ライフサイエンスコーパス: podosome

1 l signaling to F-actin polymerization at the podosome.

2 association and ventral localization at the podosome.

3 To resorb bone, OCs form podosomes.

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

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

6 rption by maintaining fast actin turnover in podosomes.

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

8 ane protrusions, as well as by disassembling podosomes.

9 have been compared with focal adhesions and podosomes.

10 d and predominantly localized to rosettes of podosomes.

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

12 t lysosomal vesicles moved to and fused with podosomes.

13 ine proteases have been found to function at podosomes.

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

15 tributes to the formation of invadopodia and podosomes.

16 o the formation of invasive adhesions termed podosomes.

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

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

19 a concomitant loss of filamentous actin-rich podosomes.

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

21 transcellular pore formation in response to podosomes.

22 ted structures in NIH 3T3 fibroblasts called podosomes.

23 eoclasts, where it is primarily localized in podosomes.

24 tent protrusions formed at sites enriched in podosomes.

25 somes, a collective term for invadopodia and 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 ture DCs are flatter and fail to disassemble podosomes, a specialized structure for cell-matrix adhes

31 ng DCs, in dynamic coordination with nascent podosome actin cores.

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

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

34 1 localized to lamellipodial protrusions and podosomes, actin-rich structures associated with adhesio

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

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

37 ncrease in activated alphavbeta3 integrin in podosome and focal adhesion matrix adhesion sites.

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

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

40 on of the late-stage MK invagination system, podosome and PPF, and PP branching.

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

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

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

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

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

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

47 Podosomes and invadopodia are actin-rich structures that

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

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

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

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

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

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

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

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

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

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

58 report that kindlin-3 recruits leupaxin into podosomes and thereby regulates paxillin phosphorylation

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

60 etal remodeling, especially the formation of podosomes and.

61 a-catenin colocalization on trophoblast cell podosomes, and ACTN4 down-regulation suppressed the E-ca

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

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

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

65 rganize the cytoskeleton of lamellipodia and podosomes, and thus modulating cell motility and invasio

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

67 We demonstrate that podosomes are abundant in primary murine megakaryocytes

68 Podosomes are actin-based proteolytic microdomains of th

69 Podosomes are actin-rich structures that function in adh

70 Podosomes are compartmentalized actin-rich adhesions, de

71 Podosomes are cytoskeletal-based structures involved in

72 Podosomes are dynamic cell adhesions that are also sites

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

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

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

76 Podosomes are multimolecular mechanosensory assemblies t

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

78 continuous assembly and disassembly and that podosomes are precursors of these structures.

79 rin alpha(M)beta(2), and other components of podosomes are present in ZLSs.

80 Podosomes are protrusive structures implicated in macrop

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

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

83 Podosomes are ubiquitous cellular structures important t

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

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

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

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

88 cules involved in actin core organization in podosomes, as well as cells treated with the inhibitors

89 Podosome assembly was aberrant and associated with dysre

90 ules to link phosphatidylinositol signals to podosome assembly.

91 th PLD1 and PLD2 control the early stages of podosome assembly.

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

93 5, mature Lpar1(-/-) osteoclasts had reduced podosome belt and sealing zone resulting in reduced mine

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

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

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

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

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

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

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

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

102 otected both the microtubule network and the podosome belt.

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

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

105 t only activates and clusters integrins into podosomes but also regulates their lifetime by recruitin

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

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

108 ts presence in these early adhesion patches, podosomes can form in the absence of paxillin or any pax

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

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

111 Podosome clusters appear as self-organized contact areas

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

113 her understanding the collective behavior of podosome clusters.

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

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

116 Structurally, podosomes consist of a protrusive actin core surrounded

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

118 o1e) is enriched at the ventral layer of the podosome core in a PI(3,4,5)P3-dependent manner.

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

120 vealing ring-like tensile forces surrounding podosome cores.

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

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

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

124 We show that podosome development occurs through initial mobilization

125 Podosome disassembly caused by TLR signaling occurs norm

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

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

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

129 Stress-induced podosome displacements increased nonlinearly with applie

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

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

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

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

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

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

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

137 r pharmacological inhibitors led to striking podosome elimination.

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

139 Matrix remodeling by endothelial podosomes facilitates invasion and thereby vessel format

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

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

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

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

144 Podosome formation and assembly are regulated by cytoske

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

146 role of PLD1 and PLD2 isoforms in regulating podosome formation and dynamics in human primary DCs by

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

148 wever, the mechanisms underlying endothelial podosome formation and function remain unclear.

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

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

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

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

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

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

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

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

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

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

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

160 Therefore, targeting of Septin2-mediated podosome formation is a potentially attractive anti-angi

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

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

163 Podosome formation requires the function of Rho family g

164 Podosome formation requires the Wiskott-Aldrich syndrome

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

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

167 D) and its product phosphatidic acid (PA) in podosome formation, but the spatiotemporal control of th

168 During podosome formation, distinct phosphatidylinositol 3,4,5-

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

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

171 s filamentous actin (F-actin) and diminished podosome formation, whereas the tubulin cytoskeleton rem

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

173 tion of an autoregulatory loop that promotes podosome formation.

174 d) in mouse peritoneal macrophages inhibited podosome formation.

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

176 y of the Arp2/3 complex decreased fusion and podosome formation.

177 ng matrix metalloproteinase-2 expression and podosome formation.

178 inhibiting cytoskeletal remodeling, that is, podosome formation.

179 o determine whether MAPK signaling regulates podosome formation.

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

181 the Src phosphorylation site did not support podosome formation.

182 of N-WASP and Arp2/3 in the initial phase of podosome formation.

183 strains F-actin polymerization, and inhibits podosome formation.

184 binding residues of Septin2 are required for podosome function.

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

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

187 Septin2 localizes around the perimeter of podosomes in close proximity to the basolateral plasma m

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

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

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

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

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

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

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

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

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

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

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

199 quired for maturation of nascent endothelial podosomes into matrix-degrading organelles.

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

201 membranes, suggesting that the transition of podosomes into ZLSs is induced by bridging plasma membra

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

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

204 we show that Septin2-mediated regulation of podosomes is critical for endothelial cell invasion asso

205 ode with leupaxin, paxillin recruitment into podosomes is kindlin-3 independent.

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

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

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

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

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

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

223 This work deepens our understanding of podosome mechanotransduction and contributes tools that

224 Podosomes mediate cell migration and invasion by coordin

225 oth PLD1 and PLD2 activity are important for podosome-mediated matrix degradation.

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 Our findings redefine podosome nanoscale architecture and reveal a paradigm fo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

247 10 plays a role in osteoclast attachment and podosome positioning by direct linkage of actin to the m

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

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

250 modular actin nano-architecture that enables podosome protrusion and mechanosensing.

251 Although podosome protrusion forces have been quantified, the mag

252 The podosome protrusive core contains a central branched act

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

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

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

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

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

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

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

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

261 As podosome rings changed size or shape, tractions undernea

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

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

264 vesicular structures transiently contacting podosome rings.

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

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

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

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

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

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

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

272 on the dynamics and degradative functions of podosome rosettes.

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

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

275 Podosome stability and dynamics depend on actin cytoskel

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

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

278 to create probes that measure and manipulate podosome tensile forces with molecular piconewton (pN) r

279 re initialized from the ventral layer of the podosome, TH12 precedes the recruitment of N-WASP and Ar

280 s, such as focal adhesions, invadopodia, and podosomes, that are directly implicated in oncogenic eve

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

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

283 ton forms a diffusive barrier around nascent podosomes to promote their maturation.

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

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

286 ereby regulates paxillin phosphorylation and podosome turnover.

287 Thus, podosomes use pN integrin forces to sense and respond to

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

289 the formation of actin-based protrusions and podosomes, was also impaired both in vitro and in vivo.

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

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

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

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

294 activity is required for the maintenance of podosomes, whereas both PLD1 and PLD2 control the early

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

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

297 dritic cells and mediates the dissolution of podosomes, which dendritic cells use to adhere to extrac

298 assemble actomyosin-based structures called podosomes, which mediate adhesion and degradation of ext

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