ライフサイエンスコーパス: anchorage

1 e hydrophobic patch responsible for membrane anchorage.

2 and complementation (DSC) and cleft-mediated anchorage.

3 pid-anchor probe derived from Lyn's membrane anchorage.

4 orates only tissue contraction and localized anchorage.

5 as we lack tools to directly challenge this anchorage.

6 be required for the maintenance of the RCs' anchorage, a function previously unrecognized because of

7 t branching is critical for plants to secure anchorage and ensure the supply of water, minerals, and

8 ted to impact signalling as well as synaptic anchorage and may thereby influence AMPAR clustering dur

9 s have well-established functions in nuclear anchorage and migration in interphase, but little is kno

10 -associated striated fibers (SFs) promote BB anchorage and orientation into ciliary rows.

11 ater and nutrients from the soil, as well as anchorage and stability for the whole plant.

12 and desmin serve redundant roles in nuclear anchorage and that the loss of nuclear anchorage in skel

13 ctivation of c-kit provides signaling, niche-anchorage, and synergies with integrin-mediated adhesion

14 ility of cancer cells to survive and grow in anchorage- and serum-independent conditions is well corr

15 We propose integrin-mediated anchorage as an evolutionarily conserved mechanism of ge

16 Epithelial invasion required matrix anchorage as well as signaling through Src, PI3K, and Ra

17 cER to the young bud followed by subsequent anchorage at its tip ensures the faithful inheritance of

18 mother tip and is required for mitochondrial anchorage at that site, independent of the previously id

19 asynaptically through radixin (Rdx)-mediated anchorage at the actin cytoskeleton.

20 ontractile energy is not transferred to cell anchorage but instead is involved in actin network dynam

21 e ensured by two opposing processes: bud-tip anchorage by mitochondrial fusion and Mmr1p, which favor

22 ing its nutrient/water uptake as well as its anchorage capacity.

23 Theoretical arguments suggest that GPI anchorage could be important for these receptors to expa

24 SH domain of ANC-1, both result in a nuclear anchorage defect in C. elegans.

25 ached fibroblasts, which might indicate that anchorage-dependence of cell growth signaling is disturb

26 gration of a wide range of surface sensitive anchorage dependent cell types.

27 B-231 cell migration, Matrigel invasion, and anchorage-dependent and -independent growth.

28 Inhibition of anchorage-dependent and -independent proliferation, colo

29 broad range of human tumors inhibited their anchorage-dependent and anchorage-independent growth by

30 ranslational mechanisms, and suppresses PDAC anchorage-dependent and anchorage-independent growth.

31 skeleton organization, signaling, apoptosis, anchorage-dependent and independent growth, migration an

32 y delivered small hairpin RNA decreased both anchorage-dependent and independent proliferation of hum

33 Active hirsutinolides inhibited anchorage-dependent and three-dimensional spheroid growt

34 Anchorage-dependent cells (OV-90AD) were grown in tissue

35 es the acquisition of AnR, a process whereby anchorage-dependent cells become resistant to cell death

36 Industrial applications of anchorage-dependent cells require large-scale cell cultu

37 CP) that facilitates digital mass culture of anchorage-dependent cells.

38 h MLK4 expression impaired proliferation and anchorage-dependent colony formation.

39 hat renders PDA cells more invasive and less anchorage-dependent for growth in vitro, as well as more

40 ed in metabolic shift to glycolysis, loss of anchorage-dependent growth and acquired invasive phenoty

41 that (i) VPA affects GSC lines viability and anchorage-dependent growth by inducing differentiative p

42 d samples and between Cdc6 and total Chk1 in anchorage-dependent growth derived protein samples.

43 , migration, invasion, colony formation, and anchorage-dependent growth in HCC cell lines.

44 PL inhibited anchorage-independent and anchorage-dependent growth of multiple breast cancer cel

45 ession levels in OSCC cells with a decreased anchorage-dependent growth, invasion and wound healing.

46 ENP7S exhibit greater cell proliferation and anchorage-dependent growth.

47 kinase-independent mb-KitL/c-kit clustering, anchorage, F-actin polymerization, and Tyr567-dependent

48 al ligament (PDL) include tooth eruption and anchorage, force absorption, and provision of propriocep

49 y malignant cells to survive the stresses of anchorage-free growth in peritoneal fluid and ascites, a

50 de insight into the DNA remodeling and polar anchorage functions of the protein.

51 e of applications, from using as a molecular anchorage in single-molecule force spectroscopy studies

52 clear anchorage and that the loss of nuclear anchorage in skeletal muscle results in a pathological r

53 omplex, critical for nuclear positioning and anchorage in skeletal muscle, and is thought to provide

54 g understanding of the importance of nuclear anchorage in skeletal muscle.

55 The chemokine receptor CXCR4 mediates cell anchorage in the bone marrow (BM) microenvironment and i

56 attachment of anionic lipopolysaccharide for anchorage in the outer membrane.

57 , UNC-84, functions in nuclear migration and anchorage in the soma.

58 by targeting a CSC-like cell population with anchorage independence and invasive potential.

59 ves as an antiapoptotic factor, facilitating anchorage independence and metastasis.

60 They showed higher anchorage independence growth (AIG) in colony formation

61 Altogether, our comprehensive study of anchorage independence in human ILC cell lines provides

62 gether, the data indicate that adaptation to anchorage independence requires a fundamental change in

63 transformed primary mouse and human cells to anchorage independence similarly to mutant H-Ras.

64 ired redundant compensatory signals enabling anchorage independence via ERK and PI3K bypass cascades

65 tumor cells to survive estrogen deprivation, anchorage independence, and invasion.

66 pic mTOR inhibitor repressed CSC generation, anchorage independence, cell survival, and chemoresistan

67 homeostasis and growth during adaptation to anchorage independence.

68 dent increases in SOD2 mRNA during sustained anchorage-independence.

69 oduction and the capacity of MCF-7 cells for anchorage independent growth in soft agar were dependent

70 bypass the requirement for oncogenic Ras in anchorage independent growth in vitro and tumor formatio

71 Anchorage independent growth is one of the hallmarks of

72 Proliferation, migration, and anchorage independent growth were evaluated.

73 uired to support replicative immortality and anchorage independent growth, a predictor of tumorigenes

74 ULK2 overexpression inhibited anchorage independent growth, inhibited astrocyte transf

75 5 and -1976 suppress CRC cell proliferation, anchorage independent growth, metastatic potential, and

76 In 2-dimensional, and in quantitative anchorage-independent 3-dimensional cell culture, ERalph

77 PL inhibited anchorage-independent and anchorage-dependent growth of

78 nd its target genes and to the impairment of anchorage-independent and clonogenic growth, consistent

79 into the proteomic changes that occur during anchorage-independent cancer cell aggregation.

80 lular calcium levels play a critical role in anchorage-independent cancer sphere formation.

81 Finally, anchorage-independent cell growth ability was tested by

82 ses global phosphotyrosine content, promotes anchorage-independent cell growth and activates several

83 In MECs, ectopic expression of PAF induces anchorage-independent cell growth and breast CSC marker

84 Anchorage-independent cell growth and tumor formation in

85 GEF activity is critical for PREX1-dependent anchorage-independent cell growth and xenograft tumor gr

86 Indeed, SOX9 knockdown inhibited anchorage-independent cell growth in vitro and lung colo

87 ng down RSK1 or MSK2, cell proliferation and anchorage-independent cell growth were markedly inhibite

88 pic expression of LKB1 decreased glycolysis, anchorage-independent cell growth, and cell migration an

89 CIP1) PREX1-mediated ERK1/2 phosphorylation, anchorage-independent cell growth, and cell migration we

90 ologic transformation, cell focus formation, anchorage-independent cell growth, and invasion.

91 The impaired anchorage-independent cell growth, apoptosis, and ERK1/2

92 on of miR-29b suppressed cell proliferation, anchorage-independent cell growth, cell migration, invas

93 s inhibitory to Ewing Sarcoma clonogenic and anchorage-independent cell growth, even at modest overex

94 chromatin assembly, facilitated FA-mediated anchorage-independent cell growth.

95 m of PREX1 and contributes to PREX1-mediated anchorage-independent cell growth.

96 ld-type but not GEF-inactive PREX1 increased anchorage-independent cell growth.

97 mor cell proliferation, colony formation and anchorage-independent cell growth.

98 t c-Met-sustained signalling on ARE supports anchorage-independent cell survival and growth, tumorige

99 In vitro ELT3-245 cells exhibit enhanced anchorage-independent cell survival, resistance to anoik

100 RTK, c-Met, from inside the cell, to promote anchorage-independent cell survival.

101 identified a molecular pathway critical for anchorage-independent cell survival.

102 were grown in tissue culture flasks, whereas anchorage-independent cells (OV-90AI) were grown in susp

103 ed hormone independence and HT resistance in anchorage-independent cells revealed distinct context-de

104 ition, SIRT3 inhibits glycolytic capacity in anchorage-independent cells thereby contributing to meta

105 a-mediated down-regulation of ESRRA impaired anchorage-independent colony formation and invasion of O

106 ERK2 knockdown significantly inhibited anchorage-independent colony formation and mammosphere f

107 s inhibited cell proliferation and repressed anchorage-independent colony formation and migration, bu

108 senescence but permitted ICN1 to facilitate anchorage-independent colony formation and xenograft tum

109 PF MPCs manifested an increased capacity for anchorage-independent colony formation compared to CD44(

110 w SPRIGHTLY regulates cell proliferation and anchorage-independent colony formation in primary human

111 AP knockout increases tumorsphere formation, anchorage-independent colony formation, cell migration i

112 s with low endogenous GRHL1 levels abrogated anchorage-independent colony formation, inhibited prolif

113 sed the ability of IGROV cells to grow under anchorage-independent conditions and form aberrant acini

114 ival and induced their ability to grow under anchorage-independent conditions, outcomes that could be

115 breast cancer cells from self-renewing under anchorage-independent conditions, whereas ectopic overex

116 so that cancer cells are able to grow under anchorage-independent conditions.

117 tially rely on SHOC2 for ERK signaling under anchorage-independent conditions.

118 mourigenesis cell-autonomously, by mediating anchorage-independent cytokinesis via RhoA.

119 These cells (hNCPCs(V600E)) acquired anchorage-independent growth ability and were weakly tum

120 osis, epithelial-mesenchymal transition, and anchorage-independent growth activities in vitro and on

121 CHPT1 silencing inhibited anchorage-independent growth and cell proliferation, als

122 ons, ectopic expression of Myc-nick promotes anchorage-independent growth and cell survival at least

123 ive melanoma and lung cancer cells increased anchorage-independent growth and elevated the expression

124 ependency of tumor cells on HR signaling for anchorage-independent growth and highlights how the meta

125 hat LARP1 promotes cell migration, invasion, anchorage-independent growth and in vivo tumorigenesis.

126 colorectal cancer cell lines increased their anchorage-independent growth and inhibited TGFB signalin

127 ermore, depletion of K-Ras and RalB inhibits anchorage-independent growth and invasion and interferes

128 ing ATAD3A also results in loss of both cell anchorage-independent growth and invasion and suppressio

129 nt-derived colon cancer cell line suppressed anchorage-independent growth and reduced tumor growth in

130 operties of MCF10-2A cells with induction of anchorage-independent growth and self-renewal in 3D-sphe

131 (KO) in LN-229 glioblastoma cells suppresses anchorage-independent growth and spheroid invasion in vi

132 t pathways to promote cell proliferation and anchorage-independent growth and survival.

133 egulated kinase pathway activation, promoted anchorage-independent growth and tumor formation in mice

134 cells harboring wild-type PPP2R1A increased anchorage-independent growth and tumor formation, and tr

135 Phosphorylation of WASp at Y102 enhances anchorage-independent growth and tumor growth in an in v

136 ies associated with tumorigenesis, including anchorage-independent growth and tumor progression.

137 nhibits proliferation, NF-kappaB activation, anchorage-independent growth and tumorigenesis.

138 c and/or Akt and examined the cell lines for anchorage-independent growth and tumorigenesis.

139 Results of MTT- and anchorage-independent growth assays and cell cycle analy

140 mors inhibited their anchorage-dependent and anchorage-independent growth by inducing senescence and/

141 1)/S transition of the cell cycle as well as anchorage-independent growth capability of breast cancer

142 y active forms of Akt1 and Akt2 restores the anchorage-independent growth capability of HeLa cells de

143 nder magnesium-deprived situations and under anchorage-independent growth conditions, demonstrating a

144 cy on Nrf2 could be recapitulated in certain anchorage-independent growth environments and was not pr

145 ificantly reduced cellular proliferation and anchorage-independent growth from control melanomas, whe

146 whereas independently of PI3K, Rac1 mediated anchorage-independent growth in a GTPase-independent man

147 cancer cell growth, migration, invasion and anchorage-independent growth in both MCF7 and MCF7-Cd ce

148 ound that FATE1 is required for survival and anchorage-independent growth in Ewing sarcoma cells via

149 ms underlying acquisition and restoration of anchorage-independent growth in HR(+) tumors.

150 d that its depletion inhibits clonogenic and anchorage-independent growth in multiple patient-derived

151 , morphological transformation and increased anchorage-independent growth in response to FGF2 ligand

152 ormation between GRIN1 and GRIN2A, increased anchorage-independent growth in soft agar, and increased

153 o-mesenchymal transition phenotype, acquired anchorage-independent growth in soft agar, and led to en

154 ILC cells exhibit anchorage-independent growth in ultra-low attachment (UL

155 s of contact growth inhibition and increased anchorage-independent growth in vitro and in vivo.

156 colon cancer cells reduces cell survival and anchorage-independent growth in vitro and inhibits tumor

157 encing inhibits NSCLC cell proliferation and anchorage-independent growth in vitro and tumor formatio

158 ific expression of CD24 (NLS-CD24) increased anchorage-independent growth in vitro and tumor formatio

159 ispensable for breast cell proliferation and anchorage-independent growth in vitro and tumor growth i

160 tion of ETS1 in breast cancer cells promotes anchorage-independent growth in vitro and tumor growth i

161 sufficient to promote cell proliferation and anchorage-independent growth in vitro and tumorigenesis

162 s to tumor cell proliferation, invasion, and anchorage-independent growth in vitro.

163 inhibited oral cancer cell invasiveness and anchorage-independent growth in vitro.

164 ls significantly increased proliferation and anchorage-independent growth in vitro.

165 ilization, G2/M growth arrest induction, and anchorage-independent growth inhibition of cancer cells.

166 gulation of survivin, which in turn supports anchorage-independent growth of alphavbeta6-expressing c

167 -binding motif of Claudin-2 is necessary for anchorage-independent growth of cancer cells and is requ

168 entiation and impaired the proliferation and anchorage-independent growth of cells with protective al

169 ificantly reduced cell growth, migration and anchorage-independent growth of CRC cells.

170 f focal complexes, is also essential for the anchorage-independent growth of HeLa cervical carcinoma

171 antiandrogens induced anoikis by abrogating anchorage-independent growth of HR(+) cancer cells but e

172 not RKI-11 inhibits migration, invasion and anchorage-independent growth of human breast cancer cell

173 preading of murine embryonic fibroblasts and anchorage-independent growth of human cancer cell lines.

174 AF8 and AF10 inhibited the anchorage-independent growth of human colorectal cancer

175 lture, the knockdown of which diminished the anchorage-independent growth of ILC cell lines through c

176 ounds disrupt NR0B1 complexes and impair the anchorage-independent growth of KEAP1-mutant cancer cell

177 Depletion of AR suppressed Sema4D-induced anchorage-independent growth of LNCaP and LNCaP-LN3 cell

178 gammaS inhibited, whereas adenosine promoted anchorage-independent growth of MDA-MB-231 cells.

179 x), resulting in increased proliferation and anchorage-independent growth of melanoma cells.

180 Aspirin decreased viability and anchorage-independent growth of mutant PIK3CA breast can

181 INPP4B increases proliferation and triggers anchorage-independent growth of normal colon epithelial

182 a2 or SPRK3 inhibited both proliferation and anchorage-independent growth of RMS cells.

183 plasma membrane, where its activity promoted anchorage-independent growth of the cell cultures.

184 hosphatases significantly reduced growth and anchorage-independent growth of TNBC cells to a greater

185 t cannot be phosphorylated by AMPK increased anchorage-independent growth of tumor cells and helped t

186 s Wnt/beta-catenin activation, as well as an anchorage-independent growth phenotype.

187 Anchorage-independent growth reprogrammes a metabolic ne

188 ere we report that p100 inhibits cancer cell anchorage-independent growth, a hallmark of cellular mal

189 These cell lines exhibit anchorage-independent growth, a lack of contact inhibiti

190 ction to ECM-induced signals is required for anchorage-independent growth, a property of most maligna

191 of apico-basal polarity in 3D cultures, and anchorage-independent growth, accompanied by expression

192 ns for CAP1 in cancer cell proliferation and anchorage-independent growth, again in a cell context-de

193 ing FGFR3 and kdFGFR3 reduced clonogenicity, anchorage-independent growth, and disintegration of the

194 gnificantly decreased cell proliferation and anchorage-independent growth, and impaired migration and

195 cluded rates of proliferation and apoptosis, anchorage-independent growth, and invasiveness, were ass

196 transforming prostate epithelial cells into anchorage-independent growth, and MAPK4 knockdown inhibi

197 KSRP decreased cell proliferation, reversed anchorage-independent growth, and reduced migration/inva

198 n to reduce cellular motility, invasiveness, anchorage-independent growth, and responsiveness to TGFb

199 , KAP1, CHD1, and EIF3L collectively support anchorage-independent growth, and the SUMOylation of KAP

200 s exhibit epithelial-to-mesenchymal changes, anchorage-independent growth, and upregulated RAS/MAPK s

201 ockdown inhibited cancer cell proliferation, anchorage-independent growth, and xenograft growth.

202 of cancer, loss of cell-to-cell adhesion and anchorage-independent growth, are both dependent on cell

203 tive-tissue growth factor (CTGF), as well as anchorage-independent growth, capacity to invade Matrige

204 each variant on NB cell adhesion, migration, anchorage-independent growth, co-precipitation with alph

205 ts in vitro and in vivo including changes to anchorage-independent growth, interaction with activated

206 like phenotype with increased proliferation, anchorage-independent growth, invasion, and migration.

207 cells, miR-22 decreased cell proliferation, anchorage-independent growth, invasiveness, and promoted

208 s treated with bisphosphonates inhibited the anchorage-independent growth, migration and invasion of

209 eads to markedly increased cell motility and anchorage-independent growth, reduced endocrine sensitiv

210 Hemizygous deletion promoted anchorage-independent growth, revealing that PKCbeta is

211 Overexpression of HOXD9 increases anchorage-independent growth, shortens population-doubli

212 tively inhibits melanoma cell proliferation, anchorage-independent growth, tumorigenesis, and tumor m

213 ic cell line U251 reduces their capacity for anchorage-independent growth, two-dimensional migration,

214 ivity and for suppressing cell migration and anchorage-independent growth.

215 well as for Ewing sarcoma proliferation and anchorage-independent growth.

216 ncer-like gene expression but do not exhibit anchorage-independent growth.

217 h Cat-1, the cells are again able to undergo anchorage-independent growth.

218 ogate its actions as a negative regulator of anchorage-independent growth.

219 cell proliferation, migration, invasion, and anchorage-independent growth.

220 ion forces, cell migration and invasion, and anchorage-independent growth.

221 r (CTGF) and Cyr61 target genes, and exhibit anchorage-independent growth.

222 7b overexpression on migration, invasion and anchorage-independent growth.

223 vPK also augments cellular proliferation and anchorage-independent growth.

224 ain prostate cancer migration, invasion, and anchorage-independent growth.

225 ed cell growth, clonogenicity, mobility, and anchorage-independent growth.

226 er proliferation, cell cycle progression and anchorage-independent growth.

227 cy, including cell migration, metastasis and anchorage-independent growth.

228 4C-E) resulted in a significant increase in anchorage-independent growth.

229 towards ULK1 and require ULK1 for sustained anchorage-independent growth.

230 ndrial function, cellular proliferation, and anchorage-independent growth.

231 with CK2alpha had enhanced proliferation and anchorage-independent growth.

232 lticellular spheroids that were generated by anchorage-independent growth.

233 ll death and reducing metabolic activity and anchorage-independent growth.

234 esults in preventing migration, invasion and anchorage-independent growth.

235 oncogenic MET-induced cell migration but not anchorage-independent growth.

236 and suppresses PDAC anchorage-dependent and anchorage-independent growth.

237 is associated with reduced proliferation and anchorage-independent growth.

238 ared with WT, especially under conditions of anchorage-independent growth.

239 t wild-type doubling times, cytokinesis, and anchorage-independent growth.

240 for optimal cancer cell proliferation in an anchorage-independent manner.

241 ntly impairs their capacity for growth in an anchorage-independent manner.

242 n subunits showed that spheroids formed from anchorage-independent melanoma cells expressed increased

243 Cnk1 inhibition decreased anchorage-independent mut-KRas cell growth more so than

244 Furthermore, dyskerin attenuation impaired anchorage-independent proliferation and tumor growth.

245 It also impacted clonogenic survival and anchorage-independent proliferation while also decreasin

246 f HNRNPA2B1 significantly reduced viability, anchorage-independent proliferation, and formation of xe

247 g small hairpin RNAs and measured viability, anchorage-independent proliferation, and growth of xenog

248 achment from monolayer culture and growth as anchorage-independent tumour spheroids was accompanied b

249 er of cell colonies capable of growing in an anchorage-independent way.

250 The balloons provide anchorage into the colonic wall for a bio-inspired inchw

251 When anchorage is disrupted, both the adaptor Protein 4.1B an

252 site preparation to guarantee apical implant anchorage is recommended.

253 ly diverse ways, such as for settlement, egg anchorage, mating, active or passive defence, etc.

254 lian spindle in space-time and dissect local anchorage mechanics and mechanism.

255 c resolution evidence for the extended lipid anchorage model for cytochrome c/cardiolipin binding.

256 e across the NE in processes such as nuclear anchorage, nuclear migration, and homologous chromosome

257 mber of adsorbed dye molecules per site (n), anchorage number (n'), receptor sites density (NM), adso

258 and hazel selectively destroy integrity and anchorage of columnar respiratory epithelial cells, but

259 tively and irreversibly damage integrity and anchorage of columnar respiratory epithelial cells.

260 Schwann cell lipid metabolism regulating the anchorage of juxtaparanodal Kv1-channels.

261 Conversely, increasing the accumulation and anchorage of mitochondria in the bud tip by overexpressi

262 t a role for mitochondrial fusion in bud-tip anchorage of mitochondria.

263 Proper localization and anchorage of nuclei within skeletal muscle is critical f

264 RCs, is required for the maintenance of the anchorage of RCs to the PM to withstand the increased me

265 local activation of integrin beta1 and focal anchorage of surface ectoderm cells to a shared point of

266 ol FA formation through YAP to stabilize the anchorage of the actin cytoskeleton to the cell membrane

267 f-reading, whereby only reactions supporting anchorage of the bacterium are maintained.

268 D, including its possible role in the direct anchorage of the cadherin-catenin complex to the actin c

269 tes these distal appendages and disrupts the anchorage of the centrosome to the apical membrane, resu

270 are scaffold proteins that play key roles in anchorage of the contractile ring at the cell equator du

271 and the divergent regulatory logics for the anchorage of the contractile ring through the anillin/Mi

272 generated by cell constriction and localized anchorage of the epithelium to the cuticle via the apica

273 le, achieved by dynein-driven transport, and anchorage of the mother centriole to the plasma membrane

274 erone-subunit complex and the cleft-mediated anchorage of the subunit C-terminus additionally assist

275 Here we show that anchorage of this axoglial complex to the axon cytoskele

276 uggests that ADAMTSL4 is required for stable anchorage of zonule fibers to the lens capsule.

277 Upon anchorage, pi-stacking interactions with the graphene sh

278 thy murine enthesis, and other extraskeletal anchorage points including the aortic root and the cilia

279 tendon, ligament, and joint capsule skeletal anchorage points that are termed entheses.

280 density and distribution of integrin/ligand anchorage points with the substrate.

281 te, independent of the previously identified anchorage protein Num1p.

282 e, causing isoform-specific silencing of the anchorage reporter p66(Shc) and blocking anoikis in vitr

283 Once in the plasma membrane, anchorage requires enzyme activity, which suggests co-sy

284 3 and ANC-1 to mediate nuclear migration and anchorage, respectively.

285 nduced damage to respiratory epithelial cell anchorage resulted in increased infection by the host-sp

286 red with physical interactions, the chemical anchorage results in a higher intrinsic work of adhesion

287 hanism, we found that TUFM serves as a novel anchorage site, recruiting Beclin-1 to mitochondria, pro

288 FAK), a key transmitter of growth factor and anchorage stimulation, is aberrantly overexpressed or ac

289 multiagency workgroup hosted a symposium in Anchorage that brought internationally-recognized expert

290 ere, we investigate the influence of motors' anchorage to a lipid bilayer on the collective transport

291 se and in heterogeneous phase by pi-stacking anchorage to graphene-based electrodes.

292 ding to alpha-SA favors a strong multivalent anchorage to JAM-A.

293 Anchorage to NPCs allows SUMO removal by the SENP SUMO p

294 chains was sufficient to bypass the need for anchorage to NPCs and the inhibitory effect of poly-SUMO

295 le cilia polarization requires intracellular anchorage to the cytoskeleton; however, the molecular ma

296 integrin-containing adhesions, which provide anchorage to the pancreatic extracellular matrix and are

297 activities: recruitment to endocytic sites, anchorage to the plasma membrane, Arp2/3 activation, and

298 ion by c-kit blocking mAbs and provided cell anchorage under physiological shear stresses.

299 th regard to skeletal muscle, DKO myonuclear anchorage was dramatically decreased compared with wild-

300 Using it as mechanically stable anchorage, we demonstrate the applications in single-mol