118 y integrin alpha6beta4 expression, including S100A4, FST, PDLIM4, CAPG, and Nkx2.2.

119 Our findings uncover a novel S100A4 function and highlight its importance in controll

120 s demonstrate that significant inhibition of S100A4 function occurs only at TFP concentrations that p

121 ation of just Cys81 is sufficient to inhibit S100A4 function with respect to myosin-IIA binding and d

122 development of reagents that interfere with S100A4 function.

123 azines as inhibitors of myosin-II associated S100A4 function.

124 S100A4 gain of function was sufficient to confer fibroti

125 Mechanistically, S100a4 haploinsufficiency decreases myofibroblast and ma

126 present study we tested the hypothesis that S100a4 haploinsufficiency or inhibition of S100a4 signal

127 through a cell non-autonomous process, with S100a4 haploinsufficiency promoting regenerative tendon

128 S100A4 has been shown to be increased in osteoarthritic

129 The relationship between Scx and S100a4 has not been explored.

130 e) also enhanced the chemotactic activity of S100A4 in a synergistic manner.

131 binding studies and the crystal structure of S100A4 in complex with a 45-residue-long myosin heavy ch

132 To address the role of S100A4 in normal mammary gland, its spatial and temporal

133 adly relevant to the physiologic function of S100A4 in other cell and tissue types.

134 GF-beta1, supporting a non-canonical role of S100A4 in pancreatic cancer.

135 alpha-smooth muscle actin and expression of S100A4 in proximal tubular epithelial cells.

136 tor-1, platelet-derived growth factor-b, and S100A4 in R-cells were downregulated by valproic acid an

137 hat TFP binds to the target binding cleft of S100A4 in solution.

138 ere we report the crystal structure of human S100A4 in the active calcium-bound state at 2.03 A resol

139 , defining required signaling pathway(s) for S100A4 in this setting.

140 The role of S100A4 in tumor progression was studied by using an orth

141 S100A4, in a reciprocal manner, activates geminin-overex

142 of a significant number of genes, including S100A4, in the myofibroblastic signature; however, DNA c

143 In 3D culture models, topical addition of S100A4 induced a significant increase in the TGFalpha me

144 king of sumoylation and nuclear transport of S100A4 inhibited the IL-1beta-induced production of MMP-

145 iscovered that metastasis-associated protein S100A4 interacts with the Rho-binding domain (RBD) of Rh

146 ar expression of the calcium-binding protein S100A4 is a biomarker of increased invasiveness in chola

147 hibitor blocked this effect, suggesting that S100A4 is a downstream effector of EGFR activation.

148 S100A4 is a member of the S100 family of calcium-binding

149 Here, we show that S100A4 is a novel biomarker of GSCs.

150 These observations suggest that S100A4 is an excellent target for therapeutic interventi

151 0A4 as a reporter of EMT, we discovered that S100A4 is an upstream regulator of the master EMT regula

152 Additionally, increased S100A4 is associated with only one of the tumors.

153 These findings provide evidence that S100A4 is developmentally regulated and that it plays a

154 The calcium-binding protein S100A4 is expressed at elevated levels in human cancers,

155 S100A4 is expressed in many tissues, including smooth mu

156 n addition to its expression in tumor cells, S100A4 is expressed in normal cells and tissues, includi

157 S100A4 is implicated in metastasis and chronic inflammat

158 Numerous studies indicate that S100A4 is not simply a marker for metastatic disease, bu

159 Thus, S100A4 is one effector of the paracrine action of E2 in

160 We have previously shown that S100A4 is overexpressed in diseased cartilage and that e

161 tin immunoprecipitation, we demonstrate that S100A4 is regulated by NFAT5, thus identifying the first

162 As a DAMP, S100A4 is sensitive to oxidation whereas uric acid (UA)

163 S100A4 is widely expressed in many tissues including smo

164 trated that S100 calcium-binding protein A4 (S100a4) is a driver of tendon scar formation and marks a

165 oblast-specific protein 1 (FSP1, also called S100A4) is considered a marker of fibroblasts in differe

166 S100A4 knockdown also resulted in an increased sensitivi

167 ionally, we demonstrate that markers Scx and S100a4 label distinct populations in tendon during homeo

168 The mechanism by which S100A4 leads to increased cancer aggressiveness has yet

169 of TMD cells, while Paclitaxel decreased the S100A4 level and reduced TMD's cellular motility.

170 f CD16A-CY by PKC in vitro, and reduction of S100A4 levels in vivo enhances receptor phosphorylation

171 Moreover, S100a4-lineage cells become alpha-SMA(+) myofibroblasts,

172 is that deletion of the PGE2 receptor EP4 in S100a4-lineage cells would decrease adhesion formation.

173 x found in the organized bridging tissue and S100a4 localized throughout the entire scar region.

174 the source of elevated elastase (NE) in the S100A4 lung, and NE mRNA and protein levels are greater

175 did not express alpha-smooth muscle actin or S100A4, markers of myofibroblasts and fibroblasts.

176 ractions provides a mechanism for inhibiting S100A4-mediated cellular activities and their associated

177 e S100A4/myosin-IIA interaction and inhibits S100A4-mediated depolymerization of myosin-IIA filaments

178 Assays examining the ability of TFP to block S100A4-mediated disassembly of myosin-IIA filaments demo

179 We suggest that S100A4-mediated effects during branching morphogenesis p

180 cal macrophage motility and demonstrate that S100A4 mediates macrophage recruitment and chemotaxis in

181 Here, we have examined whether S100A4 mediates MPC fibrogenicity.

182 S100A4 (metastasin) is a member of the S100 family of ca

183 d in cell motility and metastasis, including S100A4/metastasin.

184 intimal lesions and elastin fragmentation in S100A4 mice 6 months after viral infection.

185 greater in PA smooth muscle cells (SMC) from S100A4 mice than from C57 mice.

186 increase in lung elastase activity occurs in S100A4 mice, 7 days after M1-MHV-68, unrelated to inflam

187 Homozygous S100A4(-/-) mice are fertile, grow normally and exhibit

188 bone marrow macrophages (BMMs) derived from S100A4(-/-) mice display defects in chemotactic motility

189 ed that bone marrow-derived macrophages from S100A4(-/-) mice exhibit defects in directional motility

190 Two sumoylation sites were identified on the S100A4 molecule, Lys(22) and Lys(96).

191 Exogenous EGF increased S100A4 mRNA levels in 231BR-EGFP cells (1.40+/-0.02-fold

192 METHODS AND Both S100A4/Mts1 (500 ng/mL) and BMP-2 (10 ng/mL) induce migr

193 ced CLIC4 expression does not interfere with S100A4/Mts1 internalization or its interaction with myos

194 lecule necessary for motility in response to S100A4/Mts1 or BMP-2.

195 es demonstrate how a single ligand (BMP-2 or S100A4/Mts1) can recruit multiple cell surface receptors

196 We hypothesized that S100A4/Mts1-mediated hPASMC motility might be enhanced b

197 identified as an inhibitor that disrupts the S100A4/myosin-IIA interaction and inhibits S100A4-mediat

198 hibition in which phenothiazines disrupt the S100A4/myosin-IIA interaction by sequestering S100A4 via

199 identified as an inhibitor that disrupts the S100A4/myosin-IIA interaction.

200 The structure of the S100A4-NMIIA complex reveals a unique mode of interactio

201 Here, we investigate the mechanism of S100A4-NMIIA interaction based on binding studies and th

202 gn of specific drugs that interfere with the S100A4-NMIIA interaction.

203 he Ca(2+)-dependent binding of myosin-IIA to S100A4, NSC 95397 was identified as an inhibitor that di

204 is study, we provide evidence that targeting S100A4 nuclear import by low-dose paclitaxel, a microtub

205 curs only at TFP concentrations that promote S100A4 oligomerization.

206 , we provide evidence that cells depleted in S100A4 or NDUFS2 shift their metabolism toward glycolysi

207 Importantly, we noted that S100A4 or NDUFS2 silencing inhibits mitochondrial comple

208 In the presence of S100A4 or UA, MSCs gained an immunosuppressive capabilit

209 s in which the staining profile for the MIPs S100A4, osteopontin, anterior gradient-2, and S100P has

210 pulmonary artery (PA) neointimal lesions in S100A4-overexpressing, but not in wild-type (C57), mice.

211 S100A4 plays a critical function in the regulation of ai

212 The results show that S100A4 plays a critical role in tension development in a

213 These findings support that S100A4 plays an important role in pancreatic cancer prog

214 The Ca(2+)-S100A4/prochlorperazine (PCP) complex exhibits a similar

215 We now show that the loss of S100A4 produces two mechanistically distinct phenotypes

216 ressing Cre recombinase under control of the S100A4 promoter crossed with mice carrying VEGF-A allele

217 viral thymidine kinase under control of the S100A4 promoter to specifically ablate S100A4(+) stromal

218 in pancreatic cancer progression in vivo and S100A4 promotes tumorigenic phenotypes of pancreatic can

219 Intravenously injected S100A4 protein induced expression of SAA proteins and cy

220 e three-dimensional structure of the dimeric S100A4 protein upon calcium binding.

221 The structure of the active form of S100A4 provides insight into its interactions with its b

222 TSP1, TSP2, EGFR, EpCAM, GPC1, WNT-2, EphA2, S100A4, PSCA, MUC13, ZEB1, PLEC1, HOOK1, PTPN6, and FBN1

223 In concert, geminin-overexpression, S100A4/RAGE and Gas6/AXL signaling promote the invasive

224 s, which, along with annexin-binding protein S100A4, regulated fusogenic activity of syncytin 1.

225 Investigating how S100A4 regulates metabolism, we found that S100A4 deplet

226 S100A4 regulates the motility of metastatic cancer cells

227 ved in EP4cKO(S100a4) suggesting that EP4cKO(S100a4) repairs heal with increased infiltration of EP4

228 S100a4-Cre; EP4 (flox/flox) (EP4cKO(S100a4)) repairs healed with improved gliding function a

229 Interestingly, EP4cKO(S100a4) resulted in only transient deletion of EP4, sugg

230 of a novel solvatochromatic reporter dye to S100A4 results in a sensor that, upon activation, underg

231 no overt abnormalities; however, the loss of S100A4 results in impaired recruitment of macrophages to

232 The depletion of S100A4, RhoA or rhotekin from airway SM tissues using sh

233 22alpha) and an increase in synthetic marker S100A4 (S100 calcium binding protein A4) compared with c

234 We found that S100A1, S100A2, S100A4, S100A6 and S100B proteins bound different p63 an

235 biophysically the binding of S100A1, S100A2, S100A4, S100A6 and S100B to homologous domains of p63 an

236 Here, we found that S100A1, S100A2, S100A4, S100A6, and S100B bound to two subdomains of the

237 Real-time PCR confirmed that STMN3, S100A4, S100A6, c-Myb, estrogen receptor alpha, growth h

238 ls of genes associated with metastasis NPTN, S100A4, S100A9, and with epithelial mesenchymal transiti

239 taining for the metastasis-inducing proteins S100A4, S100P, osteopontin, and AGR2 (P < or = 0.002).

240 Within the tumor, MSCs differentiate into S100A4-secreting cancer-associated fibroblasts (CAFs).

241 f this study was to examine the mechanism of S100A4 secretion by chondrocytes.

242 00 family proteins, of which two, S100A2 and S100A4, showed in vitro the ability to repress exogenous

243 t S100a4 haploinsufficiency or inhibition of S100a4 signaling improves tendon function following acut

244 g hexokinase expression and that suppressing S100A4 signaling sensitizes lung cancer cells to glycoly

245 Moreover, inhibition of S100a4 signaling via antagonism of its putative receptor

246 Short hairpin RNA-mediated S100A4 silencing in 231BR-EGFP cells decreased their mig

247 immunoprecipitation assays demonstrated that S100A4 specifically and directly binds to Rhotekin RBD,

248 in diseased cartilage and that extracellular S100A4 stimulates MMP-13 production, a major type II col

249 n studies demonstrated that these effects of S100A4(+) stromal cells are attributable to local non-bo

250 s have been examined, the functional role of S100A4(+) stromal cells in metastasis is largely unknown

251 To study the contribution of S100A4(+) stromal cells in metastasis, we used transgeni

252 Depletion of S100A4(+) stromal cells significantly reduced metastatic

253 f the S100A4 promoter to specifically ablate S100A4(+) stromal cells.

254 The Ca(2+)-bound S100A4 structure reveals a large conformational change i

255 ouble-positive cells were observed in EP4cKO(S100a4) suggesting that EP4cKO(S100a4) repairs heal with

256 Partial silencing of S100A4 suppressed migratory capabilities of TMD cells, w

257 ies provide the foundation for understanding S100A4 target recognition and may support the developmen

258 entification of small molecules that disrupt S100A4/target interactions provides a mechanism for inhi

259 EP4 and impaired gliding function in EP4cKO(S100a4) tendon repairs.

260 nding results in the assembly of five Ca(2+)-S100A4/TFP dimers into a tightly packed pentameric ring.

261 e cooperative formation of a similarly sized S100A4/TFP oligomer in solution.

262 n flies overexpressing mutant Ras(Val12) and S100A4, there was a significant increase in activation o

263 established the relationship between Scx and S100a4 throughout both homeostasis and healing.

264 ese lysine residues abolished the ability of S100A4 to be sumoylated and to translocate into the nucl

265 endent conformational change is required for S100A4 to bind peptide sequences derived from the C-term

266 Calcium-activated binding of S100A4 to CD16A, promoted by the initial calcium flux, a

267 t interaction of S100A4 and Rhotekin permits S100A4 to complex with RhoA and switch Rho function from

268 atory mechanism for mediating the binding of S100A4 to myosin-IIA.

269 The binding of S100A4 to NM myosin was required for NM myosin polymeriz

270 To examine the contribution of S100A4 to normal physiology, we established S100A4-defic

271 of evolutionarily conserved pathways used by S100A4 to promote metastatic dissemination, with potenti

272 lanine significantly impaired the ability of S100A4 to promote myosin-IIA filament disassembly.

273 Ch (acetylcholine) stimulated the binding of S100A4 to the NM myosin heavy chain, which was catalysed

274 ng domain (RBD) of Rhotekin, thus connecting S100A4 to the Rho pathway.

275 lar chondrocytes, we show that intracellular S100A4 translocated into the nucleus upon interleukin-1b

276 angiocarcinoma cell lines expressing nuclear S100A4 triggered a marked reduction in nuclear expressio

277 The expression of S100a6 and S100a4, two highly upregulated genes, is closely correla

278 Downregulation of S100A4 using shRNA significantly reduced TGFalpha induce

279 documented the heightened susceptibility of S100A4 versus C57 PA elastin to degradation by elastase.

280 IL-7 stimulates chondrocyte secretion of S100A4 via activation of JAK/STAT signaling, and then S1

281 RhoA GTPase regulated the activation of S100A4 via rhotekin, which facilitated the formation of

282 100A4/myosin-IIA interaction by sequestering S100A4 via small molecule-induced oligomerization.

283 A) 1 and SAA3 are transcriptional targets of S100A4 via Toll-like receptor 4 (TLR4)/nuclear factor-ka

284 lization of YFP with the mesenchymal markers S100A4, vimentin, alpha-SMA, or procollagen 1alpha2, alt

285 Increased expression of S100A4 was also observed in the medulla and papilla, but

286 Nuclear S100A4 was bound to the promoter region of MMP-13 in IL-

287 High expression of either S100A2 or S100A4 was independent poor prognostic factors in a trai

288 Secretion of S100A4 was measured in conditioned media by immunoblotti

289 Chondrocyte secretion of S100A4 was observed after treatment with IL-6 or IL-8 bu

290 t analysis, S100 calcium-binding protein A4 (S100A4) was aligned to a principal axis associated with

291 The effects of loss or gain of S100A4 were examined in pancreatic cancer cell lines.

292 MMP13 correlated more closely with levels of S100A4, whereas MMP9 levels correlated more closely with

293 hat IPF MPCs had increased levels of nuclear S100A4, which interacts with L-isoaspartyl methyltransfe

294 clude that Ca(2+) binds to the EF2 domain of S100A4 with micromolar affinity and that the K(d) value

295 ACh stimulated the interaction of S100A4 with NM myosin II in airway SM at the cell cortex

296 lament assembly, and that the interaction of S100A4 with NM myosin in response to contractile stimula

297 The interaction of S100A4 with NM myosin may also play an important role in

298 hydrophobic target binding pocket of Ca(2+)-S100A4 with no significant conformational changes observ

299 To examine the interaction of S100A4 with TFP, we determined the 2.3 A crystal structu

300 a marked reduction in nuclear expression of S100A4 without modifying its cytoplasmic levels, an effe