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1 IGFBP-1 acts via beta1-integrin and focal-adhesion-kinas
2 IGFBP-1 can affect cellular functions independently of I
3 IGFBP-1 phosphorylation, which markedly increases its af
4 IGFBP-2 bound RPTPbeta, which led to its dimerization an
5 IGFBP-2 enhanced IGF-I-stimulated VSMC migration and pro
6 IGFBP-2 knockdown led to decreased PTEN tyrosine phospho
7 IGFBP-3 activation was significantly reduced following t
8 IGFBP-3 further inhibits TNF-alpha, CRP and high glucose
9 IGFBP-3 level remained positively associated with T2DM i
10 IGFBP-3 was positively associated with diabetes (OR(q5-q
11 IGFBP-3NB administration resulted in a significant decre
12 IGFBP-3NB partially restored VEGF-induced in vivo permea
13 IGFBP-5 is the most conserved IGFBP, and contains 18 cys
14 IGFBPs are composed of cysteine-rich amino- (N-) and car
15 1.16; 95% CI: 1.08-1.24; P(trend) < 0.001), IGFBP-2 (1.18; 1.06-1.31; P(trend) < 0.01) and IGFBP-3 (
17 nsulin-like growth factor binding protein 1 (IGFBP-1) are associated with insulin resistance and pred
18 nsulin-like growth factor binding protein 1 (IGFBP-1) is a potentially interesting marker for liver f
20 es (ir) of the IGF-I, IGF binding protein-1 (IGFBP-1) and glycogen synthase kinase 3beta (GSK3beta),
21 nsulin-like growth factor binding protein-1 (IGFBP-1) mRNA in the endothelium and decreased serum IGF
22 her insulin growth factor binding protein-1 (IGFBP-1) were associated with higher analgesic sensitivi
23 nsulin-like growth factor-binding protein-1 (IGFBP-1), which is expressed and released from central n
25 sma 25-hydroxyvitamin D (25(OH)D) and IGF-1, IGFBP-3 as well as C-peptide levels in 499 cases and 992
27 participants with high 25(OH)D and low IGF-1/IGFBP-3 ratio (reference group), participants with a hig
28 ipants with high 25(OH)D and low molar IGF-1/IGFBP-3 ratio and low C-peptide levels (reference group)
30 ants with a combination of either high IGF-1/IGFBP-3 ratio or high C-peptide were at elevated risk fo
31 rence group), participants with a high IGF-1/IGFBP-3 ratio were at elevated risk of colorectal cancer
32 I: 0.80, 1.57; Ptrend = 0.51), and the IGF-1:IGFBP-3 molar ratio (IRR = 0.94, 95% CI: 0.66, 1.34; Ptr
34 FBP-3: IRR = 1.85, 95% CI: 1.08, 3.16; IGF-1:IGFBP-3: IRR = 1.57, 95% CI: 0.85, 2.88) but not among w
35 s (Nix, PUMA) and tumor suppression (GDF-15, IGFBP-6), particularly in cells with high integrin expre
36 vels of GH, IGF-1 and IGF-binding protein 2 (IGFBP-2) after gastric sleeve surgery in healthy obese i
37 nsulin-like growth factor binding protein 2 (IGFBP-2) may protect against type 2 diabetes, but popula
38 insulinlike growth factor-binding protein 2 (IGFBP-2), nerve growth factor (b-NGF), platelet-derived
39 of insulin growth factor-binding protein-2 (IGFBP-2), which is secreted thereby promoting angiogenes
42 nsulin-like growth factor-binding protein 3 (IGFBP-3) might raise the risk of type 2 diabetes mellitu
43 nsulin-like growth factor binding protein 3 (IGFBP-3) signaling would produce neuronal changes in the
45 nsulin-like growth factor binding protein 3 (IGFBP-3), adiponectin, C-reactive protein (CRP), and int
46 nsulin-like growth factor binding protein 3 (IGFBP-3), testosterone, androstenedione, androstanediol
48 nsulin-like growth factor binding protein-3 (IGFBP-3) activation in retinal endothelial cells (REC) t
49 nsulin-like growth factor binding protein-3 (IGFBP-3) belongs to a family of six IGF binding proteins
51 sequently, IGF-1- and IGF-binding protein-3 (IGFBP-3) were analyzed using enzyme-linked immunosorbent
52 tein levels of IGF-I, IGF binding protein-3 (IGFBP-3), pregnancy-associated plasma protein A (PAPP-A2
54 nsulin-like growth factor binding protein-4 (IGFBP-4), a well documented inhibitor of the IGF-1/IGF-1
56 e interval (CI): 0.61, 1.27; Ptrend = 0.48), IGFBP-3 (IRR = 1.12, 95% CI: 0.80, 1.57; Ptrend = 0.51),
58 draw (IGF-1: IRR = 1.60, 95% CI: 0.86, 2.98; IGFBP-3: IRR = 1.85, 95% CI: 1.08, 3.16; IGF-1:IGFBP-3:
59 ere done after transfection with the S(156)A IGFBP-3 mutation (key phosphorylation site involved in D
64 equires functional cooperation with adjacent IGFBP and TSP1 domains to stimulate MMP-1 expression.
65 bition of tumor growth in vivo with adjuvant IGFBP-3-Fc with erlotinib versus erlotinib after treatme
68 result of lipotoxicity, and whether altered IGFBP-3 could affect pathways that are involved in hepat
70 such as low dose irradiation, may promote an IGFBP-4 release in bloodstream both in mice irradiated w
71 ic GH (12.32 vs. 50.97 pg/mL, p < 0.001) and IGFBP-2 levels (51.86 vs. 68.81 pg/mL, p < 0.001) were e
72 FBP-2 (1.18; 1.06-1.31; P(trend) < 0.01) and IGFBP-3 (1.27; 1.19-1.36; P(trend) < 0.001), but not IGF
73 compared with 1.7 (1.6, 2.0); P = 0.02], and IGFBP-3 by 6% (mean +/- SEM: 2420 +/- 29 compared with 2
74 ed that IGF-1 (odds ratio, 0.89; P=0.04) and IGFBP-3 (odds ratio, 0.09; P=0.03) are independent risk
75 t IGF-I and its binding proteins IGFBP-1 and IGFBP-2 have potentially beneficial effects on diabetes
77 ociations between plasma levels of IGF-1 and IGFBP-3 and laparoscopically confirmed endometriosis in
78 vestigated serum concentrations of IGF-1 and IGFBP-3 and their molar ratio in relation to T2DM incide
79 The initial screening showed that IGF-1 and IGFBP-3 are differentially expressed in CAV compared wit
81 ectional insulin, IGF-I, IGF-II, IGFBP-2 and IGFBP-3 in the Boyd Orr cohort (n = 182 men, 223 women).
82 t roles for circulating IGF-II, IGFBP-2, and IGFBP-3 in PSA-detected prostate cancer, in support of r
85 e report interactions between CSNK-2beta and IGFBP-1 as well as mTOR and CSNK-2beta, providing strong
87 erent effects on levels of STC2, PAPP-A, and IGFBP-4, thereby explaining the distinct metabolic effec
90 dy suggests that improved circulating GH and IGFBP-2 levels may mediate the beneficial effects of gas
92 r to extend beyond the regulation of IGF and IGFBP-4, as neither PAPP-A nor STC2 were discernibly aff
93 e associations of insulin, IGF-I, IGF-II and IGFBP-3 with physical performance in the UK-based Caerph
94 iated plasma protein A (PAPP-A2), IGF-II and IGFBP-5 in 838 children (3-18 years) from the Cincinnati
99 d ELISA analyses were done to verify PKA and IGFBP-3 knockdown, as well as to measure apoptotic marke
102 ol study to investigate circulating IGFs and IGFBPs in PSA-detected prostate cancer with regard to th
104 distinct growth factor signaling pathways as IGFBP-4 inhibited FGF-2- and IGF-1-stimulated angiogenes
105 ributed to loss of growth factor-attenuating IGFBPs, changes in local expression of contraction-promo
107 was fivefold lower among women with baseline IGFBP-2 levels in the top versus bottom quintile (odds r
108 d establishes a positive correlation between IGFBP-3 proteolysis and adiposity parameters as well as
109 lycemia to determine the interaction between IGFBP-3 and TNF-alpha, as data indicate that both protei
110 otential perinuclear co-localization between IGFBP-1 and CSNK-2beta and a nuclear co-localization bet
111 tion assay (PLA) indicated proximity between IGFBP-1 and CSNK-2beta as well as mTOR and CSNK-2beta bu
114 e the prospective association of circulating IGFBP-2 concentrations and of differential methylation i
119 d on bioinformatics analyses, the deduced Cq-IGFBP was shown to share high sequence homology with IGF
122 y on prostate cancer development, we crossed IGFBP-3KO mice with a c-Myc-driven model of CaP that dev
125 indicate that the three N-terminal domains (IGFBP, VWC, and TSP1), but not the C-terminal CT domain,
129 (95% CI: 1.00, 1.76; P for trend = 0.04) for IGFBP-3, and 0.77 (95% CI: 0.57, 1.03; P for trend = 0.0
132 g affinities for PHB2 are 9.0 +/- 1.0 nM for IGFBP-6 and 10.2 +/- 0.5 nM for mIGFBP-6, a non-IGF-bind
134 nship of measured serum levels with SHR (for IGFBP-3) and birth weight (for IGFBP-5) than with height
135 nt showed markedly amplified PLA signals for IGFBP-1 and CSNK-2beta (approximately 18-fold, P = 0.000
136 We synthesized a HBD peptide specific for IGFBP-2 and demonstrated in vitro that it rescued the mi
139 icient to regulate other FoxO1 target genes (IGFBP-1 and PEPCK) but not serpinB1 expression in mouse
140 s underlie the favorable association of high IGFBP-1 levels with insulin sensitivity and whether thes
141 he general study population, although higher IGFBP-3 levels might raise T2DM risk independent of IGF-
144 estational weeks 10-14, both IGF-I and IGF-I/IGFBP-3 were positively associated with GDM risk; adjust
146 ectiveness of IGF1/IGF binding protein (IGF1/IGFBP) complex dissociation using sodium dodecyl sulfate
147 iscovered that in addition to IGF1 and IGF2, IGFBP-3 binds bFGF, HGF, neuregulin, and PDGF AB with na
148 and cross-sectional insulin, IGF-I, IGF-II, IGFBP-2 and IGFBP-3 in the Boyd Orr cohort (n = 182 men,
149 ally important roles for circulating IGF-II, IGFBP-2, and IGFBP-3 in PSA-detected prostate cancer, in
153 that mice that are genetically deficient in IGFBP-3 exhibit weaker growth of primary prostate tumors
154 ontaneous prostate tumors did not develop in IGFBP-3KO mice, but splenic lymphomas occurred in 23% of
157 at hypoxia and rapamycin treatment increased IGFBP-1 phosphorylation at Ser98/Ser101/Ser119/Ser174 bu
158 to prevent REC apoptosis through increasing IGFBP-3 levels, which are reduced in response to hypergl
159 DNA-PK is required for Compound 49b-induced IGFBP-3 expression, leading to inhibition of REC cell de
161 TEF-1 expression and significantly inhibited IGFBP-1 transcription in endothelial cells in a dose-dep
167 a key role in this IGF-independent action of IGFBP-6 and suggest a possible therapeutic target for RM
171 hibition of PAPP-A and increased cleavage of IGFBP-4 in vitro, resulting in higher bioavailability of
172 tly (Ki = 68 pm) inhibits PAPP-A cleavage of IGFBP-4, and we show in a cell-based assay that STC1 eff
174 gest that the RGD integrin-binding domain of IGFBP-1 may be a promising candidate for therapeutic dev
177 in obese mice to investigate the effects of IGFBP-1 and its RGD domain on insulin sensitivity, insul
179 vity restored the anti-angiogenic effects of IGFBP-4 on VEGF-induced blood vessel growth in vivo.
180 P-3 in circulation and reduced expression of IGFBP-3 in macrophages in obesity may result in suppress
182 se findings provide a molecular framework of IGFBP-3's IGF-independent antiangiogenic antitumor activ
184 r localization and potential interactions of IGFBP-1, CSNK-2beta, and mTOR as a prerequisite for prot
185 hese findings suggest that reduced levels of IGFBP-3 in circulation and reduced expression of IGFBP-3
188 s not only establish a disulfide bond map of IGFBP-5 but also define a general approach that takes ad
194 ights into the transcriptional regulation of IGFBP-1 and contribute to our understanding of the role
195 novel mechanism for coordinate regulation of IGFBP-2 and IGF-I signaling functions that lead to stimu
197 notoxic stressors may promote the release of IGFBP-4 and the molecular pathways associated with the i
201 ate inhibits hepatic macrophage secretion of IGFBP-3, thereby releasing the brake and enhancing palmi
202 = 3), IGFBP3 (n = 3), acid-labile subunit of IGFBP (IGFALS; n = 2), IGF1 receptor (IGF1R; n = 4), and
203 ans may similarly result in the secretion of IGFBPs, with important ramifications for diseases associ
204 verall, these data suggest that, if IGF-1 or IGFBP-3 plays a role in the etiology of endometriosis, i
205 s, ternary complex formation with IGFBP-3 or IGFBP-5 and the auxillary protein, acid labile subunit,
210 Immunoprecipitation for total and phospho-IGFBP-3, cell proliferation and cell death measurements
211 measurement of fasting serum phosphorylated IGFBP-1 (fS-pIGFBP-1) helps to predict liver fat compare
212 g 4-week intermittent fasting (VPS8, POLRMT, IGFBP-5) and 1 week after 4-week intermittent fasting (P
213 insulin-like growth factor-binding protein (IGFBP) 1 mRNAs to be downregulated and upregulated, resp
214 insulin-like growth factor-binding protein (IGFBP) and von Willebrand factor type C (vWC) domains.
215 y the insulin growth factor binding protein (IGFBP) homolog ImpL2, an antagonist of insulin signaling
218 Insulin-like growth factor binding protein (IGFBP)-1 influences fetal growth by modifying insulin-li
220 Insulin-like growth factor binding protein (IGFBP)-3 regulates cell proliferation and apoptosis in e
222 insulin-like growth factor-binding protein (IGFBP)-4 and hence release within tissues of bioactive I
223 in-like growth factor (IGF)-binding protein (IGFBP)-6 decreases cancer cell proliferation and surviva
225 suggest that IGF-I and its binding proteins IGFBP-1 and IGFBP-2 have potentially beneficial effects
226 rmation about IGFs and IGF-binding proteins (IGFBP) in cancers detected by the prostate-specific anti
228 insulin-like growth factor-binding proteins (IGFBPs) comprise a conserved family of secreted molecule
229 that several secreted IGF-binding proteins (IGFBPs) exist in mammals, our work raises the possibilit
231 Insulin-like Growth Factor Binding Proteins (IGFBPs)" route in allergic asthma and the lectin pathway
234 l IGFBP-3 levels and increase in proteolyzed IGFBP-3 in circulation when compared to their normal cou
239 knockdown, small inhibitors and recombinant IGFBP-1, we demonstrate that schwannoma cells, in contra
242 cells, in contrast to Schwann cells, release IGFBP-1 that activates the Src/FAK pathway, via integrin
243 nd better the role of IGFBP-3 in the retina, IGFBP-3 knockout (KO) mice were evaluated for neuronal,
249 vitreal injection of an endothelial-specific IGFBP-3-expressing plasmid resulted in increased differe
250 These results show that RTEF-1-stimulated IGFBP-1 expression may be central to the mechanism by wh
257 l rendering of the PLA images validated that IGFBP-1 and CSNK-2beta interactions were in the perinucl
260 mical and physical stress, we identified the IGFBP-4 protein that can be considered a general stress
262 and oscillatory potential amplitudes in the IGFBP-3 KO mice, corresponding to increased apoptosis.
265 arization, whereas ectopic expression of the IGFBP-vWC variant exacerbated pathological angiogenesis.
266 us-mediated expression of either CCN1 or the IGFBP-vWC-TSP1 form reduced ischemia-induced neovascular
267 form containing completely or partially the IGFBP and vWC domains as a surrogate marker of CCN1 acti
269 nal tubular structure formation, whereas the IGFBP-vWC-TSP1 variant suppressed cell growth and angiog
273 ts anti-inflammatory functions and therefore IGFBP-3 may present itself as a therapeutic for obesity-
274 ident diabetes with baseline levels of three IGFBPs and free IGF-I, consistent with hypotheses that t
277 ith T2DM incidence-and the ratio of IGF-1 to IGFBP-3 was inversely related with T2DM incidence--in mo
278 hree-module forms comprising, in addition to IGFBP and vWC, the thrombospondin type 1 (TSP1) repeats
279 esistance of VEGF-stimulated angiogenesis to IGFBP-4 inhibition appears to depend on sustained activa
280 ) concentrations and molar ratio of IGF-I to IGFBP-3 increased, whereas IGFBP-2 decreased throughout
281 re of palmitate-treated THP-1 macrophages to IGFBP-3-deficient conditioned medium led to a 20-fold in
282 n obese adolescents show a decrease in total IGFBP-3 levels and increase in proteolyzed IGFBP-3 in ci
283 er, the IGFBP3 signal (associated with total IGFBP-3 and IGF-II levels) colocalizes with an associati
287 ore, we demonstrated that RTEF-1 upregulates IGFBP-1 through selective binding and promotion of trans
293 IGFBP3 gene region on chromosome 7p12.3 with IGFBP-3 concentrations using a significance threshold of
294 d to REC, they worked antagonistically, with IGFBP-3 inhibiting apoptosis and TNF-alpha promoting apo
295 001) and was also negatively associated with IGFBP-1 levels (OR(q5-q1) = 0.37 [0.18-0.73]; P trend =
296 s (e.g. rs11977526) that was associated with IGFBP-3 concentrations was also associated with the oppo
298 rast to this, ternary complex formation with IGFBP-3 or IGFBP-5 and the auxillary protein, acid labil
299 s shown to share high sequence homology with IGFBP family members from both invertebrates and vertebr
301 uncorrected P = 0.008); CTBP2-rs4962416 with IGFBP-3 (uncorrected P = 0.003); 11q13.2-rs12418451 with