ライフサイエンスコーパス: podosome

1 o the capacity of certain cell types to form podosomes.

2 ane protrusions, as well as by disassembling podosomes.

3 have been compared with focal adhesions and podosomes.

4 d and predominantly localized to rosettes of podosomes.

5 MT1-MMP) was not recruited to the incomplete podosomes.

6 t lysosomal vesicles moved to and fused with podosomes.

7 ine proteases have been found to function at podosomes.

8 din plays a critical role in the assembly of podosomes.

9 tributes to the formation of invadopodia and podosomes.

10 o the formation of invasive adhesions termed podosomes.

11 alladin plays a key role in the formation of podosomes.

12 P1, ASAP3 did not localize to invadopodia or podosomes.

13 a concomitant loss of filamentous actin-rich podosomes.

14 les, is involved in the matrix degradtion of podosomes.

15 transcellular pore formation in response to podosomes.

16 ted structures in NIH 3T3 fibroblasts called podosomes.

17 eoclasts, where it is primarily localized in podosomes.

18 r leukocyte trafficking and the functions of podosomes.

19 and ASAP1b) associated with invadopodia and podosomes.

20 well as wild-type ASAP1 in the formation of podosomes.

21 ing RNA blocked formation of invadopodia and podosomes.

22 orylation levels and subsequent formation of podosomes.

23 s and formation of invasive adhesions called podosomes.

24 sts in either phase are markedly depleted of podosomes.

25 the activation of c-Src and the formation of podosomes.

26 rane remodeling and has been associated with podosomes.

27 ndrome protein (WASP), 2 major regulators of podosomes.

28 ls were unable to spread normally or to form podosomes.

29 mbrane, where it colocalized with markers of podosomes.

30 To resorb bone, OCs form podosomes.

31 gulates cyt-PTPe activity and its effects on podosomes.

32 podosome belt, and EB1-positive MTs targeted podosomes.

33 rption by maintaining fast actin turnover in podosomes.

34 ture DCs are flatter and fail to disassemble podosomes, a specialized structure for cell-matrix adhes

35 form circular structures outside and at the podosome actin ring to regulate podosome dynamics.

36 iting myosin-II-dependent tension dissipated podosome actin rings before dissipating the myosin-ring

37 gelsolin null osteoclasts failed to exhibit podosomes, actin ring was observed in these osteoclasts.

38 1 localized to lamellipodial protrusions and podosomes, actin-rich structures associated with adhesio

39 Because SH3PXD2B is predicted to be a podosome adaptor protein, these findings implicate podos

40 eopodal features and appearance of prominent podosomes along with clearance of the Stiny-1 periostin

41 ant of NaV1.6 participates in the control of podosome and invadopodia formation and suggest that intr

42 tes cellular invasion through its effects on podosome and invadopodia formation in macrophages and me

43 sealing zones, suggesting a possible role in podosome and sealing zone positioning.

44 results in disassembly of murine macrophage podosomes and a marked reduction of GTP loading on Rac.

45 nd dendritic cells, but are generally called podosomes and are thought to be more involved in cell-ma

46 Here we demonstrate that lymphocytes used podosomes and extended "invasive podosomes" to palpate t

47 eveals that PSTPIP1 regulates the balance of podosomes and filopodia in macrophages.

48 d signaling molecules within alpha(V)beta(3) podosomes and in particular the proximal binding partner

49 m chloride greatly enhanced the formation of podosomes and increased the matrix degradation.

50 nase signaling involved in the regulation of podosomes and invadopodia and speculate that ASAP1 may f

51 , our results show that SV is a component of podosomes and invadopodia and that SV plays a role in in

52 Podosomes and invadopodia are actin-rich structures that

53 CD302 colocalized with podosomes and lamellopodia structures, so we hypothesize

54 The dynamics of podosomes and of focal adhesions were different.

55 rophages showed that FXIII-A associated with podosomes and other structures adjacent to the plasma me

56 a common molecular step in the formation of podosomes and phagocytic cups.

57 g that WASP is required for the formation of podosomes and phagocytic cups.

58 ecruitment is necessary for the formation of podosomes and phagocytic cups.

59 efective MT targeting to, and patterning of, podosomes and reduced bone resorption.

60 sing active Src, where it is most evident in podosomes and regions of membrane ruffling.

61 Patterning of both podosomes and sealing zones is dependent upon an intact

62 wed that WASP bound WIP to form a complex at podosomes and that the knockdown of WIP impairs podosome

63 Moreover, Nef points out podosomes and the Hck/WASP signaling pathway as good can

64 ned the nanoscale organization of individual podosomes and their spatial arrangement within large clu

65 at adhesion sites is reminiscent of invasive podosomes and, consistent with this model, they are enri

66 etal remodeling, especially the formation of podosomes and.

67 in-based structures, including lamellipodia, podosomes, and endocytic actin networks.

68 ated with podosomes, regulates actin flux in podosomes, and promotes bone resorption by osteoclasts.

69 type PTP alpha (RPTPa), which is absent from podosomes, and the nonreceptor form of PTP epsilon (cyt-

70 veil-like membrane protrusions, disassemble podosomes, and travel from the peripheral tissues to lym

71 We demonstrate that podosomes are abundant in primary murine megakaryocytes

72 Podosomes are actin-based proteolytic microdomains of th

73 Podosomes are actin-rich structures that function in adh

74 Podosomes are cytoskeletal-based structures involved in

75 Podosomes are dynamic cell adhesions that are also sites

76 Our results suggest that podosomes are dynamic mechanosensors in which interactio

77 Podosomes are highly dynamic actin-containing adhesion s

78 stability, size, and proteolytic function of podosomes are increased via the phagocyte-specific kinas

79 We show that as podosomes are lost, TLR signaling induces prominent foca

80 Podosomes are multimolecular mechanosensory assemblies t

81 In osteoclasts (OCs) podosomes are organized in a belt, a feature critical fo

82 Podosomes are protrusive structures implicated in macrop

83 Podosomes are self-organized, dynamic, actin-containing

84 The location and dynamics of synaptic podosomes are spatiotemporally correlated with changes i

85 d invade tissues; related structures, termed podosomes, are sites of dynamic ECM interaction.

86 e cells formed recognizable podosomes, their podosome arrays were loosely packed and improperly local

87 erely defective in the formation of circular podosome arrays.

88 iridocorneal angle and the genes influencing podosomes as candidates in glaucoma.

89 ack was observed due to the rearrangement of podosomes as rosettes or clusters at the leading edge.

90 clast motility is thought to depend on rapid podosome assembly and disassembly.

91 Podosome assembly was aberrant and associated with dysre

92 At sites of residual podosome-associated actin polymerization, localization o

93 that the FAT domain of Pyk2 is essential for podosome belt and sealing zone formation as well as for

94 5, mature Lpar1(-/-) osteoclasts had reduced podosome belt and sealing zone resulting in reduced mine

95 pleting both Cbl proteins disrupted both the podosome belt and the microtubule network and decreased

96 unable to transform podosome clusters into a podosome belt at the cell periphery; instead of a sealin

97 microtubules, allowing the formation of the podosome belt in osteoclasts, and by promoting osteoclas

98 namin colocalizes with Cbl in the actin-rich podosome belt of osteoclasts and that dynamin forms a co

99 bly of focal adhesions, were observed in the podosome belt of osteoclasts.

100 ii) actin cytoskeleton reorganization into a podosome belt that forms a gasket to restrict lacunar ac

101 ound to be an early component of the nascent podosome belt, along with dynamin, supporting a role for

102 eased as OCs matured and was enriched in the podosome belt, and EB1-positive MTs targeted podosomes.

103 Calpain inhibitors disrupted the podosome belt, blocked the constitutive cleavage of the

104 ition to the effects on microtubules and the podosome belt, depleting both Cbls significantly increas

105 , talin, and Pyk2, which are enriched in the podosome belt, induced osteoclast retraction, and reduce

106 growing "plus" ends of MTs point toward the podosome belt, plus-end tracking proteins (+TIPs) might

107 otected both the microtubule network and the podosome belt.

108 or EB1 depletion resulted in the loss of the podosome belt.

109 l-length Myo10 led to increased formation of podosome belts along with larger sealing zones and enhan

110 loproteinase MT1-MMP is enriched not only at podosomes but also at distinct "islets" embedded in the

111 Thus, ARNO-ARF1 regulates formation of podosomes by inhibition of RhoA/myosin-II and promotion

112 f actin filament comet tails by Listeria and podosomes by monocytes.

113 what regulates podosome dynamics and whether podosomes can function as direct mechanosensors, like fo

114 mal motility involves matrix proteolysis and podosomes, cell structures constitutive of monocyte-deri

115 Podosome clusters appear as self-organized contact areas

116 k2-null osteoclasts were unable to transform podosome clusters into a podosome belt at the cell perip

117 her understanding the collective behavior of podosome clusters.

118 Invadopodia and podosomes, collectively referred to as invadosomes, are

119 We further showed that RhoE activates podosome component cofilin by inhibiting its Rock-mediat

120 adation sites and containing proteins of the podosome core but not of the adhesive ring.

121 WASp recruitment to podosome cores was independent of HS1, whereas HS1 recru

122 However, podosomes degrade matrix and appear to be important for

123 typal migratory cells, use the protease- and podosome-dependent mesenchymal migration mode in dense t

124 similar structures (that is, invadopodia and podosomes) described in other cell types.

125 Simultaneously, actin-rich podosomes disappear, which suggests a coordinated redepl

126 Podosome disassembly caused by TLR signaling occurs norm

127 , MMP inhibitors block TLR signaling-induced podosome disassembly, although stimulated endocytosis is

128 teoclast: dysregulation of calpain-dependent podosome disassembly, leading to abnormal actin belt for

129 membrane protrusive activity, as well as in podosome disassembly.

130 Stress-induced podosome displacements increased nonlinearly with applie

131 MT1-MMP islets become apparent upon podosome dissolution and persist beyond podosome lifetim

132 cells and fibroblasts stimulated to produce podosomes, down-regulation of the G-protein ARF1 or the

133 he AChR aggregate bear structures resembling podosomes, dynamic actin-rich adhesive organelles involv

134 the RhoE-Rock-cofilin pathway, by promoting podosome dynamics and patterning, is central for OC migr

135 Yet, it is not clear what regulates podosome dynamics and whether podosomes can function as

136 unctions including phagocytosis, chemotaxis, podosome dynamics, and matrix degradation.

137 e and at the podosome actin ring to regulate podosome dynamics.

138 r pharmacological inhibitors led to striking podosome elimination.

139 nable efficient and localized reformation of podosomes, ensuring coordinated matrix degradation and i

140 ic, actin-rich peripheral edge that contains podosomes, filopodia, and lamellipodia.

141 NA-treated cells could not properly position podosomes following microtubule disruption.

142 On glass, osteoclasts generate podosomes, foot-like processes containing a core of F-ac

143 ive analyses with osteoclasts, which utilize podosomes for migration.

144 ly, palladin knockdown resulted in decreased podosome formation and a significant reduction in transw

145 Podosome formation and assembly are regulated by cytoske

146 lowed us to reveal the nanoscale dynamics of podosome formation and dissociation throughout an entire

147 , we addressed whether Sos1 is implicated in podosome formation and function in macrophages.

148 und that lack of Tks4 resulted in incomplete podosome formation and inhibited ECM degradation.

149 Hck/Fgr-deficient macrophages showed blunted podosome formation and mesenchymal migration capacity.

150 mplex is involved in other functions such as podosome formation and phagocytosis.

151 ting podosomes with WASp being essential for podosome formation and with HS1 ensuring efficient array

152 the pattern and distribution of actin-based podosome formation are visibly altered in BMDCs lacking

153 We conclude that ERK5 promotes Src-induced podosome formation by inducing RhoGAP7 and thereby limit

154 Examination of the initial stages of podosome formation has revealed an important role for th

155 g factor 2C, and RhoGAP7 expression restored podosome formation in ERK5-deficient cells.

156 te that the WASP-WIP complex is required for podosome formation in macrophages.

157 partner of WASP, plays an important role in podosome formation in macrophages.

158 exchange factor activity, and Rac regulates podosome formation in myeloid cells and invadopodia form

159 atelet-derived growth factor (PDGF) mediates podosome formation in SMCs through the regulation of miR

160 Palladin overexpression induced podosome formation in the non-invasive MCF7 cells, which

161 Concomitantly, treatments inducing podosome formation increased the level of guanosine trip

162 However, the molecular basis for podosome formation is not fully understood.

163 toskeleton: the ability of SSeCKS to inhibit podosome formation is unaffected by cytochalasin D or ja

164 hereas the suppression of myosin-IIA rescued podosome formation regardless of ARF1 inhibition.

165 Podosome formation requires the function of Rho family g

166 Podosome formation requires the Wiskott-Aldrich syndrome

167 actin regulatory protein WASP; inhibition of podosome formation selectively blocked the transcellular

168 ll adhesion and actin dynamics by regulating podosome formation through the assembly of complexes com

169 When WASP binding to WIP was blocked, podosome formation was also impaired.

170 When podosome formation was reduced by blocking WASP binding

171 Podosome formation was restored in cortactin-depleted ce

172 rane paralleled virus-induced cytopathicity, podosome formation, and cellular fusion.

173 cued by reintroduction of Tks4, whereas only podosome formation, but not ECM degradation, was rescued

174 of membrane traffic at the Golgi, regulates podosome formation, maintenance, and function.

175 luding dendritic morphology, probing motion, podosome formation, production of interleukin-12 and oth

176 ex of WASP with WIP plays a critical role in podosome formation, thereby mediating efficient transend

177 e kinase, is implicated in the regulation of podosome formation.

178 tion of an autoregulatory loop that promotes podosome formation.

179 d) in mouse peritoneal macrophages inhibited podosome formation.

180 asts lacking Tks4 to investigate its role in podosome formation.

181 ng matrix metalloproteinase-2 expression and podosome formation.

182 inhibiting cytoskeletal remodeling, that is, podosome formation.

183 o determine whether MAPK signaling regulates podosome formation.

184 v-Src led to cellular extension and restored podosome formation.

185 the Src phosphorylation site did not support podosome formation.

186 ASP with WIP decreased, resulting in reduced podosome formation.

187 osomes and that the knockdown of WIP impairs podosome formation.

188 sidues phosphorylated by Src did not restore podosome formation.

189 tment was unable to activate c-Src or effect podosome formation.

190 ganization as rosettes and three-dimensional podosomes, (ii) regulates the proteolysis of the matrix

191 Sos1 localizes to podosomes in both murine and human macrophages, and its

192 SV localizes to the cores of Src-generated podosomes in COS-7 cells and with invadopodia in MDA-MB-

193 mulated the formation of palladin-containing podosomes in invasive, but not in non-invasive cell line

194 es the proteolysis of the matrix mediated by podosomes in macrophages, (iii) is required for podosome

195 the first time a fundamental requirement for podosomes in megakaryocyte process extension across a ba

196 We further show that podosomes in mouse DC are foci of pronounced gelatinase

197 me adaptor protein, these findings implicate podosomes in normal development of the iridocorneal angl

198 A new study now implicates podosomes in pore formation during myoblast fusion.

199 Invadopodia are different from podosomes in the localization of actin/vinculin, distrib

200 onstrated that invadopodia are comparable to podosomes in the localization of Wiskott-Aldrich syndrom

201 ronments, whereas they use the protease- and podosome-independent amoeboid mode in more porous matric

202 Thus, dynamic MTs and podosomes interact to control bone resorption.

203 rization drives extension of invadopodia and podosomes into the basement layer.

204 mology 3 domains (Tks5)/Fish is required for podosome/invadopodia formation, degradation of ECM, and

205 e are highly dynamic and colocalize with the podosome/invadopodial proteins, cortactin, Tks5, and cdc

206 topology, and pharmacological disruption of podosomes leads to rapid alterations in AChR organizatio

207 eveal a previously unrecognized phase in the podosome life cycle and identify a structural function o

208 Megakaryocyte podosome lifetime and density, but not podosome size, ar

209 e, are dependent on the type of matrix, with podosome lifetime dramatically increased on collagen fib

210 upon podosome dissolution and persist beyond podosome lifetime.

211 ding submicron-scale, actin-rich "invadosome/podosome-like protrusions" (ILPs).

212 Our studies uncover a novel invasive podosome-like structure (PLS) in a developing tissue and

213 colocalizing with the F-actin focus within a podosome-like structure (PLS), and promotes actin filame

214 is mediated by an invasive, F-actin-enriched podosome-like structure (PLS).

215 At the front, formation of a zone containing podosome-like structures (PLS) dynamically correlates wi

216 ation but is targeted to the cell cortex and podosome-like structures after stimulation with a phorbo

217 activity regulates motility associated with podosome-like structures at the cell leading edge, while

218 neutralizing antibody to TNF-alpha displayed podosome-like structures in the entire subsurface and at

219 Podosome-like structures present at the leading edge in

220 ADAM8 was not found in podosome-like structures, which are associated with prot

221 the cell periphery, and F-actin was found in podosome-like structures.

222 tes its relocalization from the cytoplasm to podosome-like structures.

223 rich sealing zone composed of densely packed podosome-like units.

224 ement membrane, and our results suggest that podosomes may have a role in proplatelet arm extension o

225 Podosomes mediate cell migration and invasion by coordin

226 on, we show that cathepsin B participates in podosomes-mediated focal matrix degradation and invasion

227 ion and stability of the belt, the MT and/or podosome molecules that mediate the interaction of the t

228 ins at the apical surface directly displaced podosomes near the basal surface.

229 main promotes bone metastases by stimulating podosome nucleation, motility, neoangiogenesis, vasculog

230 iguration (i.e. either in the disassembly of podosomes or formation of actin aggregates).

231 cellular retraction and an inability to form podosomes or induce invasion.

232 uctures "linear invadosomes." Interestingly, podosomes or invadopodia were replaced by linear invados

233 ynamic actin-rich membrane structures called podosomes or invadopodia.

234 gradation of matrix but not the formation of podosomes or invadopodia.

235 trabecular meshwork (TM) cells that resemble podosomes or invadopodia.

236 type-1 matrix metalloproteinase (MT1-MMP) to podosomes or invadosomes to break extracellular matrix b

237 ducted to determine whether TM cells exhibit podosome- or invadopodia-like structures (PILS) and whet

238 ells, ADAMTS-4 colocalized with cortactin in podosome- or invadopodia-like structures, but ADAMTS-1 a

239 nous PSTPIP1 negatively regulates macrophage podosome organization and matrix degradation.

240 The varying effects of either PTP on podosome organization in osteoclasts are caused by their

241 well as production, structure, function, and podosome organization of osteoclasts, are unchanged in m

242 ortant role of Pyk2 in microtubule-dependent podosome organization, bone resorption, and other osteoc

243 Although changes in actin dynamics during podosome patterning have been documented, the mechanisms

244 end tracking proteins (+TIPs) might regulate podosome patterning.

245 ssociation with WASP as well as formation of podosomes, peripheral microfilopodia-like structures, an

246 regulates F-actin-rich structures, including podosomes, phagocytic cups, actin comet tails, subcortic

247 Our results indicate that synaptic podosomes play critical roles in maturation of the posts

248 10 plays a role in osteoclast attachment and podosome positioning by direct linkage of actin to the m

249 osteoclasts to play a role in attachment and podosome positioning.

250 in fibroblasts induced formation of putative podosome precursors: actin-rich puncta coinciding with m

251 ity of MT1-MMP islets are reused as sites of podosome reemergence.

252 smic domain in imprinting spatial memory for podosome reformation via assembly in membrane islets.

253 d that the GTPase dynamin is associated with podosomes, regulates actin flux in podosomes, and promot

254 rminal residues of cyt-PTPe is essential for podosome regulation; attaching this sequence to the cata

255 Moreover, we identify key podosome regulators as targets of miR-143 (PDGF receptor

256 We propose actin nodules are platelet podosome-related structures required for platelet-platel

257 Podosomes represent a class of integrin-mediated cell-ma

258 cient Wiskott-Aldrich syndrome patients lack podosomes, resulting in defective chemotactic migration.

259 ortactin depletion led to a specific loss of podosomes, revealing a tight spatial compartmentalizatio

260 ion of any molecule in this complex disrupts podosome ring formation and/or decreases osteoclast migr

261 Calcitonin disrupted the podosome ring, induced osteoclast retraction, and reduce

262 associated with the outer edges of immature podosome rings and sealing zones, suggesting a possible

263 As podosome rings changed size or shape, tractions undernea

264 osome rings were generated with rotations of podosome rings in a nonmotile, nonrotating cell, suggest

265 Torsional tractions underneath the podosome rings were generated with rotations of podosome

266 vesicular structures transiently contacting podosome rings.

267 s a critical regulator of cell spreading and podosome rosette formation in immature DCs.

268 osomes in macrophages, (iii) is required for podosome rosette formation triggered by Hck, and (iv) is

269 in microtubule acetylation, which increases podosome rosette stability and is sufficient to inhibit

270 -positive staining within the electron dense podosome rosette structure.

271 n matrix degradation, due to a disruption of podosome rosettes caused by myosin-IIA overassembly, and

272 mal marker LAMP-1 localized at the center of podosome rosettes protruding into extracellular matrix u

273 on the dynamics and degradative functions of podosome rosettes.

274 d cells and contributed to the biogenesis of podosome rosettes.

275 found that RA T cells abundantly express the podosome scaffolding protein TKS5, which enables them to

276 ocyte podosome lifetime and density, but not podosome size, are dependent on the type of matrix, with

277 Podosome stability and dynamics depend on actin cytoskel

278 rescue, we show that FLNa (i) is involved in podosome stability and their organization as rosettes an

279 F7 cells, which are otherwise unable to form podosomes, suggesting that palladin plays a critical rol

280 er, although these cells formed recognizable podosomes, their podosome arrays were loosely packed and

281 onstrated that, despite exhibiting bona fide podosomes, these cells presented dysfunctional SZs.

282 se a specialized adhesive structure called a podosome to migrate.

283 al. demonstrate that lymphocytes can extend podosomes to palpate endothelial cells searching for are

284 ocytes used podosomes and extended "invasive podosomes" to palpate the surface of, and ultimately for

285 s use an actin-based membrane structure, the podosome, to migrate to inflamed tissues.

286 d filamentous (F)-actin polymerization, high podosome turnover in macrophages, and myelodysplasia.

287 However, retention of mutant proteins in podosomes was significantly impaired and associated with

288 Because FLNa has been shown to localize to podosomes, we hypothesized that the defects seen in pati

289 nged size or shape, tractions underneath the podosomes were exerted onto the substrate and were aboli

290 Podosomes were formed in NIH 3T3 fibroblasts in which en

291 Podosomes were highly dynamic, with rapid turnover of bo

292 Podosomes were restored by reconstitution of the WASP-WI

293 of granular-filamentous material and evident podosomes, were observed.

294 cytoskeleton remodeling and is localized to podosomes where it has a role in actin turnover.

295 allowed us to detect endogenous Rho[GTP] at podosomes, where it colocalized with F-actin, cortactin,

296 und to colocalize with the adhesive rings of podosomes, whereas ARF1 was localized to vesicular struc

297 itro and in vivo results in the formation of podosomes, which are actin-rich membrane protrusions inv

298 the assembly, organization, and dynamics of podosomes, which are the transient adhesion complexes of

299 tissue remodeling, have yet to be linked to podosomes with the exception of cathepsin K in osteoclas

300 nique roles for these proteins in regulating podosomes with WASp being essential for podosome formati