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1 c machinery necessary for the degradation of primary cilia.
2 n between BAV and genetic variation in human primary cilia.
3 s required for the formation and function of primary cilia.
4 ys an important role in protein transport in primary cilia.
5 esponse because of enhanced dysregulation of primary cilia.
6 s with which we detected glycylation in many primary cilia.
7 c cell types and can be motile or non-motile primary cilia.
8 hog (Hh) signaling in vertebrates depends on primary cilia.
9 rane-bound SHH, only to receiving cells with primary cilia.
10 d enrichment of the somatostatin receptor in primary cilia.
11 lex required for assembly and maintenance of primary cilia.
12 iotropic ciliopathy caused by dysfunction of primary cilia.
13 retrograde intraflagellar transport (IFT) in primary cilia.
14 ty of which encode proteins that localize to primary cilia.
15 que structural features that are not seen in primary cilia.
16 ses Hh signaling and increases the length of primary cilia.
17 n using independent approaches to manipulate primary cilia.
18 localization of SDCCAG3 to the basal body of primary cilia.
19 in UNx-mice and prevented the elongation of primary cilia.
20 ciliogenesis and in localization of cargo to primary cilia.
21 Finally, we also applied the sensor to primary cilia.
22 athway through facilitating the formation of primary cilia.
23 w concentrations of H2O2 treatment elongated primary cilia.
24 genetically encoded calcium indicator in all primary cilia.
25 h factor (PDGF)-AA/alphaalpha, are linked to primary cilia.
26 ccurs in neurons with and without detectable primary cilia.
27 ansduction, and it shares many features with primary cilia.
28 was found to regulate Hedgehog signaling in primary cilia.
29 a heteromeric polycystin channel complex on primary cilia.
30 ermining their maturation and trafficking to primary cilia.
31 iously unknown association between KIF11 and primary cilia.
32 and adult mice was performed to evaluate for primary cilia.
33 , polycystin-1 and polycystin-2, localize to primary cilia.
34 d hedgehog signaling, which is transduced by primary cilia.
35 otic spindle and templating the formation of primary cilia.
36 afficking of signaling molecules to and from primary cilia.
37 enerated mice specifically lacking beta-cell primary cilia, a cellular organelle that has been implic
38 or our understanding of protein transport in primary cilia, a critically affected process in many gen
39 mbly, increased cilia disassembly, shortened primary cilia, a retrograde IFT defect for IFT and BBS p
41 t the chemosensory function of cholangiocyte primary cilia acts as a mechanism for tumor suppression.
43 is associated with the aberrant formation of primary cilia, an organelle essential for canonical Hh s
45 re, we show that brown preadipocytes possess primary cilia and can respond to Hedgehog (Hh) signaling
46 in functional and structural maintenance of primary cilia and determined that the protein localized
47 nced accumulation of Smoothened (Smo) within primary cilia and elevated levels of full-length Gli3.
48 known link between KIF11 and the dynamics of primary cilia and further support non-mitotic functions
49 ghts into the effects of LiCl on chondrocyte primary cilia and Hedgehog signaling and shows for the f
50 load in ciliome genes, resulting in reduced primary cilia and HH pathway activation compared with na
52 lopment and highlight the current advance of primary cilia and IFT proteins in the pathogenesis of ca
56 enal disease have elongated and disorganized primary cilia and that this ciliary phenotype is specifi
57 rotein complexes direct both the assembly of primary cilia and the trafficking of signaling molecules
58 participate in the formation and function of primary cilia and usually result from disruption of retr
59 -traffic with Smoothened into the developing primary cilia and we identify EHD1 as a direct binding p
60 target of this signaling in tumors that lack primary cilia, and find that IFT20 mediates the ability
61 al transduction they dynamically localize in primary cilia, antenna-like solitary organelles present
74 in vitro and in vivo systems, we showed that primary cilia are important mediators of fluid flow to s
86 esults indicate that structurally integrated primary cilia are required for detection of electrical f
99 ilia generate fluid flow, whereas nonmotile (primary) cilia are required for sensory physiology and m
102 ed with plasma membrane protrusions, such as primary cilia, as well as extracellular vesicles derived
103 s, PI3K/mTOR hyperactivation interfered with primary cilia assembly (scenario also observed in other
106 te 3D structural model of typical epithelial primary cilia based on structural maps of full-length pr
107 ng is known about the role of glycylation in primary cilia because of limitations in detecting this m
108 showed that the use of the centriole to form primary cilia blocks centrosome formation and mitotic sp
110 s not at the level of upstream regulators or primary cilia, but rather at the level of Gli transcript
111 ing of IFT proteins at the base of mammalian primary cilia by optimizing single-particle tracking pho
115 H) binds to its receptor Patched1 (PTCH1) in primary cilia, causing its inactivation and delocalizati
116 such as cellular junctions, focal adhesions, primary cilia, caveolae, clathrin-coated pits, and plaqu
118 ransition (EMT) traits and by the absence of primary cilia compared to bile ducts and PBG cells in co
119 at the cell center, near the Golgi, forming primary cilia confined or submerged in a deep narrow pit
120 ew, we highlight central mechanisms by which primary cilia coordinate HH, G protein-coupled receptor,
121 nescent cell plasma membrane, which leads to primary cilia defects and a resultant failure to inhibit
123 d ventricle floor, apical profiles with only primary cilia define an additional uniciliated (E3) epit
124 peractivation promotes tumor progression via primary cilia degeneration and aberrant Hh signaling.
126 mber 3 A (Kif3a) to inhibit the formation of primary cilia did not affect hyperosmotic upregulation o
127 Our data demonstrate the architecture of primary cilia differs extensively from the commonly ackn
131 implications for human disorders related to primary cilia dysfunctions, such as ciliopathies and cer
132 vel GPR161 rare variants mislocalized to the primary cilia, dysregulated Shh and Wnt signaling and in
133 ced by a reduction of renal mass, results in primary cilia elongation, and this elongation is associa
136 We review these advances in our knowledge of primary cilia, focusing on brain development, and discus
137 e importance of the chemosensory function of primary cilia for the control of migration and invasion
138 l carcinoma (BCC), coinciding with increased primary cilia formation and activated hedgehog (Hh) sign
139 a pharmacological inhibitor of AURKA, causes primary cilia formation and cellular senescence by irrev
140 show that MaSC and MaTIC EMT programs induce primary cilia formation and Hedgehog (Hh) signaling, whi
141 ted the formation of BCC through suppressing primary cilia formation and Hh signaling, suggesting tha
143 nt upregulation is likely a prerequisite for primary cilia formation during Hh-dependent tumorigenesi
145 also found that AURKA is down-regulated and primary cilia formation is enhanced when cellular senesc
148 depletion of caveolin-1 expression promotes primary cilia formation through the proteasomal-dependen
149 nin and elevated AURKA expression, decreased primary cilia formation, and caused significant shorteni
150 ber 3A (Kif3a), a gene that is essential for primary cilia formation, at will in transplanted cells a
151 ed to the Golgi and its knockdown suppresses primary cilia formation, similar to pathogenic LRRK2.
156 Here, we demonstrate that disruption of primary cilia function following the selective loss of c
158 p of ciliopathies in which mutations disrupt primary cilia function, are characterized by axonal trac
160 rol patients, respectively, which identified primary cilia genes as associated with the BAV phenotype
161 e constituents, development, and function of primary cilia has advanced considerably in recent years,
162 (2+)-responsive mechanosensor hypothesis for primary cilia has been invoked to explain a large range
166 erstanding of the crosstalk between NRF2 and primary cilia/Hh signaling could not only open new avenu
170 l transduction proteins can also localize to primary cilia in a cell type-dependent manner; available
172 en described in developing heart, a role for primary cilia in adult heart has not been reported.
176 the current evidence for the localization of primary cilia in dental tissues and the impact of disrup
181 n human forebrain malformations, the role of primary cilia in forebrain morphogenesis has been little
183 ther, these results suggest a novel role for primary cilia in HBC activation, proliferation, and diff
192 that KIF11 localized to the basal bodies of primary cilia in multiple cell types, including neoplast
193 eracts with host proteins at the base of the primary cilia in neural progenitor cells, causing an aty
195 l dysplasias, implying the important role of primary cilia in skeletal development and homeostasis.
196 by Lang et al. (2020b) demonstrates loss of primary cilia in Spitzoid melanoma compared with Spitz n
197 d tongue agenesis, following the loss of the primary cilia in the CNC-derived palatal mesenchyme.
200 catenin in regulating AURKA and formation of primary cilia in the setting of VHL deficiency, opening
202 mulates on the cell surface in Drosophila or primary cilia in vertebrates, which is thought to be ess
203 man RPE1 cells, a classic model for studying primary cilia in vitro, with a genetic dissection of the
205 Kif3a, a gene essential for the formation of primary cilia, in a mouse model of SCLC induced by condi
206 of mechanically induced calcium increases in primary cilia, in tissues upon which this hypothesis has
208 lization of Hedgehog effectors to the tip of primary cilia is critical for proper signal transduction
210 nsport of membrane and cytosolic proteins in primary cilia is thought to depend on intraflagellar tra
212 y activating LKB1 and bypassing the need for primary cilia, it is possible to emulate this chemosenso
215 Akap12 expression while also ensuring normal primary cilia length and renal epithelial morphogenesis,
216 ibition is associated with a 97% increase in primary cilia length from 2.09 +/- 0.7 mum in untreated
218 his flow-induced process is dependent on the primary cilia located on the apical side of epithelial c
219 pha-tubulin and SOX9 proteins, the number of primary cilia(+) LPCs, and increased active gamma-glutam
220 cating intraflagellar transport processes in primary cilia may be more complicated than that reported
222 s during EFS, our findings also suggest that primary cilia may potentially function as a crucial calc
223 sults thus define a specific requirement for primary cilia-mediated GPCR signaling in interneuronal c
226 Together, these findings demonstrate that primary cilia not only orchestrate beta-cell-intrinsic a
227 ilia based on structural maps of full-length primary cilia obtained by serial section electron tomogr
232 rgeting of Ift88 with Wnt1-Cre, we show that primary cilia of neural crest cells (NCC), precursors of
234 8 has a highly conserved function within the primary cilia of the CNC-derived mesenchyme in the lip a
239 subtype 3 (Sstr3) is selectively targeted to primary cilia on neurons in the mammalian brain and is i
240 idence has shown that loss or malfunction of primary cilia or ciliary proteins in bone and cartilage
243 ns in proteins of the transition zone of the primary cilia or the closely associated distal end of ce
246 ital syndrome, altogether demonstrating that primary cilia play a critical role in regulation of both
247 ng a primary cilium and to determine whether primary cilia play a role in disease-related remodeling.
252 is confirmed an inverse relationship between primary cilia presence and Ras/MAPK activation, and prim
258 cilia presence and Ras/MAPK activation, and primary cilia removal in BCCs potentiated Ras/MAPK pathw
260 ons that affect the structure or function of primary cilia result in ciliopathies, a group of develop
261 ic disorder characterized by malfunctions in primary cilia resulting from mutations that disrupt the
263 f miR-219 function accelerates the growth of primary cilia, revealing a possible mechanistic link bet
265 cues that diminish Siah2-activity leading to primary cilia shortening and attenuation of the mitogeni
266 evidence indicates the important role of the primary cilia signaling pathway in bone elongation.
267 dulate axonal connectivity and that impaired primary cilia signaling underlies axonal tract defects i
268 n renal epithelia results in abnormally long primary cilia similar to that observed in Notch-signalin
269 erived stem cells (hASCs) by knocking down 2 primary cilia structural proteins, polycystin-1 and intr
271 n in centrosome number, spindle formation or primary cilia, suggesting that the major effect of BubR1
273 ation of basal stem cells uniquely possesses primary cilia that are aligned in an apical orientation
274 ining the biliary tree in the liver, express primary cilia that can detect several kinds of environme
275 ntage of cultured primary NP cells possessed primary cilia that changed length in response to osmotic
276 es with the C terminus of Ptch1 (Ptch1-C) in primary cilia to inhibit Ptch1-mediated cell death.
277 CDK10 in transducing signals received at the primary cilia to sustain embryonic and postnatal develop
278 ing Gli transcription factors, accumulate at primary cilia to transduce the Hh signal, but the mechan
279 ccurs through an indirect mechanism in which primary cilia trigger macrophage recruitment to the kidn
280 ins involved in the structure or function of primary cilia, ubiquitous antenna-like organelles essent
284 lacking both Tgifs, the number of cells with primary cilia was significantly decreased, and we observ
285 tic MT mechanisms and indeed, centrosome and primary cilia were altered and spindles were found to be
287 In addition, vesicles releasing from kidney primary cilia were observed in the structural maps, supp
289 The regulatory GTPase Arl13b localizes to primary cilia, where it regulates Sonic hedgehog (Shh) s
294 otherwise-forbidden actin polymerization in primary cilia, which excises cilia tips in a process we
295 cylation is essential for the homeostasis of primary cilia, which has important implications for huma
296 nipulations localized IGF1 receptor to their primary cilia, which maintained their signaling competen
297 equired for the assembly and function of the primary cilia, which mediate the activity of key develop
299 ic proteins in the 250-nm-wide shaft of live primary cilia with a spatiotemporal resolution of 2 ms a