コーパス検索結果 (left1)
通し番号をクリックするとPubMedの該当ページを表示します
1 SPARC (Secreted Protein Acidic and Rich in Cysteine), is
2 SPARC (secreted protein acidic rich in cysteine) is an a
3 SPARC and myocilin mRNA expression were dramatically inc
4 SPARC and myocilin protein expression paralleled changes
5 SPARC deficiency resulted in endoglin-mediated blockade
6 SPARC expression in human adipose tissue correlated with
7 SPARC expression is increased in ACC samples by 1.56 +/-
8 SPARC expression was correlated with leptin independent
9 SPARC in the stroma, but not in the tumor, was correlate
10 SPARC inhibited in vivo and adipocyte-induced homing, pr
11 SPARC interacted directly with endoglin and reduced endo
12 SPARC is a matricellular protein often associated with f
13 SPARC is a matricellular protein that is highly expresse
14 SPARC is a matricellular protein that is involved in bot
15 SPARC is a regulatory node for IOP.
16 SPARC is known to be upregulated in the tumor microenvir
17 SPARC is not synaptogenic, but specifically antagonizes
18 SPARC is secreted at high levels by pancreatic stellate
19 SPARC is thus a novel regulator of microglial proliferat
20 SPARC levels were positively correlated with GSIS in isl
21 SPARC may be a downstream regulatory node of TGF-beta2-m
22 SPARC null/CX3CR1-GFP reporter mice reveal that SPARC re
23 SPARC overexpression decreased STAT3 phosphorylation; co
24 SPARC overexpression increased the IOP of perfused human
25 SPARC overexpression increases IOP in perfused cadaveric
26 SPARC production peaks when innervation of the rat super
27 SPARC reduced carcinogen-induced inflammation and accumu
28 SPARC suppressed metabolic programming of both adipocyte
29 SPARC was expressed at measurable levels in human islets
30 SPARC was suppressed 31 +/- 13% (n = 5, P < 0.0001) by s
31 SPARC was upregulated by TGF-beta2 in the human TM cells
32 SPARC-deficient mice have been shown to exhibit impaired
33 SPARC-like 1 (SC1) is a member of the SPARC family of ma
34 SPARC-null mice demonstrate a lower IOP resulting from i
35 SPARC-null mice demonstrated a more uniform outflow patt
36 SPARC-null mice had a 23% decrease in IOP.
37 SPARC-null mice have a 15% to 20% decrease in intraocula
38 SPARC-null mice have lower intraocular pressure (IOP).
39 SPARC-null mice have lower IOPs than do their WT counter
40 SPARC-Related Modular Calcium Binding Protein-2 (Smoc-2)
41 SPARC/Osteonectin (SP/ON) is implicated in the regulatio
43 he hematopoietic system is normal, HSCs in a SPARC-deficient niche show an accelerated return to quie
46 in 6 (IL-6) and supplemented IL-6-abrogated, SPARC-mediated suppression of Notch signaling and expres
51 ecombinant leptin, insulin, and glucose, and SPARC mRNA and protein expression determined by Western
53 d two astrocyte-secreted proteins, hevin and SPARC, as regulators of excitatory synaptogenesis in vit
54 h regulation of relative levels of hevin and SPARC, astrocytes might control the formation, maturatio
55 tive models, ABSOLV, COSMOtherm, KOWWIN, and SPARC to calculate storage lipid-water partition coeffic
56 ese results identify hevin as a positive and SPARC as a negative regulator of synapse formation and s
59 ediating detachment, cultured SPARC(+/+) and SPARC(-/-) podocytes were subjected to mechanical strain
60 y revealed that thrombospondin-4 (THBS4) and SPARC-like protein 1 (SPARCL1) were enriched in serum fr
65 nce of SPARC, age-matched wild-type (WT) and SPARC-null mice underwent either transverse aortic const
67 he data supporting this relationship between SPARC and nab-paclitaxel remain largely correlative at t
75 pression in IPF fibroblasts was regulated by SPARC-mediated activation of Akt, leading to inhibition
81 ve Activity through Recombinase Competition (SPARC), a generalizable toolkit that can express any eff
83 ledge gap but highlight the need to consider SPARC protein expression in therapeutic development.
85 e had fewer excitatory synapses; conversely, SPARC-null mice had increased synaptic connections in th
86 stroke in the forelimb sensorimotor cortex, SPARC nulls demonstrate enhanced microgliosis in and aro
87 n primary prostate tumorigenesis, we crossed SPARC-null (SP(-/-)) with TRAMP (Transgenic Adenocarcino
88 for SPARC in mediating detachment, cultured SPARC(+/+) and SPARC(-/-) podocytes were subjected to me
89 ecreted protein acidic and rich in cysteine (SPARC) and collagen-I and induction of complement activa
91 creted protein, acidic and rich in cysteine (SPARC) family matricellular protein, during invasive pha
92 ecreted protein acidic and rich in cysteine (SPARC) has been implicated in multiple aspects of human
93 ecreted protein acidic and rich in cysteine (SPARC) in OvCa through multi-faceted roles inhibiting ca
94 ecreted protein acidic and rich in cysteine (SPARC) is a matricellular protein known to regulate extr
95 ecreted protein acidic and rich in cysteine (SPARC) is a matricellular protein that is important for
96 Secreted protein acidic rich in cysteine (SPARC) is a matricellular protein that modulates the act
97 ecreted protein acidic and rich in cysteine (SPARC) is up-regulated and expressed intracellularly in
98 ecreted protein acidic and rich in cysteine (SPARC) participates in the regulation of morphogenesis a
99 ecreted protein acidic and rich in cysteine (SPARC) plays a key role in post-synthetic procollagen pr
100 creted protein, acidic and rich in cysteine (SPARC) were among those substrates we biochemically conf
101 ecreted protein acidic and rich in cysteine (SPARC), a matricellular protein with counteradhesive pro
102 ecreted protein acidic and rich in cysteine (SPARC), a molecule produced by glial cells, is involved
103 ecreted Protein Acidic and Rich in Cysteine (SPARC), a protein involved in mammalian cardiac function
104 ecreted protein acidic and rich in cysteine (SPARC), although the data supporting this relationship b
106 creted Protein, Acidic and Rich in Cysteine (SPARC), originally discovered in bone as osteonectin, is
107 ecreted protein acidic and rich in cysteine (SPARC), which significantly stimulated the expression of
108 ecreted protein acidic and rich in cysteine (SPARC)-deficient mice exhibited decreased pericyte-assoc
109 reted Protein, Acidic, and Rich in Cysteine (SPARC)-null mice have a lower intraocular pressure.
113 dels revealed that tumor- and stroma-derived SPARC reduced tumor growth and metastasis through inhibi
115 our approach improves contrast because each SPARC-targeting molecule delivers a large number of nano
116 ibroblasts that is characterized by elevated SPARC, giving rise to activated beta-catenin, which regu
121 es for alkyl PAHs deviated increasingly from SPARC log K(OW) values with increasing degree of alkylat
124 oteoglycans - including fibulin, hemicentin, SPARC, agrin, and type XVIII collagen - are present in B
125 The matricellular SPARC family member hevin (SPARC-like 1/SPARCL-1/SC1/Mast9) contributes to neural d
129 nvasion of breast carcinoma cells identified SPARC, or secreted protein acidic and rich in cysteine.
130 4 integrin expression and signaling impacted SPARC expression and that SPARC facilitates beta4-mediat
135 ations form an intramolecular salt bridge in SPARC and are essential for the binding of SPARC to coll
138 e alpha-, beta-, and gamma-actin isoforms in SPARC knockout myoblasts reveals a changed expression pa
139 myocardial diastolic stiffness was lower in SPARC-null TAC mice (0.075+/-0.005) than in WT TAC mice
140 servations show that homozygous mutations in SPARC can give rise to severe bone fragility in humans.
142 Moreover, the preserved podocyte number in SPARC(-/-) mice correlates with reduced urinary levels o
143 ments suggest that aqueous turnover rates in SPARC-null mice are equal to if not greater than rates i
144 s ameliorated, and proteinuria is reduced in SPARC(-/-) mice as compared with SPARC(+/+) littermates.
145 ion of the SP1/NF-kappaB complex resulted in SPARC downregulation and leukemia growth inhibition.
146 IV, we identified two homozygous variants in SPARC (GenBank: NM_003118.3; c.497G>A [p.Arg166His] in i
147 containing human SPARC was used to increase SPARC expression in human TM endothelial cells and perfu
149 d that leptin and insulin potently increased SPARC production dose dependently in visceral adipose ti
150 ture amoeboid myeloid precursors only induce SPARC expression after they cease proliferation and migr
155 oss induced by very-low-calorie diet lowered SPARC expression by 33% and increased by 30% in adipose
160 FBI), interaction with the microenvironment (SPARC), retinoic acid signaling (RBP1), and the response
161 capable of processing and thereby modulating SPARC, a protein implicated in bone metastasis and infla
162 The selected mRNAs (IL-6, IL-8, myocilin, SPARC [secreted protein, acidic and rich in cysteine], m
165 olic function are affected by the absence of SPARC, age-matched wild-type (WT) and SPARC-null mice un
175 s segmental, and that transgenic deletion of SPARC causes a more uniform pattern that correlates with
177 herefore aimed to characterise the effect of SPARC on beta-cell function and features of diabetes.
178 partially decreased the promoting effect of SPARC on oxotremorine-M-stimulated insulin secretion.
181 gether, our data indicate that evaluation of SPARC expression has prognosticative value and SPARC is
183 -induced detachment, stable re-expression of SPARC restored detachment rates to levels comparable wit
184 ned therapy attenuates in vivo expression of SPARC, increases microvessel density, and enhances drug
185 F silencing also decreased the expression of SPARC, phospho-FAK and FAK and overexpression of SPARC a
186 -regulated DNMTs and increased expression of SPARC, which led to tumor growth suppression in bone in
187 hs post-instillation to assess the impact of SPARC on multiple stages in the development of fibrosis.
188 tion, an effect which appears independent of SPARC's modulation of obesity-induced insulin resistance
189 Our results highlight a complex influence of SPARC over the stromal and hematopoietic BM response in
191 umor tissues, the frequency and intensity of SPARC expression were inversely correlated with disease-
195 injury study to investigate whether lack of SPARC would compromise the ability to repair muscle.
198 tutively expressed increased basal levels of SPARC, plasminogen activator inhibitor-1 (PAI-1), and ac
199 wild-type littermates, we found that loss of SPARC accelerated the development of urothelial preneopl
201 in Drosophila and suggest that modulation of SPARC gene expression may ameliorate cardiac dysfunction
202 C, phospho-FAK and FAK and overexpression of SPARC abrogated the inhibitory effect of CTGF silencing
203 w that adenoviral-mediated overexpression of SPARC cDNA (Ad-DsRed-SP) elevated the expression of the
206 h signaling is suppressed in the presence of SPARC, as well as the Notch effector basic helix-loop-he
207 action increased secretion and processing of SPARC, as did co-cultures of bone marrow stromal cells w
211 ray data, confirmed the expected reversal of SPARC gene suppression after treating HT-29 cells with 5
213 is protective effect is not due to a role of SPARC in HSCs, but rather is due to its function in the
216 e a novel and functionally important role of SPARC in OvCa and not only bridge the knowledge gap but
217 of this study is to investigate the role of SPARC in OvCa interactions with omental adipocytes and i
220 of this study was to investigate the role of SPARC in the regulation of beta cell growth and survival
224 ving further support to the potential use of SPARC as a therapeutic candidate for medulloblastoma tre
225 ar fragment approaches (EPISuite's KOCWIN or SPARC), poly parameter linear free energy relationship (
228 se (ALPL), osteocalcin (BGLAP), osteonectin (SPARC) and osteopontin (SPP1) were detected in NU-CD271(
229 rotein, acidic, cysteine-rich (osteonectin) (SPARC) gene, which encodes a matricellular protein that
230 rophin, along with required binding partners SPARC/SPARCL1 and HSP90B, as key mediators of this chemo
232 es the stromal-derived matricellular protein SPARC as a novel regulator of islet survival and beta ce
234 e implication of the multifunctional protein SPARC (Secreted protein acidic and rich in cysteine)/ost
239 is study demonstrate that beta4 can regulate SPARC expression and that SPARC is an effector of beta4-
240 c microglia rapidly downregulate and release SPARC at the lesion, concomitant with reactive, hypertro
242 of secreted protein, acidic, cysteine rich (SPARC), myocilin, angiopoietin-like factor (ANGPTL)-7, a
243 Secreted protein, acidic, cysteine-rich (SPARC) is a glycoprotein that binds to collagen type I a
244 , FBLN1, FHL1, FN, NKTR, OGN, PARVA, S100A6, SPARC, STC1 and ZEB1 proteins showed specific and varied
246 of the secreted matricellular protein SMOC2 (SPARC related modular calcium binding 2) presenting seve
247 istinct contributions of tumoral and stromal SPARC to tumorigenesis and progression are unclear.
248 To determine the contribution of stromal SPARC, we evaluated subcutaneous tumor growth of TRAMP c
249 tor: nongerminal center B cell-like subtype, SPARC (secreted protein, acidic, and rich in cysteine) <
251 engineered to display a peptide that targets SPARC glycoprotein, which is overexpressed in various ca
254 -) mice and BM chimeras, we demonstrate that SPARC contributes to the development of significant stro
261 Therefore, we tested the hypothesis that SPARC in human adipose tissue is influenced by glucose m
265 We show using immunohistochemistry that SPARC is expressed by stromal cells within islets and ca
271 RC null/CX3CR1-GFP reporter mice reveal that SPARC regulates the distribution and branching of mature
277 Taken together, our results suggest that SPARC induces expression of neuronal markers in medullob
278 in bone in vivo These findings suggest that SPARC plays a key role in maintaining the dormancy of pr
280 in myopathies, which together suggests that SPARC might serve a specific role within muscle cells.
282 n levels and patterns are not altered in the SPARC null mouse, suggesting that SC1 does not compensat
283 collagen that was soluble was greater in the SPARC-null TAC mice (14+/-2%) than in WT TAC mice (1+/-2
284 collagen that was insoluble was less in the SPARC-null TAC mice (86+/-2%) than in WT TAC mice (99+/-
285 portance of addressing the complexity of the SPARC family and provides a new framework to explain the
289 Hevin is expressed in TM but, in contrast to SPARC, does not appear to be regulated by TGF-beta2.
296 e upregulated genes were SNAI2, FGFBP1, VIM, SPARC (osteonectin), and SERPINE1, while the downregulat
300 6-ring parent PAHs, and correlated well with SPARC octanol/water coefficients (K(OW)) (correlation co