ライフサイエンスコーパス: anchorage

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

2 orates only tissue contraction and localized anchorage.

3 over particle size, distribution and surface anchorage.

4 e hydrophobic patch responsible for membrane anchorage.

5 and complementation (DSC) and cleft-mediated 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 ater and nutrients from the soil, as well as anchorage and stability for the whole plant.

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

12 ns including nutrient and water uptake, soil anchorage, and symbiotic interactions.

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 Tip cell anchorage antagonizes forward-directed, TGF-beta-guided

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

24 ermore, S3I-1757, but not S3I-1756, inhibits anchorage-dependent and -independent growth, migration,

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

26 on caused a DLC1-dependent decrease in NSCLC anchorage-dependent and -independent proliferation.

27 the ability of CaP cells to form colonies in anchorage-dependent and anchorage-independent conditions

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

29 upport of this, PRLrYDmut expression reduced anchorage-dependent and anchorage-independent growth.

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

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

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

33 MUC4 promotes proliferation, anchorage-dependent and-independent growth of TNBC cells

34 Loss of p120 in anchorage-dependent breast cancer cell lines strongly pr

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

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

37 F1R) cross-talk) in non-transformed cells in anchorage-dependent conditions.

38 d by signals from cell-matrix interaction in anchorage-dependent conditions.

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

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

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

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

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

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

49 enable proliferation independently of matrix anchorage identified a cell adhesion molecule PVRL4 (pol

50 Finally, loss of nuclear anchorage in DKO mice coincided with a fibrotic response

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

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

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

54 The terminal bulb of the pedicle provided anchorage in soft sediment.

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 ure water and nutrient uptake and to provide anchorage in the soil.

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

59 s myogenic sarcoma cell migration, invasion, anchorage independence and invadopodia formation, and dy

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

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

62 cted cell viability, migratory potential and anchorage independence by attenuating oxidative injury.

63 ased cell viability, augmented migration and anchorage independence in a cell-type-specific manner.

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

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

66 homeostasis and growth during adaptation to anchorage independence.

67 PVRL4 promotes anchorage-independence by driving cell-to-cell attachmen

68 ditions and require HIF-1 for ERBB2-mediated anchorage-independence, three-dimensional culture growth

69 tive CCND1/CDK2 activity effectively confers anchorage independent growth by inhibiting p53 or replac

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 nhibition of sAPPalpha significantly reduced anchorage independent growth of the cancer cells.

73 biased determination of colony formation and anchorage independent growth over time.

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

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

76 ULK2 overexpression inhibited anchorage independent growth, inhibited astrocyte transf

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

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

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

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

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

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

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

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

85 Anchorage-independent cell growth and tumor formation in

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

87 D1 transcription, cell cycle transition, and anchorage-independent cell growth by up-regulating trans

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

89 Consistently, cell cycle transition and anchorage-independent cell growth were also attenuated i

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

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

92 tion of AKT2 impaired cell proliferation and anchorage-independent cell growth, and decreased the sec

93 pe characterized by increased proliferation, anchorage-independent cell growth, anoikis resistance an

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

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

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

97 ion promotes tumor progression by supporting anchorage-independent cell growth.

98 cellular proliferation, focus formation, and anchorage-independent cell growth.

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

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

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

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

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

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

105 r a PTK6-FAK-AKT signaling axis in promoting anchorage-independent cell survival.

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

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

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

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

110 ic expression of BRAF K578R mutant inhibited anchorage-independent colony formation of MCF7 breast ca

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

112 erference resulted in a dramatic decrease in anchorage-independent colony formation.

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

114 s suggest that 1) IGF1 induces signals under anchorage-independent conditions and that 2) R36E/R37E a

115 We studied if IGF1 can induce signaling in anchorage-independent conditions in transformed Chinese

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

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

118 However, under anchorage-independent conditions, WT IGF1 enhanced cell

119 to form colonies in anchorage-dependent and anchorage-independent conditions.

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

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

122 antly, Orai3 knockdown selectively decreased anchorage-independent growth (by approximately 58%) and

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

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

125 n a subset of these cell lines inhibits both anchorage-independent growth and cell invasion in a GAP-

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

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

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

129 n immortalized cells, although essential for anchorage-independent growth and evasion of apoptosis, d

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

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

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

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

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

135 bset of lung cancer cell lines reduces their anchorage-independent growth and significantly decreases

136 abrogated the ability of hypoxia to increase anchorage-independent growth and significantly reduced t

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

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

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

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

141 nally important in alveolar rhabdomyosarcoma anchorage-independent growth and tumor-cell proliferatio

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

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

144 tion of EGFR expression reduced HER2-induced anchorage-independent growth and tumorigenesis.

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

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

147 melanocytes and in melanoma cells increased anchorage-independent growth by providing GAB2-expressin

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

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

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

151 PC re-expression exerted profound effects in anchorage-independent growth conditions, however, includ

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

153 transcripts identified in this tumor induced anchorage-independent growth in 3T3 cells and tumor form

154 tivity in maintaining metabolic activity and anchorage-independent growth in breast cancer cells.

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

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

157 by growth factor-independent proliferation, anchorage-independent growth in soft agar, and enhanced

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

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

160 reased cell proliferation, colony formation, anchorage-independent growth in soft agar, cell migratio

161 functionally relevant; through induction of anchorage-independent growth in TGF-beta1-dependent norm

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

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

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

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

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

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

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

169 cancer cell stemness in a mammosphere assay, anchorage-independent growth in vitro, and lung cancer c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 depletion of srGAP3 promotes Rac dependent, anchorage-independent growth of partially transformed hu

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

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

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

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

190 This diminished both cell proliferation and anchorage-independent growth required for cancer progres

191 pha silencing in ras-transformed IEC reduced anchorage-independent growth, a criterion for malignant

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

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

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

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

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

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

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

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

200 orrelated with increased cell proliferation, anchorage-independent growth, and migration and invasion

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

202 duced apoptosis, inhibited proliferation and anchorage-independent growth, and rendered glioma cells

203 ogic transformation by H-RasV12 or K-RasV12, anchorage-independent growth, and survival of anoikis of

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

205 changes, an increase in cell proliferation, anchorage-independent growth, and tumor growth in vivo.

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

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

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

209 icted by Helios found ten conferred enhanced anchorage-independent growth, demonstrating Helios's exq

210 y and cellular transformation as assessed by anchorage-independent growth, focus formation, invasion,

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

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

213 gnant properties such as cell proliferation, anchorage-independent growth, migration, invasion, and a

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

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

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

217 ced migration and colony formation, impaired anchorage-independent growth, slower xenograft tumor gro

218 is, they exhibit much greater invasiveness, anchorage-independent growth, spheroid formation, and dr

219 malignant melanoma cell proliferation and/or anchorage-independent growth, suggesting key and non-ove

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

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

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

223 4C-E) resulted in a significant increase in anchorage-independent growth.

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

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

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

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

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

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

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

231 suppressed HCC cell migration, invasion, and anchorage-independent growth.

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

233 ploidy cells, and attenuation of cancer cell anchorage-independent growth.

234 T352A) attenuated the induction of PDAC cell anchorage-independent growth.

235 xpressed in TNBCs and 10 proved critical for anchorage-independent growth.

236 l lines reduced cell migration, invasion and anchorage-independent growth.

237 increased the proliferation rate and induced anchorage-independent growth.

238 t expression reduced anchorage-dependent and anchorage-independent growth.

239 of epithelial characteristics and decreased anchorage-independent growth.

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

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

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

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

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

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

246 7b overexpression on migration, invasion and anchorage-independent growth.

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

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

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

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

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

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

253 Under anchorage-independent overgrowth conditions, Oct1 associ

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

255 trast to KIT, activation of PDGFRA increased anchorage-independent proliferation and was required for

256 pha1-ACT inhibits cell-cycle progression and anchorage-independent proliferation of HCC cells.

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

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

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

260 sed in normal breast or ovary, PTK6 promotes anchorage-independent survival of breast and ovarian tum

261 n and invasion, as well as proliferation and anchorage-independent survival.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 Remarkably, anchorage of the embryoid colony from the 3D matrix to c

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

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

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

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

283 Anchorage of tissue cells to their physical environment

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

285 Three anchorage phases can be distinguished: (i) Bronze Age pr

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

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

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

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

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

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

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

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

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

295 le, before the start of septum formation and anchorage to the cell wall.

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

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 ge proto-harbours that correspond to natural anchorages, with minor human impacts; (ii) semi-artifici