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1 s a growth-suppressing factor, as well as an IGF-binding protein.
2 otein-3 (IGFBP-3) belongs to a family of six IGF binding proteins.
3 GF signalling by the increased expression of IGF-binding proteins.
4 by transmembrane receptors and modulated by IGF-binding proteins.
5 een insulin-like growth factor 1 (IGF-I) and IGF binding protein 1 (IGFBP-1) have recently been disco
6 calcium, zinc, and sodium] and serum IGF-I, IGF binding protein 1 (IGFBP-1), IGF binding protein 3 (
7 selected from IGF-1 (n = 9), IGF-2 (n = 1), IGF binding protein 1 (IGFBP1; n = 3), IGFBP3 (n = 3), a
8 trypsin, alpha-fetal protein, ceruloplasmin, IGF binding protein 1, transferrin, apolipoprotein(AI) [
9 [insulin-like growth factor 1], and IGFBP1 [IGF binding protein 1] and IGFBP3]), ILA, and mortality.
10 uble human IGF-I receptor, recombinant human IGF-binding protein 1, and sIGF-II/MPR with similar kine
12 or the immunoreactivities (ir) of the IGF-I, IGF binding protein-1 (IGFBP-1) and glycogen synthase ki
14 hat insulin-like growth factor-I (IGF-I) and IGF binding protein-1 (IGFBP-1) could be important deter
15 a), insulinlike growth factor-I (IGF-I), and IGF binding protein-1 (IGFBP-1) in 14 subjects with CF (
18 y that IGF-I is dependent on the presence of IGF binding protein-1 (IGFBP-1) to act as a wound healin
22 ns with time were statistically significant (IGF binding protein-1, P-heterogeneity = .0016; sIL6R, P
25 oncentrations of insulin-like growth factor (IGF) binding protein-1 (IGFBP1) are associated with insu
26 had higher serum insulin-like growth factor (IGF) binding protein-1 levels (21.0 +/- 8.9 ng/mL versus
27 G6Pase, and a third insulin-regulated gene, IGF-binding protein-1 (IGFBP1); suggests a high degree o
28 hat the hypoxia-inducible factor 1a (HIF-1a)-IGF binding protein 2 (IGFBP2) axis and the tumor-specif
33 we investigated the levels of GH, IGF-1 and IGF-binding protein 2 (IGFBP-2) after gastric sleeve sur
34 we identified angiopoietin-like proteins and IGF-binding protein 2 (IGFBP2) as new hormones that, tog
35 Addition of either angiopoietin-like 5 or IGF-binding protein 2 to the cultures led to a sizable e
37 IGF binding protein-3 levels, and increased IGF binding protein-2 levels, a pattern suggestive of di
38 was accompanied by a significant increase in IGF binding protein-2 levels, a slight reduction in IGF
39 sion was associated with increased levels of IGF-binding protein-2 (IGFBP-2) in the uterus and ovary,
40 , IGF-I is ultrafiltered in conjunction with IGF-binding protein-2 and is present in proximal tubular
43 150-kDa complex including the IGF molecule, IGF binding protein 3 (IGFBP-3), and the acid labile sub
44 erum IGF-I, IGF binding protein 1 (IGFBP-1), IGF binding protein 3 (IGFBP-3), and the IGF-I:IGFBP-3 m
45 F-I) concentrations, frequently adjusted for IGF binding protein 3 (IGFBP-3), have been associated wi
47 n assessment using Western blot analysis for IGF binding protein 3 (IGFBP3), IGF-1 receptor (IGF-1R),
48 iously diminished muscle levels of IGF-1 and IGF binding protein 3 both increased following PRT (P <
49 F-I) and the concentration ratio of IGF-I to IGF binding protein 3 were lower in the low-protein, low
50 ternary complex formed by the association of IGF binding protein 3-IGF complexes with a serum protein
52 bust increase of insulin-like growth factor (IGF) binding protein 3 expression in AR-deficient stroma
54 ix et al. demonstrate that downregulation of IGF-binding protein 3 (IGFBP-3) and -4, the negative reg
56 pproximately 13-fold (P < 0.001) increase in IGF-binding protein 3 (IGFBP-3) protein levels were also
57 like growth factor (IGF-I) content and IGF-I:IGF-binding protein 3 (IGFBP-3) ratio as risk factors fo
58 complexes with acid-labile subunit (ALS) and IGF-binding protein 3 (IGFBP-3) to maintain its circulat
60 een insulin-like growth factor 1 (IGF-1) and IGF-binding protein 3 (IGFBP3) so that the free form of
61 apamil decreases the expression of beta-cell IGF-binding protein 3 (IGFBP3), whereas IGFBP3 is increa
62 at verapamil reduces beta-cell expression of IGF-binding protein 3 (IGFBP3), whereas IGFBP3 was incre
63 ng IGF1 secretion through the suppression of IGF-binding protein 3 expression in prostatic stromal ce
64 1 signaling by ablating IGF-1 and increasing IGF-binding protein 3, increased vSMC apoptosis, and dec
65 to direct expression of rat IGF-I and human IGF binding protein-3 (IGFBP-3) to mammary tissue during
66 thors assessed the associations of IGF-1 and IGF binding protein-3 (IGFBP-3) with cardiovascular dise
67 However, des(1-3)IGF-I, which weakly binds IGF binding protein-3 (IGFBP-3), induced IGF-IR phosphor
68 S of measured serum protein levels of IGF-I, IGF binding protein-3 (IGFBP-3), pregnancy-associated pl
69 proteins insulin-like growth factor (IGF) 1, IGF binding protein-3 and acid-labile subunit, along wit
72 ding protein-2 levels, a slight reduction in IGF binding protein-3 levels, and an increase in levels
73 1% decrease at 1 and 2 wk, respectively) and IGF binding protein-3 levels, and increased IGF binding
76 evels of insulin-like growth factor (IGF)-1, IGF binding protein-3, growth hormone (GH), and somatost
77 rmone, insulin-like growth factor-I (IGF-1), IGF binding protein-3, insulin, cortisol, parathyroid ho
86 ed and validated insulin-like growth factor (IGF)-binding protein-3 (IGFBP3) as a novel miR-21 target
94 nation of the specificity and sensitivity of IGF-binding protein-3 as an index of nutrition or anabol
95 on into the study and was analyzed for serum IGF-binding protein-3 concentration (by radioimmunoassay
98 y should be considered when evaluating serum IGF-binding protein-3 concentrations as a marker of nutr
99 F-1 concentrations changed coordinately with IGF-binding protein-3 concentrations in females and male
100 s of the present study were to measure serum IGF-binding protein-3 concentrations in trauma patients
101 y must be considered when interpreting serum IGF-binding protein-3 concentrations in trauma patients.
103 der were not significant predictors of serum IGF-binding protein-3 concentrations when all patients w
106 cal illness, but there is little research on IGF-binding protein-3, which regulates the bioactivity o
110 had no effect on apolipoprotein D (ApoD) or IGF binding protein 5 (IGFBP5) expression, but E2/T and
111 n, muscle creatine kinase, beta-enolase, and IGF binding protein 5 and activated the myocyte enhancer
112 H (but not other myofibrillar proteins) and IGF binding protein 5, which may favor cell protein loss
113 parin binding to insulin-like growth factor (IGF)-binding protein 5 (IGFBP-5) leads to a 17-fold decr
116 ously shown that insulin-like growth factor (IGF) binding protein- 5 (IGFBP-5) is overexpressed in lu
118 Therefore, elucidation of the identity of IGF binding protein-5 (BP-5) protease produced by osteob
120 vel of upstream signaling molecules, such as IGF binding protein-5 (IGFBP-5), IGF-1 receptor (IGF-1R)
121 determine whether IGF-I action was altered, IGF binding protein-5, which is synthesized in response
122 Recent studies support the concept that IGF-binding protein-5 (IGFBP-5) stimulates bone formatio
123 sed in MK-PTEN mammary tissue, including the IGF-binding protein-5 (Igfbp5) gene, and others whose ex
126 e inhibitor metalloproteinase-2 (TIMP-2) and IGF-binding protein-7 (IGFBP7) have been validated for r
128 his IGF-II 'binding-hotspot', revealing that IGF-binding proteins and IGF2R have converged on the sam
129 and acromegaly on locally produced IGF1 and IGF binding proteins are uncertain and in need of furthe
130 BI-31772, which displaces IGF-I from all six IGF-binding proteins at low nanomolar concentrations fro
131 etween common genetic variation in the IGF1, IGF binding protein (BP) 1, and IGFBP3 genes with IGF-I
132 plasma levels of insulin-like growth factor (IGF) binding protein (BP)-2 or IGFBP-3 would predict can
133 on of insulin-like growth factor (IGF)-I and IGF-binding protein (BP) 3 with cancer and cardiovascula
134 fically cleaving insulin-like growth factor (IGF) binding proteins, causing increased IGF bioavailabi
136 s (A6-A11, A7-B7, and A20-B19) maintained by IGF-binding proteins; IGF-swap has alternative pairing (
137 uded demonstrating the effectiveness of IGF1/IGF binding protein (IGF1/IGFBP) complex dissociation us
138 levels of IGF-I with concomitant lowering of IGF binding protein (IGFBP)-3 are associated with increa
141 isoform of IGF-1 with decreased affinity for IGF binding proteins (IGFBP) due to a 3-amino acid delet
144 he expression of insulin-like growth factor (IGF)-binding protein (IGFBP)-1, a secreted protein that
146 kDa consisting of one molecule each of IGF, IGF-binding protein (IGFBP) 3, and an acid labile subuni
149 ) complexed with its natural binding protein IGF-binding protein (IGFBP)-3 (rhIGF-I/IGFBP-3) is a nov
150 muscle, while recent evidence suggests that IGF-binding protein (IGFBP)-3 acts as an insulin antagon
151 th and increases lymphocyte numbers and that IGF-binding protein (IGFBP)-3 has an opposing effect, in
152 In this study, the endogenous expression of IGF-binding protein (IGFBP)-3 was examined in human reti
154 tor I (IGF-I) knockout mice demonstrate that IGF-binding protein (IGFBP)-5, an important bone formati
155 e is still little information about IGFs and IGF-binding proteins (IGFBP) in cancers detected by the
156 questered into binary complexes with several IGF-binding proteins (IGFBP-2, IGFBP-3, and IGFBP-5).
157 reatment of cells with either alphaIR3 or an IGF-binding protein, IGFBP-3, led to a 75% inhibition of
159 ong induction of insulin-like growth factor (IGF)-binding protein IGFBP5, an antagonist of IGF signal
160 rowth, the specific contributions of the six IGF binding proteins (IGFBPs 1-6) to these processes are
161 els of insulin-like growth factor 1 (IGF-1), IGF binding proteins (IGFBPs) 1 and 3, insulin, osteocal
171 However, an unrelated class of proteins, the IGF-binding proteins (IGFBPs) also bind IGF-1 in the ser
172 on bone, and alterations in the IGFs and/or IGF-binding proteins (IGFBPs) could be responsible for t
174 le of insulin-like growth factor (IGF)-I and IGF-binding proteins (IGFBPs) in the regulation of vascu
175 between IGF-1/2, the IGF-1 receptor, and the IGF-binding proteins (IGFBPs) leads to elevated IGF-1 se
177 of insulin-like growth factor I (IGF-I) and IGF-binding proteins (IGFBPs) occur in children with end
178 metabolism yet control of their activity by IGF-binding proteins (IGFBPs) remains controversial.
180 mainly by the liver and circulates bound to IGF-binding proteins (IGFBPs), either as binary complexe
182 ce of insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs), which promoted or inhibit
186 of high affinity, specific binding proteins (IGF-binding proteins; IGFBPs) that are present in the in
190 59, 60, Ala31)hIGF-I] with high affinity to IGF-binding proteins (Ki = 0.3-3.9 nM) and no biological
191 Neither IGF-1 analogues with low affinity to IGF binding proteins nor proteinase inhibitors obliterat
192 nding protein 4 (IGFBP-4), the most abundant IGF-binding protein produced by rodent smooth muscle cel
193 IGF-I, rescued from structural ambiguity by IGF-binding proteins, reflects fine-tuning of signal tra
194 re medium (R0), and to avoid interference by IGF-binding proteins, secreted IGF peptides were isolate
195 ound mostly to a family of six high affinity IGF-binding proteins, which form stable complexes with I