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1  formed from two cell lineages, myogenic and fibroblastic.
2 ne serum, to cause the keratocytes to become fibroblastic.
3 re aggressive, less differentiated, and more fibroblastic.
4 mas included one secretory meningioma and 11 fibroblastic, 11 transitional, 14 meningothelial, and tw
5 minant isoform, was ectopically expressed in fibroblastic 3T3-L1 pre-adipocytes that normally lack th
6                                              Fibroblastic 3T3-L1 progenitor cells expressed very low
7 tified in our study, may explain some of the fibroblastic abnormalities previously observed in patien
8 tain all the bone-marrow colony-forming-unit fibroblastic activity and can be propagated as non-adher
9  been postulated that certain drugs increase fibroblastic activity through alterations in levels of v
10 a product, tenv could induce cytotoxicity to fibroblastic and B-lymphoid cells but not to T-lymphoid
11 o their release is the ablation of VCAM-1 by fibroblastic and by endothelial cells.
12  Similar behavior was observed not only with fibroblastic and epithelial cell lines but also explants
13                   During cell division, both fibroblastic and epithelial cells exhibit an increased l
14 siently transfected into human cell lines of fibroblastic and epithelial origins that differed in the
15            We showed that these cells become fibroblastic and scattered, with increased N-cadherin ex
16                                    Reticular fibroblastic and vascular stromal cells, important for s
17  in vitro, keratocytes proliferate, becoming fibroblastic, and lose biosynthesis of unique corneal ma
18 s cultured in 10% FBS proliferated, appeared fibroblastic, and synthesized only 9% of the total glyco
19                      The colony-forming unit-fibroblastic assay was used for MSC enumeration.
20               Nestin is expressed in several fibroblastic but not epithelioid cell lines.
21 te that primary cultures of keratocytes made fibroblastic by exposure to serum can return to their ke
22 d passage were transformed and designated as fibroblastic CECs (fCECs).
23 a signaling in the cancer-associated stromal fibroblastic cell compartment.
24 orneal stroma with the appropriate number of fibroblastic cell layers and Descemet's membrane of appr
25 teoblastic cell line (MC3T3-E1), and a mouse fibroblastic cell line (NIH3T3).
26 id progenitor cell line K562, and the murine fibroblastic cell line NIH 3T3.
27 8383, and peritoneal macrophages, but not in fibroblastic cell line NRK49F.
28 ism in the embryo itself, we derived primary fibroblastic cell lines from foetuses affected by NTDs a
29  of myosin VI at the Golgi complex, immortal fibroblastic cell lines of Snell's waltzer mice lacking
30 vated receptor (PPAR) gamma in non-precursor fibroblastic cell lines resulted in conversion to adipoc
31 but not in the endothelial, hemolymphoid, or fibroblastic cell lines tested.
32 arget, equine macrophages, permissive equine fibroblastic cell lines, and an engineered mouse cell li
33 d by Gi- but not Gs-linked receptors in many fibroblastic cell lines, we observed the opposite in PC1
34 n of TIMP-3 was associated with a scattered, fibroblastic cell morphology, as well as enhanced prolif
35 , PYK2 increases actin polymerization at the fibroblastic cell periphery.
36  stromal interleukin-1beta signaling between fibroblastic cell populations.
37 now show that for some melanoma, sarcoma, or fibroblastic cell types that survive without integrin-me
38          It remains unknown how myogenic and fibroblastic cell-cell interactions affect cell fate det
39 litate relevant studies of cancer-associated fibroblastic cell/cholangiocarcinoma cell interactions t
40 ine-rich peptide synthesized and secreted by fibroblastic cells after activation with transforming gr
41 ells from OC-activated livers yield Thy-1(+) fibroblastic cells and a population of E-cadherin(+) mes
42                            Adhesions between fibroblastic cells and extracellular matrix have been st
43 genic capacity to stimulate the migration of fibroblastic cells and promote their ability to secrete
44 n microtubule organization at centrosomes in fibroblastic cells and provide new insights into dynacti
45 totic effects of lipopolysaccharide (LPS) on fibroblastic cells and to investigate the role that the
46                                        Since fibroblastic cells are not targets of BCR-ABL-induced on
47   Expression of wild-type INO80 in patients' fibroblastic cells corrected their hypersensitivity to h
48 e mechanisms through which cancer-associated fibroblastic cells crosstalk with cholangiocarcinoma cel
49 eractive pathways by which cancer-associated fibroblastic cells crosstalk with cholangiocarcinoma cel
50 phosphatidic acid (LPA)-induced migration of fibroblastic cells derived from beta1-null mouse embryon
51                                              Fibroblastic cells derived from embryonic stem cells car
52 ollagenase (MMP-13; collagenase-3) gene from fibroblastic cells directly adjacent to macrophages with
53                                              Fibroblastic cells expressing mouse or human TIM-3 bound
54 , control DCs and IL-4-transduced T cells or fibroblastic cells failed to alter the course of the dis
55                                              Fibroblastic cells forced to express lefty by retroviral
56 ogenic progenitors form muscle cells whereas fibroblastic cells give rise to the supportive connectiv
57 duction of sustained transgene expression in fibroblastic cells in mice using a chimeric gene encodin
58 ooth muscle actin-positive cancer-associated fibroblastic cells in promoting intrahepatic cholangioca
59 ooth muscle actin-positive cancer-associated fibroblastic cells in the stroma of intrahepatic cholang
60 en found to transform both hematopoietic and fibroblastic cells in vitro, while inducing predominantl
61 y demonstrated that LPS induces apoptosis of fibroblastic cells in vivo, largely through TNF-alpha.
62                               Whereas stroma fibroblastic cells lost the PAF-R gene expression found
63 ts revealed low to absent staining of Fas in fibroblastic cells of fibroblast foci.
64 stitutive activation of TGFbeta signaling in fibroblastic cells of mice after birth caused a marked f
65 poptosis of resident non-bone marrow-derived fibroblastic cells of the corneal stroma is strongly cor
66 al neural crest (CNC) cells give rise to the fibroblastic cells of the tongue skeletal muscle in mice
67 lturing normal rat kidney epithelial and 3T3 fibroblastic cells on a collagen-coated polyacrylamide s
68                                 In contrast, fibroblastic cells or mammary tumor cells, which co-expr
69 xperiments in other neuron-like cells and in fibroblastic cells revealed that N-glycosylation of neur
70 n in the dermal layer of cell aggregates and fibroblastic cells surrounded by a pericellular matrix e
71 and associated stromal components, including fibroblastic cells that contribute to tumor growth and p
72 arge number of genes that favor apoptosis of fibroblastic cells that is dependent upon activation of
73                               Medium for the fibroblastic cells was replaced on day 4 with serum-free
74                                 Many stromal fibroblastic cells were also Gli2+.
75 astic prostate revealed that FGF7-expressing fibroblastic cells were present in higher numbers near t
76  we report that stimulation of epithelial or fibroblastic cells with G protein-coupled receptor agoni
77                        In contrast, in human fibroblastic cells with inactivated p53, the SOD1 RNAi i
78 ate that PDL cells are a mixed population of fibroblastic cells, capable of forming a mineralized mat
79                 In both epithelial cells and fibroblastic cells, EEA1 and a transfected apical endoso
80                          These cells include fibroblastic cells, endothelial cells, and cells of hema
81 en bacteria were cocultured with Detroit 532 fibroblastic cells, ExoS-producing 388 bacteria caused a
82                             In epithelial or fibroblastic cells, Gem or Rad expression resulted in st
83  fully functional brown fat program in naive fibroblastic cells, including skin fibroblasts from mous
84 esent in inflamed tissues and joints rich in fibroblastic cells, no significant data on fibrin(ogen)-
85                               In contrast to fibroblastic cells, T or B cells expressing TIM-3 formed
86 asement membrane into dissociated and motile fibroblastic cells.
87 type I collagen, together with proliferating fibroblastic cells.
88 , loss of contact inhibition, and multilayer fibroblastic cells.
89 ty of cell types, including osteoblastic and fibroblastic cells.
90  can be modulated by the adherence status of fibroblastic cells.
91 nt in regulating E2F-4 and E2F-5 activity in fibroblastic cells.
92  in 14 d, compared with 28 d for age-matched fibroblastic cells.
93  that zonal organization of osteoblastic and fibroblastic cellular phenotypes can be engineered by a
94                            We differentiated fibroblastic CFU-Fs (Fibro-CFU-Fs) from mixed CFU-Fs, ba
95 fraction of Nestin(+) cells, containing most fibroblastic CFUs, mesenspheres, and self-renewal capaci
96 val connective tissue were isolated that had fibroblastic characteristics.
97 (low) sub-population, which possesses higher fibroblastic colony-forming units (CFUs) and mesensphere
98                                        After fibroblastic commitment, the ability of MSCs to differen
99                        Heterotypic epithelio-fibroblastic contacts, like homotypic contacts between f
100 ation: human embryonic stem cells (hESCs), a fibroblastic differentiated derivative of the hESCs, and
101 e overload does not trigger significant EPDC fibroblastic differentiation.
102 se their keratocyte markers when they become fibroblastic during corneal wound healing.
103                              Taken together, fibroblastic epigenetic changes causative of DNA damage,
104                         ROCK is expressed in fibroblastic, epithelial, endothelial, and muscle cells
105                                              Fibroblastic expression of both uPA and uPAR were positi
106                Although patients with strong fibroblastic expression of uPA showed a tendency toward
107                                              Fibroblastic expression of uPAR was only related to the
108 P = 0.012; fibroblasts, P < 0.001), but only fibroblastic expression was related to the presence of i
109 to the hepatic mesenchyme where they exhibit fibroblastic features.
110 l pneumonia had a higher median profusion of fibroblastic foci (1.75 vs. 1.0, p = 0.003).
111 ance of four individual histologic features (fibroblastic foci [FF], interstitial mononuclear cell in
112 ated usual interstitial pneumonia have fewer fibroblastic foci and improved survival.
113  STAT3 was not present in alpha-SMA-positive fibroblastic foci but was observed in the nuclei of cell
114                               In IPF tissue, fibroblastic foci contained cells expressing Ki67 and th
115 lung specimens of IPF, myofibroblasts within fibroblastic foci demonstrated diminished PTEN expressio
116  decrease in the number of myofibroblasts at fibroblastic foci in animals treated with SD-208 but not
117                           IHC examination of fibroblastic foci in IPF lung tissue demonstrates the pr
118 eomycin-induced lung fibrosis in mice and in fibroblastic foci of human subjects with IPF, using phos
119 ning revealed increased IGF-II expression in fibroblastic foci of SSc lungs.
120                                The extent of fibroblastic foci present on lung biopsy predicts surviv
121  59.42; p = 0.002 for a one-unit increase in fibroblastic foci score).
122                                 Profusion of fibroblastic foci was the most discriminative feature fo
123 of granulation/connective tissue deposition (fibroblastic foci).
124                                   Near these fibroblastic foci, an abnormal adjacency of alveolar wal
125 ty is regionally decreased in IPF within the fibroblastic foci, and that within these areas PEDF was
126 ased attenuation very likely correspond with fibroblastic foci.
127  accumulation of fibroblasts in areas called fibroblastic foci.
128 ression are low in myofibroblasts within IPF fibroblastic foci.
129 is demonstrated absent Thy-1 staining within fibroblastic foci.
130 ent 0, mild 1, moderate 2, and marked 3) for fibroblastic foci.
131 , we hypothesized that they would have fewer fibroblastic foci.
132 al interstitial pneumonia is the presence of fibroblastic foci.
133 studies revealed that SHP2 was absent within fibroblastic foci.
134  CCN1 protein was predominantly localized to fibroblastic foci.
135 fibroblasts (FL-fibroblasts) in areas called fibroblastic foci.
136  presence of inactive FoxO3a in cells within fibroblastic foci.
137 th IPF expressed increased levels of pVHL in fibroblastic foci.
138 rly within the fibrotic interstitium and the fibroblastic focus, and prominently within the epitheliu
139 within the epithelium directly overlying the fibroblastic focus.
140 2 patients), telangiectatic (four patients), fibroblastic (four patients), small cell (one patient),
141             Changes in serum levels of basic fibroblastic growth factor (bFGF) were correlated with t
142 diocytes with interleukin-1 (IL-1) and basic fibroblastic growth factor (bFGF), with some induction a
143                                              Fibroblastic growth factor 23 (FGF23) is a circulating p
144                                              Fibroblastic growth factor 23 (FGF23) regulates renal ph
145 ing levels of the novel phosphaturic hormone fibroblastic growth factor 23 (FGF23).
146                                              Fibroblastic growth factor receptor 1 (FGFR1) signaling
147 gene expression in response to either PMA or fibroblastic growth factor-2 (FGF-2).
148 ells modestly enhanced that seen with acidic fibroblastic growth factor.
149 S) are part of a wide spectrum of disordered fibroblastic growth that display striking clinical and p
150 lates were morphologically heterogeneous and fibroblastic, had a normal-appearing actin cytoskeleton
151 urface mesenchymal epitopes, expressed broad fibroblastic hallmarks, and increasingly synthesized col
152 um-free medium appeared dendritic and became fibroblastic in appearance when exposed to medium contai
153 ted beta-catenin mutants are dispersed, more fibroblastic in morphology, and less efficient in formin
154 ally infect (invade) mouse cytokine-treated, fibroblastic L929 cells and macrophagelike RAW264.7 cell
155         Neuroblastoma-derived N2a-PK1 cells, fibroblastic LD9 cells, and CNS-derived CAD5 cells can b
156                              This promotes a fibroblastic-like morphology and expression of the mesen
157 ell line, MCF-7, altered its morphology to a fibroblastic-like phenotype, which exhibited protein mar
158 -1 and vimentin, indicating that they are of fibroblastic lineage and express a well-characterized ad
159  differentiation of mesenchymal cells into a fibroblastic lineage while repressing their transformati
160                                 While murine fibroblastic lines are comparable to human T-cell lines
161 dicted size of 37.8 kDa in neural, glial and fibroblastic lines by western blot analysis.
162 action and physiology, and downregulation of fibroblastic markers.
163  (a) alveolar collapse, (b) incorporation of fibroblastic material into alveolar walls, and (c) cigar
164 s in histogram measures of CP and CS between fibroblastic meningiomas and other subtypes were observe
165           The best model for differentiating fibroblastic meningiomas from other subtypes consisted o
166 xpression of adipocyte-specific genes, and a fibroblastic morphological appearance.
167  altered the shape of CECs from polygonal to fibroblastic morphologies in a time- and dose-dependent
168           We previously showed that CVC have fibroblastic morphology and express several osteoblastic
169 tumor progression, with the development of a fibroblastic morphology characteristic of metastatic cel
170 R inhibition resulted in a transition from a fibroblastic morphology to a more epithelial phenotype i
171 acteristics; i.e., change from epithelial to fibroblastic morphology, enhanced cell motility, decreas
172 1 in Madin-Darby canine kidney cells induced fibroblastic morphology, increased intercellular junctio
173 way, which induces EMT-like reprogramming to fibroblastic morphology, loss of cell polarity, contact
174 ed with changing cell shape into a flattened/fibroblastic morphology, suppression of E-cadherin expre
175 l motility; and (iv) converted epithelial to fibroblastic morphology.
176 ntrast, cells in 10% FBS developed a bipolar fibroblastic morphology.
177 in transfectants revealed a reversion from a fibroblastic, motile phenotype to a more stationary epit
178 A-null mice, suggesting that a uPA-dependent fibroblastic nAChRalpha1 pathway promotes renal fibrosis
179 the absence of RhoA and p160ROCK activity in fibroblastic NIH 3T3 cells and its presence in epithelia
180 ppeared dendritic on AM, even in 10% FBS but fibroblastic on plastic.
181 cells which may differentiate along either a fibroblastic or an osteoblastic pathway.
182 ocyte-specific genes to one that resembles a fibroblastic or chondroprogenitor-like pattern.
183  and most have used immortalized epithelial, fibroblastic, or hematopoietic cell lines that may not n
184 ggests that induced cells are most likely of fibroblastic origin.
185 ells of B-cell, endothelial, epithelial, and fibroblastic origin; however, in all cases, infection pr
186 emonstrate a lipogenic-to-myogenic switch in fibroblastic phenotype during fibrosis formation.
187 rsed the loss of differentiation markers and fibroblastic phenotype in Bcl-2-deficient chondrocytes.
188 the corneal endothelium, and they maintained fibroblastic phenotype on day 14.
189 ighly proliferative component demonstrated a fibroblastic phenotype that readily underwent myofibrobl
190 ls which expressed the transgene exhibited a fibroblastic phenotype, co-localized with sites of activ
191 ini branching, indicative of a more invasive fibroblastic phenotype.
192 cell attachment defects, and a more invasive fibroblastic phenotype.
193 e stroma of colon tumors and to cells with a fibroblastic phenotype.
194 patients do not display any TLR3-IFN-related fibroblastic phenotype.
195 of these cells to an epithelial, rather than fibroblastic, phenotype.
196                                              Fibroblastic preadipocyte cells are recruited to differe
197 al reorganization and cell shape change from fibroblastic preadipocytes to spherical adipocytes occur
198  differed depending on whether astrocytic or fibroblastic processes were present.
199 s cultured in fetal bovine serum also become fibroblastic, proliferate, and lose these markers.
200                                              Fibroblastic proliferation accompanies many angiogenesis
201 nd repair process associated with persistent fibroblastic proliferation.
202 adenocarcinoma, associated with a pronounced fibroblastic reactive stroma activation surrounding pros
203 ocytic) and, to a lesser degree, peripheral (fibroblastic) regions of normal, degenerative uncalcifie
204 osthetic mesh induces a chronic foreign-body fibroblastic response creating scar tissue that imparts
205        Surgical exploration revealed a dense fibroblastic response encompassing the polypropylene mes
206 trated that Prx-2 affected a number of fetal fibroblastic responses believed to be important in media
207                                  Loss of the fibroblastic reticular cell (FRC) network in lymphoid ti
208 eukin (IL)-7 that is 'posted' on the stromal fibroblastic reticular cell (FRC) network on which T cel
209   The underlying structural elements of LTs, fibroblastic reticular cell (FRC) network, not only form
210 ll access to the survival factor IL-7 on the fibroblastic reticular cell (FRC) network, resulting in
211 sly showed that lymphotoxin signaling in the fibroblastic reticular cell (FRC) stromal subset was req
212 nd intravital microscopy, we showed that the fibroblastic reticular cell network regulated naive T ce
213 tial association of dendritic cells with the fibroblastic reticular cell network within lymph nodes a
214 ce the distance between intersections in the fibroblastic reticular cell network, suggesting that at
215 h T cells largely move along conduits of the fibroblastic reticular cell network, they appear to exec
216 ll responses and pathological alterations of fibroblastic reticular cell networks in the draining lym
217 CAM-1 expression, and disrupted perivascular fibroblastic reticular cell organization, the re-establi
218                                 Mice lacking fibroblastic reticular cell PDPN or platelet CLEC-2 exhi
219 eatment altered stromal subset, particularly fibroblastic reticular cell, production of cytokines and
220  node paracortex is composed of a network of fibroblastic reticular cells (FRC) and reticular fibers
221 infection, we demonstrate viral targeting of fibroblastic reticular cells (FRC) in the lymphoid organ
222 eled into follicles via conduits secreted by fibroblastic reticular cells (FRC).
223 on conditioning caused a loss of T-cell zone fibroblastic reticular cells (FRCs) and CCL21 expression
224 t by podoplanin (PDPN) signalling in stromal fibroblastic reticular cells (FRCs) and its modulation b
225                                              Fibroblastic reticular cells (FRCs) and lymphatic endoth
226                                              Fibroblastic reticular cells (FRCs) are known to inhabit
227                                              Fibroblastic reticular cells (FRCs) are lymphoid stromal
228                              In lymph nodes, fibroblastic reticular cells (FRCs) form a collagen-base
229 that, as recently described for lymph nodes, fibroblastic reticular cells (FRCs) form a network in th
230                                              Fibroblastic reticular cells (FRCs) form the cellular sc
231                                              Fibroblastic reticular cells (FRCs) in the T cell zone o
232                                              Fibroblastic reticular cells (FRCs) showed enrichment fo
233 zones are organized in a rigid 3D network of fibroblastic reticular cells (FRCs) that are a rich cyto
234                              gp38(+) stromal fibroblastic reticular cells (FRCs) that express VEGF ar
235  Lymph node (LN) stromal cells, particularly fibroblastic reticular cells (FRCs), provide critical st
236                                              Fibroblastic reticular cells (FRCs), through their expre
237                               We report that fibroblastic reticular cells (FRCs), which reside in the
238  also includes the lymphatic vasculature and fibroblastic reticular cells (FRCs).
239 okine Ccl19-expressing host cells, including fibroblastic reticular cells and follicular dendritic ce
240 driven by the synergistic cross-talk between fibroblastic reticular cells and interstitial flow.
241 some transgenic IL-7-Cre mice, we found that fibroblastic reticular cells and LECs strongly up-regula
242                   Of the major LNSC subsets, fibroblastic reticular cells and lymphatic endothelial c
243 PN is expressed by lymphatic endothelial and fibroblastic reticular cells and promotes blood-lymph se
244 tissues, only follicular dendritic cells and fibroblastic reticular cells exhibited staining.
245 sion of adhesion molecules and chemokines by fibroblastic reticular cells most likely facilitates the
246     These stromal cells expressed markers of fibroblastic reticular cells of lymphoid organs and were
247                                              Fibroblastic reticular cells responded rapidly to DST by
248 s regulation occurs in the lymph node, where fibroblastic reticular cells support the maintenance of
249  a meshwork of collagen fibers ensheathed by fibroblastic reticular cells that connects the subcapsul
250                                              Fibroblastic reticular cells were flow-sorted at differe
251 dence suggests that the extensive network of fibroblastic reticular cells within the T cell areas hel
252 ht the varied immunoregulatory properties of fibroblastic reticular cells, we reviewed the most recen
253 analyses demonstrated that PDPN expressed on fibroblastic reticular cells, which surround HEVs, funct
254 (-) stromal cells, a profile associated with fibroblastic reticular cells.
255 ritic cells, follicular dendritic cells, and fibroblastic reticular cells.
256 , CXCL12, CCL5, CCL21 and IL-6 expression in fibroblastic reticular cells.
257 idered to be derived mainly from T-cell zone fibroblastic reticular cells.
258  of lymph node vasculature, expansion of the fibroblastic reticular network and maintenance of lympho
259  The induced defect in the remodeling of the fibroblastic reticular system results in the loss of nor
260 tribution and caused cells to adopt the more fibroblastic, RhoA mutant phenotype.
261 steoblastic ROS17/2.8 cells) or inactive (in fibroblastic ROS24/1 cells) using chromatin immunoprecip
262 ated that murine keratocytes also acquired a fibroblastic shape and lost keratocan expression after f
263  towards the more flattened and more spread, fibroblastic shape of wild type NIH3T3 cells.
264  acquisition correlated with transition to a fibroblastic spindle shape, assembly of actin stress fib
265 l proliferation at low doses and induced the fibroblastic spindle-shape and express alpha-sm actin at
266  included cell proliferation, adoption of a "fibroblastic" spindle-shaped morphology associated with
267                In summary, tumors form their fibroblastic stroma predominantly from precursors presen
268  basal or PTH-stimulated RANKL expression in fibroblastic stromal cell models.
269 een studied extensively, the contribution of fibroblastic stromal cells as portals of entry into the
270  requirement for RANKL gene transcription in fibroblastic stromal cells but may enhance responsivenes
271                          Activated meningeal fibroblastic stromal cells have the capacity to rapidly
272  we have uncovered a pathogenic function for fibroblastic stromal cells in alloimmune reactivity that
273 , and the role of Notch ligands expressed by fibroblastic stromal cells in alloimmunity.
274  to relapse are harbored in association with fibroblastic stromal cells in the bone marrow.
275  inactivation of Dll1 and Dll4 in subsets of fibroblastic stromal cells that were derived from chemok
276 ne (C-X-C motif) ligand 13 in epithelial and fibroblastic stromal cells that, in turn, is pivotal for
277                          Here, we used liver fibroblastic stromal cells to mimic the liver microenvir
278 ipheral T cells or Notch ligands on putative fibroblastic stromal cells, we show that Notch signaling
279 ptor activator of NFkappaB ligand (RANKL) by fibroblastic stromal cells, which some evidence suggests
280 nt interactions with Notch ligand-expressing fibroblastic stromal cells.
281 GF-overexpressing tumors exhibited extensive fibroblastic stromal content, a clinical feature called
282 two-branched differentiation pathway of five fibroblastic subtypes was predicted using SLICE.
283 ulation of tumour-stromal cross-talk through fibroblastic TGF-beta pathway may depend on fibroblast p
284                     To determine the role of fibroblastic TGF-beta pathway on breast cancer cells, we
285 ment of a novel, inducible, conditional, and fibroblastic TGF-beta type II receptor knockout (Tgfbr2(
286                     Consistent with elevated fibroblastic TGF-beta3, fmod(-/-) fibroblasts were signi
287  and cells were generally flattened and more fibroblastic than epithelial in morphology.
288 n in four (100%) telangiectatic, three (75%) fibroblastic, three (25%) chondroblastic, three (6%) con
289  complete occlusion of the airway lumen with fibroblastic tissue and collagen scar by day 28 after tr
290 nhibited obliteration of the airway lumen by fibroblastic tissue.
291 o a fibronectin matrix and conversion from a fibroblastic to a more epithelial-like phenotype.
292 in the transition of epithelial cells from a fibroblastic to a polarized structure and function by di
293  RNA gene knockdown in MCF-7 cells triggered fibroblastic transformation and cell invasion, resulting
294 lial cells, which may promote mesothelial to fibroblastic transition (MFT) in an NLRP3-dependent mann
295 e process of asbestos-induced mesothelial to fibroblastic transition and its amelioration in caspase-
296 suggest that asbestos induces mesothelial to fibroblastic transition in an inflammasome-dependent man
297 xperiments, we found that asbestos induces a fibroblastic transition of mesothelial cells with a gain
298  immunophenotyping, we studied a group of 59 fibroblastic tumors with variable protein expression pat
299 that dendritic cells can stimulate increased fibroblastic VEGF, suggesting the scenario that lymph no
300 cts when high TGF-beta3 levels disrupt early fibroblastic wound ingress.

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