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1                                              IGF-1 (insulin-like growth factor 1) expression was incr
2                                              IGF-1 (insulin-like growth factor-1) is markedly decreas
3                                              IGF-1 also induced expression of the redox regulator nuc
4                                              IGF-1 elevation led to the accumulation of FOXO3A in the
5                                              IGF-1 is thus a valid aid to antifibrotic treatment, wit
6                                              IGF-1 receptor (IGF1R) signaling promotes keratinocyte p
7                                              IGF-1 rhythms are disrupted in Cry-deficient mice, and I
8                                              IGF-1-mediated increases in myotube diameter (1.27 +/- 0
9                Insulin-like growth factor 1 (IGF-1) administration increases fetal cardiomyocyte prol
10 ng in enhanced insulin-like growth factor 1 (IGF-1) expression and activation of proliferative ERK1/2
11          Human insulin-like growth factor 1 (IGF-1) is a 70 amino acid protein hormone, with key impa
12                Insulin-like Growth Factor 1 (IGF-1) is associated with cardiovascular disease, itself
13                Insulin-like growth factor 1 (IGF-1) is known to have diverse effects on brain structu
14 nal actions of insulin-like growth factor 1 (IGF-1) produced by the liver have been well described, b
15 es insulin and insulin-like growth factor 1 (IGF-1) reset circadian clocks in vivo and in vitro by in
16 y, the insulin/insulin-like growth factor 1 (IGF-1) signaling pathway, mechanistic target of rapamyci
17 of the insulin/insulin-like growth factor 1 (IGF-1) signaling pathway.
18 nduced insulin/insulin-like growth factor 1 (IGF-1) signalling (IIS) via phosphatidyl inositol-3-kina
19  the impact of insulin-like growth factor 1 (IGF-1) treatment on CDKL5 null mice to restore the synap
20 could be rescued by insulin growth factor 1 (IGF-1), a drug that is currently in clinical trials for
21 via binding of insulin-like growth factor 1 (IGF-1), an insulin-like hormone that is involved in gluc
22 cose, insulin, insulin-like growth factor 1 (IGF-1), insulin-like growth factor binding protein 3 (IG
23 lished that an insulin-like growth factor 1 (IGF-1)-inducible mitochondrial UTP carrier (PNC1/SLC25A3
24 of insulin and insulin-like growth factor 1 (IGF-1).
25  expression of insulin-like growth factor 1 (IGF-1).
26 ver function tests, insulin growth factor-1 (IGF-1) and 25-hydroxy vitamin D (25- OH D).
27  also contains insulin-like growth factor-1 (IGF-1) and its associated binding proteins, although the
28 or-A (VEGF-A), insulin-like growth factor-1 (IGF-1) and Klotho, in the blood and brain of normal rats
29                Insulin-like growth factor-1 (IGF-1) and signal transducer and activator of transcript
30 ophage-derived insulin-like growth factor-1 (IGF-1) and tumor cell IGF-1 receptor (IGF-1R).
31  (TGFbeta) and insulin-like growth factor-1 (IGF-1) are known to promote fibrosis; however, myofibrob
32 ic infusion of insulin-like growth factor-1 (IGF-1) exerts anti-inflammatory and antioxidant effects
33 x hormones and insulin-like growth factor-1 (IGF-1) in animals.
34      Exogenous Insulin-Like Growth Factor-1 (IGF-1) is neuroprotective in animal models of brain inju
35 gh circulating insulin-like growth factor-1 (IGF-1) levels increase the risk of prostate cancer.
36  Activation of insulin-like growth factor-1 (IGF-1) receptor (IGF1R) signaling induces keratinocyte m
37 retreated with insulin-like growth factor-1 (IGF-1) showed resolution of the same amount of initial D
38  a link to the insulin-like growth factor-1 (IGF-1) signaling pathway.
39 ein (ERG), and insulin-like growth factor-1 (IGF-1) were measured simultaneously with sub-fg/mL LODs
40 stingly, (1-3) insulin-like growth factor-1 (IGF-1), a small peptide under clinical trial testing for
41 rin, and cargo insulin-like growth factor-1 (IGF-1), in thiolated gelatin (gelatin-SH)/ poly(ethylene
42 protein (ERG), insulin-like growth factor-1 (IGF-1), pigment epithelial-derived factor (PEDF), and se
43 e polypeptide, insulin-like growth factor-1 (IGF-1), which activates IGF-1 receptor prosurvival signa
44 unger participants (aged 50-60 y, n = 1400), IGF-1 was associated with lower odds of hearing impairme
45 lin and insulin-like growth factors 1 and 2 (IGF-1 and -2) activate insulin receptors (IR-A and -B) a
46 estradiol on insulin-growth factor-1 and -2 (IGF-1, -2) signaling and metabolic function in primary c
47                           In addition, (1-3) IGF-1 treatment corrected aberrant excitability and netw
48 ckdown of TRalpha1/alpha2 blocked the T(3) + IGF-1 reduction of BrdU uptake and dramatically reduced
49                       NH3 blocked the T(3) + IGF-1 reduction of BrdU uptake without altering the phos
50 mRNA expression of CD36 (-50%), CD14 (-43%), IGF-1 (-53%), and IL-6 (-40%) was reduced in CX3CR1-defi
51  the NMR structure of the less active Asp-58-IGF-1 variant.
52 ike growth factor-1 (IGF-1), which activates IGF-1 receptor prosurvival signaling and improves cardia
53  CRC models and the efficacy of MEDI-573, an IGF-1/2-neutralizing antibody.
54 , MCF-7 cells with acquired resistance to an IGF-1 receptor (IGF-1R) tyrosine kinase inhibitor exhibi
55 tions and progressively increasing IL-10 and IGF-1 concentrations.
56 els of hepatocyte growth factor, FGF-13, and IGF-1, but not FGF-2, were significantly higher by up to
57 ion, including PDGF-A, IGFBP-3, IGFBP-2, and IGF-1.
58 stosterone (-6.6%; 95% CI: -10.1, -2.8%) and IGF-1 (-5.6%; -8.2, -2.9%); and PFNA and IGF-1 (-3.8%; 9
59 cantly improved in dual delivery of ADSC and IGF-1 in Coa encapsulated in gelatin-SH/PEGDA IPN hydrog
60                       Further, both BDNF and IGF-1 expressions are decreased in MeCP2 T158A mice.
61 RNA level and protein expression of BDNF and IGF-1 in MeCP2 T158A mice.
62 ocyte-derived neurotrophic factors, BDNF and IGF-1, and the glutamate transporter, GLT-1 after ischem
63 ocyte-derived neurotrophic factors, BDNF and IGF-1, as well as the astrocytic glutamate transporter,
64 Here we report that IGF-1 level in blood and IGF-1 signaling demonstrates circadian rhythms.
65 bitors is associated with increased CD20 and IGF-1 transcript levels in tumors and IGF-1 expression i
66 oxorubicin (DXR) and growth factors (EGF and IGF-1).
67 to the intricate relationship between GH and IGF-1, the relative contribution of each hormone to the
68  Y333 in response to stromal signals HGF and IGF-1, respectively, and IGF-1 expression was regulated
69 006 and analyzed for PFAS, sex hormones, and IGF-1.
70                                  Insulin and IGF-1 actions in vascular smooth muscle cells (VSMC) are
71 omeostatic functions, we propose insulin and IGF-1 are primary signals of feeding time to cellular cl
72                                  Insulin and IGF-1 enhance muscle protein synthesis through their rec
73 hy, as corroborated by increased insulin and IGF-1 plasma concentrations in multiple system atrophy p
74                                  Insulin and IGF-1 receptor signaling is sufficient to determine esse
75 Previous studies have shown that insulin and IGF-1 signaling in the brain, especially the hypothalamu
76 leting IR decreases responses to insulin and IGF-1.
77 egree of homology, insulin receptor (IR) and IGF-1 receptor (IGF1R) mediate distinct cellular and phy
78 inactivated both insulin receptors (IRs) and IGF-1 receptors (IGF1Rs) in the hippocampus (Hippo-DKO)
79 al inhibition of PRMT1 impaired mERalpha and IGF-1 signaling.
80 hms are disrupted in Cry-deficient mice, and IGF-1 level is reduced by 80% in these mice, which leads
81  glucose, inhibit keratinocyte migration and IGF-1-induced chemotaxis in association with inhibition
82 and IGF-1 (-5.6%; -8.2, -2.9%); and PFNA and IGF-1 (-3.8%; 95% CI: -6.4, -1.2%).
83 e expression and downregulation of PPARG and IGF-1, respectively.
84  between ribosomal RNA (rRNA) production and IGF-1-mediated myotube hypertrophy in vitro Primary skel
85 mal signals HGF and IGF-1, respectively, and IGF-1 expression was regulated by the Sonic Hedgehog (Sh
86 y across quartiles for both testosterone and IGF-1 in relation to PFOS, and for IGF-1 and PFNA in gir
87  PFAS and estradiol, total testosterone, and IGF-1 in 2,292 children (6-9 years of age) from the C8 H
88 20 and IGF-1 transcript levels in tumors and IGF-1 expression in tumor-associated B cells.
89 produce a variety of growth factors, such as IGF-1, VEGF-alpha, TGF-beta, and Wnt proteins that regul
90  roles in receptor binding, but mutations at IGF-1 position 58 and IGF-2 position 57 affected the bin
91                    However, the link between IGF-1 and the occurrence of hearing impairment is untest
92 a exhibited a sustained release of bioactive IGF-1 over 3 weeks.
93  unique inhibitor, NT157, which targets both IGF-1 receptor (IGF-1R) and STAT3, we show that these pa
94  but not IRS-1-mediated activation of AKT by IGF-1.
95 e uptake by epithelial cells was enhanced by IGF-1 and led to decreased inflammatory responses by epi
96 myocyte physiological hypertrophy induced by IGF-1 (insulin-like growth factor 1).
97 way of fibrosis and opacity was inhibited by IGF-1, and further with SAHA in particular, and with hal
98 ions on extrahepatic tissues are mediated by IGF-1.
99       The effects of the FMD are reversed by IGF-1 treatment and recapitulated by PKA and mTOR inhibi
100 XCL2, STAT3, NUPR1, Jun, CSF1, CYR61, CEBPB, IGF-1, EGFR1, SPP1, and TGM2) within these important pat
101 -like growth factor-1 (IGF-1) and tumor cell IGF-1 receptor (IGF-1R).
102     In MCF-7 and ZR75.1 breast cancer cells, IGF-1 induces peroxisome proliferator-activated receptor
103 igate the impact of the elevated circulating IGF-1 on prostate cancer development in vivo.
104 r (GHR) results in reductions in circulating IGF-1 and hepatic steatosis, associated with systemic in
105 se model (HIT) to increase their circulating IGF-1 levels to investigate the impact of the elevated c
106                 However, whether circulating IGF-1 levels directly aggravate prostate cancer remains
107                          In the full cohort, IGF-1 was not associated with subsequent hearing impairm
108                It appears that ICR decreases IGF-1 and leptin and increases adiponectin in geneticall
109 -type HNPCs, RIT1 (-/-) HNPCs show deficient IGF-1-dependent Akt signaling and neuronal differentiati
110                               B-cell-derived IGF-1 is critical for resistance of melanomas to BRAF an
111 mediated by tumor-associated B cells-derived IGF-1.
112 r data support a role for macrophage-derived IGF-1 as a key neurotrophic and sensitizing factor in en
113 ally, we demonstrate that macrophage-derived IGF-1 promotes sprouting neurogenesis and nerve sensitiz
114 e data identify that dopamine neuron-derived IGF-1 acts as a regulator of dopamine neurons and regula
115 ditional deletion of dopamine neuron-derived IGF-1 in adult mice leads to decrease of dopamine conten
116 escribed, but the role of neuronally derived IGF-1 remains largely unexplored.
117 t exogenous DHEA significantly downregulated IGF-1 and its receptor in both HCFs and HKCs with HKCs s
118         Suppression of rRNA synthesis during IGF-1 treatment did not prevent early increases in AKT (
119 wth hormone (GH) and its downstream effector IGF-1 increase and play critical roles in bone acquisiti
120 ed ERK1/2 phosphorylation in response to EGF/IGF-1 stimulation, resulting in induction of the cell cy
121 d gestation (term = 147 d), receiving either IGF-1 LR3 or vehicle.
122                                     Elevated IGF-1/insulin-like growth factor-1 receptor (IGF-1R) aut
123 cell activity and is modulated by endogenous IGF-1/VEGF-A signaling.
124  activate PI3K in the presence of endogenous IGF-1.
125 We show that Rab7a siRNA inhibition enhances IGF-1 and HGF signalling in beta cells and increases exp
126 H and increasing concentrations of exogenous IGF-1 triggers synergistic IRS1 tyrosine phosphorylation
127 Coa-mediated delivery of chondrogenic factor IGF-1 with the aid of adipose-derived stem cells (ADSCs)
128 trating B cells to produce the growth factor IGF-1.
129  -13, and type 1 insulin-like growth factor (IGF-1), which enhance neuronal survival and functions, w
130 een mature human insulin-like growth factors IGF-1 and IGF-2 makes serological discrimination by immu
131  proliferation and heart mass, but how fetal IGF-1 treatment affects coronary growth and function is
132  was preserved on a per-gram basis following IGF-1 treatment, adenosine and nitric oxide contributed
133 rogenesis is significantly blunted following IGF-1 infusion in knockout (RIT1 (-/-) ) mice.
134 (95% CI: 0.57, 1.03; P for trend = 0.03) for IGF-1:IGFBP-3 ratio.
135 al (CI): 0.68, 1.23; P for trend = 0.31) for IGF-1, 1.33 (95% CI: 1.00, 1.76; P for trend = 0.04) for
136 ence--in models that included adjustment for IGF-1 concentrations (P for trend < 0.05).
137 erone and IGF-1 in relation to PFOS, and for IGF-1 and PFNA in girls.
138 d domains being proposed to be essential for IGF-1 mediated hypertrophy.
139  it does not appear to be a prerequisite for IGF-1-induced myotube hypertrophy in vitro.
140 omal biogenesis response is not required for IGF-1-mediated hypertrophy of human primary myotubes.
141 dies, molecular evidence suggests a role for IGF-1 in hearing function.
142                                          GH, IGF-1 and IGFBP-2 levels were evaluated by ELISA at base
143                                          GH, IGF-1, and IGFBP-2 were not correlated with insulin or l
144 his study, we investigated the levels of GH, IGF-1 and IGF-binding protein 2 (IGFBP-2) after gastric
145 wth hormone-insulin-like growth factor-1 (GH-IGF-1) axis.
146 in response to enhanced activation of the GH-IGF-1 axis.
147 males potentially by interacting with the GH/IGF-1 axis.
148 dehydroxamic acid (SAHA) or halofuginone +/- IGF-1.
149 s the AP2A1/2 pathway predominates at higher IGF-1 concentrations.
150 al treatment with rhIGF-1 (recombinant human IGF-1)/BP3 (binding peptide 3) improves lung growth and
151 ary function in advanced IPF; (2) identifies IGF-1's C1 promoter as mediating the increase in IGF-1 t
152                                 Importantly, IGF-1 supplementation or anti-IL-6 treatment rescued the
153 content (-16 +/- 2% vs. IGF-1; P < 0.001) in IGF-1-treated myotubes.
154  that mutagenesis and skin carcinogenesis in IGF-1-deficient geriatric skin may be caused by defects
155                       There was no change in IGF-1 level from before to after surgery.
156    Prolactin caused no significant change in IGF-1 levels and an increase in IGF-2 in HKCs correlatin
157 1's C1 promoter as mediating the increase in IGF-1 transcription by TGFbeta in pulmonary fibroblasts;
158 lated GTPase, RIT1, plays a critical role in IGF-1-dependent neurogenesis.
159 -mediated coronary vasodilation similarly in IGF-1-treated and Control fetuses, and the relationships
160 ting FFAs and adipokines/cytokines including IGF-1, VEGF, and MCP-1, along with decreased AR, Ki67, a
161 pathways but together with the DAF-2/insulin IGF-1 receptor (IIR) signaling pathway to promote germli
162 s known that growth factors such as insulin, IGF-1 and HGF support beta cell growth and survival, but
163              Tyramine stimulates the insulin-IGF-1 signalling (IIS) pathway and precludes the inducti
164 founds effects on lifespan of daf-2 (insulin/IGF-1 signalling), daf-12 (steroid hormone signalling),
165 abditis elegans and long-lived daf-2/insulin/IGF-1 and glp-1/Notch mutants throughout adulthood.
166 d insulin resistance (i.e. decreased insulin/IGF-1) have been reported in other neurodegenerative dis
167     In addition, in the hippocampus, insulin/IGF-1 signaling is important for spatial learning and me
168 mutations within the growth-hormone, insulin/IGF-1 or mTOR signalling pathways.
169 sing evidence also suggests impaired insulin/IGF-1 signalling in multiple system atrophy, as corrobor
170     In well-fed males, insulin-like (insulin/IGF-1 signaling [IIS]) and transforming growth factor be
171 oxia-inducible factor hif-1, and the insulin/IGF-1 pathway components daf-2, age-1, and daf-16 all al
172 ffects in regulating proteins in the insulin/IGF-1 signaling cascade in vivo in physiological states
173                                  The Insulin/IGF-1 signalling (IIS) pathway plays an essential role i
174                                  The insulin/IGF-1 signalling (IIS) pathway plays an important role i
175                                  The insulin/IGF-1 signalling pathway is a key regulator of metabolis
176                                Thus, insulin/IGF-1 signaling has common roles in the hippocampus and
177 ody organs that sense and respond to insulin/IGF-1, the adipose tissue has a central role in both the
178  spatial learning and memory whereas insulin/IGF-1 signaling in the central amygdala controls thermog
179                                Intriguingly, IGF-1 induced beta-catenin and PKM2 expression and enhan
180 The Flot-1 pathway is more responsive to low IGF-1 concentrations, whereas the AP2A1/2 pathway predom
181 between anthropometric z-scores and the mean IGF-1 and (25- OH D) values (p > 0.05).
182                                     The mean IGF-1 and (25- OH D) values were significantly correlate
183 els of growth hormone (GH) and its mediator, IGF-1, associate with hepatic lipid accumulation.
184 therapy inhibiting (anti-IL-6) or mimicking (IGF-1) the cardiac hMSC secretome can rescue arrhythmia
185                  Exogenous administration of IGF-1 rescued defective rpS6 phosphorylation, spine dens
186      We investigated serum concentrations of IGF-1 and IGFBP-3 and their molar ratio in relation to T
187                            Concentrations of IGF-1 were elevated in peritoneal fluid from women with
188 ular mechanism for the therapeutic effect of IGF-1.
189 a and PRC with siRNA reverses the effects of IGF-1 and disrupts mitochondrial morphology and membrane
190  atherogenesis, but the potential effects of IGF-1 on their function are unknown.
191                     Pro-epileptic effects of IGF-1 were mediated by Akt-mTOR signaling.
192 in neonatal mice with impaired expression of IGF-1 and IGFBP3.
193  macrophages exhibit increased expression of IGF-1 in an in vitro model of endometriosis-associated m
194 The physiological and clinical importance of IGF-1 prompted challenging chemical and biological trial
195  levels might raise T2DM risk independent of IGF-1 levels.
196 d overall insulin resistance, independent of IGF-1.
197      Experiments using several inhibitors of IGF-1 receptor signaling revealed that inhibiting the Ra
198       These findings expand our knowledge of IGF-1's role as a novel fibrotic-switch, bringing us one
199 owth factor alpha genes, and a high level of IGF-1 and osteopontin genes compared to mdx(5cv) control
200 observational evidence that higher levels of IGF-1 appeared to confer some protection against hearing
201 nal Study of Ageing provided serum levels of IGF-1 in 2008 and again in 2012.
202 Monocytes/macrophages express high levels of IGF-1 receptor (IGF1R) and play a pivotal role in athero
203          Immunoreactivity and mRNA levels of IGF-1, TGF-beta1, and beta3-adrenoceptor were increased
204 ociated with T2DM incidence-and the ratio of IGF-1 to IGFBP-3 was inversely related with T2DM inciden
205 d a statistically significantly reduction of IGF-1 in CRvs.AL by 50 to 70% in WT mice at several dail
206                           Down-regulation of IGF-1 upon Cry deficiency correlates with reduced Igf-1
207                               Restoration of IGF-1 improved overall insulin sensitivity and lipid pro
208 sting findings included a protective role of IGF-1 (insulin-like growth factor 1) in systolic blood p
209              Here, we considered the role of IGF-1 in development of epilepsy after brain injury, usi
210 enotype, thereby increasing the secretion of IGF-1 and CCL20, which promoted tumor progression and st
211    Lifespan extension via the suppression of IGF-1/insulin-like signaling (IIS) offers a possibility
212 w method for the total chemical synthesis of IGF-1 analogs, which entails the solid-phase synthesis o
213                                 Targeting of IGF-1 and PI3K(p85alpha) by miR-29b is required for indu
214 ple types of muscle atrophy via targeting of IGF-1 and PI3K(p85alpha), and that suppression of miR-29
215  Akt-mTOR and MAPK are downstream targets of IGF-1 signaling that are activated after brain injury.
216 ever, myofibroblast specific upregulation of IGF-1 in the initiation and progression of TGFbeta-induc
217 rent study (1) documents the upregulation of IGF-1 via TGFbeta in myofibroblasts and fibrotic lung ti
218  signaling with small-molecule inhibitors or IGF-1 withdrawal partially abrogates both the phosphoryl
219 cates to the plasma membrane upon insulin or IGF-1 treatment, for which the unique C-terminal domain
220 oles, we delete insulin receptor (SMIRKO) or IGF-1 receptor (SMIGF1RKO) in VSMC and in mice.
221 d increased anabolic intracellular pathways (IGF-1-mTOR-p70S6sk-1 axis; MyoD) in muscles of trained a
222 been ascribed to the IGF-1 and its receptor, IGF-1 receptor (IGF-1R), and subsequent activation of th
223                                 T(3) reduced IGF-1 stimulated proliferation by ~50% in 100 dGA and by
224 e increased fetal norepinephrine and reduced IGF-1 and insulin.
225 multiple system atrophy patients and reduced IGF-1 brain levels in a transgenic mouse model of multip
226 nt results showed that SCI bladders released IGF-1 and TGF-beta1 to stimulate elastin and collagen fo
227                       Subsequently, released IGF-1 from Coa could effectively induce chondrogenic dif
228                              Serum and renal IGF-1 and EPO were significantly increased in UPI/OIR co
229 , products of microbial metabolism, restores IGF-1 and bone mass to levels seen in nonantibiotic-trea
230  We discovered that dopamine neurons secrete IGF-1 from the cell bodies following depolarization, and
231 ventional mice, in contrast, decreases serum IGF-1 and inhibits bone formation.
232 mechanism by which microbiota increase serum IGF-1.
233 lin/insulin-like growth factor-1 signalling (IGF-1) and insulin resistance (i.e. decreased insulin/IG
234 or the development of exceptionally specific IGF-1 and IGF-2 monoclonal antibodies.
235  There is an urgent need for highly specific IGF-1 and IGF-2 antibodies, yet only a short sequence el
236 se model, Hi-Myc mice, with a liver-specific IGF-1 transgenic mouse model (HIT) to increase their cir
237 oth injury in mice with odontoblast-specific IGF-1 receptor ablation exhibited a reduced tertiary den
238 autonomous fashion to regulate GH-stimulated IGF-1 expression in the liver of neonatal mice, which pl
239                                Subsequently, IGF-1-induced beta-catenin and PKM2 complex translocated
240                       These findings support IGF-1 as a potential strategy to increase cardiac myocyt
241 , but not early, infarct size by suppressing IGF-1 degradation and, consequently, diminished cardiac
242                          These new synthetic IGF-1 analogs are unique examples of disulfide bonds' ri
243 eurons electroporated with a shRNA targeting IGF-1 receptor failed to migrate to the upper cortical l
244 ells electroporated with the shRNA targeting IGF-1 receptor were unable to form an axon and, therefor
245 cted by electroporation with shRNA targeting IGF-1 receptor.
246 ll bodies following depolarization, and that IGF-1 controls release of dopamine in the ventral midbra
247                             We conclude that IGF-1 signaling is essential for sustaining cancer cell
248                             We conclude that IGF-1-stimulated fetal myocardial growth is accompanied
249 nal precursor cells (HNPCs) demonstrate that IGF-1 stimulates a RIT1-dependent increase in Sox2 level
250                           We also found that IGF-1 - mediated increase in epileptic activity led to n
251                          Here, we found that IGF-1 treatment of MCF-7 cells induced rapid ERalpha met
252 ed to epilepsy, raising the possibility that IGF-1 may be epileptogenic.
253                              We propose that IGF-1 Glu-58 interacts with IGF-1R Arg-704 and belongs t
254                          Here we report that IGF-1 level in blood and IGF-1 signaling demonstrates ci
255                            Here we show that IGF-1 stimulates mitochondrial biogenesis in a range of
256         In neurons in culture we showed that IGF-1 receptor activation is important for growth cone a
257                      These data suggest that IGF-1 promotes DNA repair in irradiated parotid glands t
258                                          The IGF-1/IGF-2 positions 51/50 and 54/53 did not appear to
259 vate insulin receptors (IR-A and -B) and the IGF-1 receptor (IGF-1R) is crucial for understanding the
260  inhibition of SirT-1 activity decreased the IGF-1-mediated resolution of DSB.
261 nt of its analogs as molecular tools for the IGF-1 receptor (IGF1-R) studies and as new therapeutics.
262  to be a limiting step in muscle growth, the IGF-1 growth pathway remained functional despite the del
263 PK activation is selectively involved in the IGF-1 signaling, because another Ras protein, H-ras loca
264 rformance of our method by interrogating the IGF-1/AKT signaling pathway, showing that even rarely ob
265                            Cells lacking the IGF-1 receptor remain arrested as multipolar forming a h
266  of the insulin receptor (M-IR-/- mice), the IGF-1 receptor (M-IGF1R-/- mice), or both (MIGIRKO mice)
267 ation of the predefined epitopes, namely the IGF-1 and IGF-2 loops.
268 1 in alveolar fibroblasts or deletion of the IGF-1 receptor from ILC precursors interrupted ILC3 biog
269 the intracellular pathways downstream of the IGF-1 receptor that contribute to these diverse physiolo
270      Our findings suggest that targeting the IGF-1/FOXO3A/BIM signaling axis could be an attractive s
271                         We conclude that the IGF-1/ephrinB1 axis plays significant roles in the early
272 pertrophy has primarily been ascribed to the IGF-1 and its receptor, IGF-1 receptor (IGF-1R), and sub
273  to contribute to muscle hypertrophy via the IGF-1 growth pathway.
274                      In agreement with this, IGF-1 robustly induced BNIP3 accumulation in mitochondri
275 rst demonstration to our knowledge of tissue IGF-1 regulation through proteolytic degradation and sug
276 ecrease in sensitivity to IGF-1 alone and to IGF-1 supplemented with EGF (P < 0.001).
277 interacts with IGF-1R Arg-704 and belongs to IGF-1 site 1, a finding supported by the NMR structure o
278 the dynamic ribosomal biogenesis response to IGF-1, myotube diameter and protein accretion were susta
279 ty to increase glucose uptake in response to IGF-1.
280 on, and leads to a lack of responsiveness to IGF-1, cell cycle arrest and decreased viability of canc
281  P < 0.001) and a decrease in sensitivity to IGF-1 alone and to IGF-1 supplemented with EGF (P < 0.00
282 reted to reflect a heightened sensitivity to IGF-1 stimulation upon HFD feeding.
283  do not confirm an association between total IGF-1 concentrations and risk of T2DM in the general stu
284  inflammation in conjunction with transgenic IGF-1 overexpression to improve postnatal growth.
285 ich entails the solid-phase synthesis of two IGF-1 precursor chains that is followed by the Cu(I)-cat
286                    The connection of the two IGF-1 precursor chains by the triazole-containing moieti
287  IGF-1R and that PRMT1 became activated upon IGF-1 stimulation.
288 and serum and mRNA of liver and kidney VEGF, IGF-1, and erythropoietin (EPO) were determined.
289 0.001) and total RNA content (-16 +/- 2% vs. IGF-1; P < 0.001) in IGF-1-treated myotubes.
290 uced 45S pre-rRNA expression (-64 +/- 5% vs. IGF-1; P < 0.001) and total RNA content (-16 +/- 2% vs.
291 omarker of therapeutic dosing of AE, whereas IGF-1 is a key molecule coupled to gene expression of ot
292 ability, providing a novel mechanism whereby IGF-1 exerts antiatherogenic effects.
293              To determine mechanisms whereby IGF-1 reduces atherosclerosis and to explore the potenti
294 eased in normal preterm infants, but whether IGF-1 treatment can prevent BPD or PH is unknown.Objecti
295 mad3 to the nucleus, also when combined with IGF-1.
296                         Guided fibrosis with IGF-1 and antifibrotic substances might maintain corneal
297 s was increased after both AE and NMES, with IGF-1 being a signaling molecule that correlated with MC
298                            Pretreatment with IGF-1 increased SirT-1 protein levels and increased deac
299  Primary skeletal myotubes were treated with IGF-1 (50 ng/ml) with or without 0.5 microM CX-5461 (CX)
300 ackground, the keratocytes were treated with IGF-1, and suberoylanilidehydroxamic acid (SAHA) or halo

 
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