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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
10 ng in enhanced insulin-like growth factor 1 (IGF-1) expression and activation of proliferative ERK1/2
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
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
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
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
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
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
48 ckdown of TRalpha1/alpha2 blocked the T(3) + IGF-1 reduction of BrdU uptake and dramatically reduced
50 mRNA expression of CD36 (-50%), CD14 (-43%), IGF-1 (-53%), and IL-6 (-40%) was reduced in CX3CR1-defi
52 ike growth factor-1 (IGF-1), which activates IGF-1 receptor prosurvival signaling and improves cardia
54 , MCF-7 cells with acquired resistance to an IGF-1 receptor (IGF-1R) tyrosine kinase inhibitor exhibi
56 els of hepatocyte growth factor, FGF-13, and IGF-1, but not FGF-2, were significantly higher by up to
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
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,
65 bitors is associated with increased CD20 and IGF-1 transcript levels in tumors and IGF-1 expression i
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
71 omeostatic functions, we propose insulin and IGF-1 are primary signals of feeding time to cellular cl
73 hy, as corroborated by increased insulin and IGF-1 plasma concentrations in multiple system atrophy p
75 Previous studies have shown that insulin and IGF-1 signaling in the brain, especially the hypothalamu
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)
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
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
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
93 unique inhibitor, NT157, which targets both IGF-1 receptor (IGF-1R) and STAT3, we show that these pa
95 e uptake by epithelial cells was enhanced by IGF-1 and led to decreased inflammatory responses by epi
97 way of fibrosis and opacity was inhibited by IGF-1, and further with SAHA in particular, and with hal
100 XCL2, STAT3, NUPR1, Jun, CSF1, CYR61, CEBPB, IGF-1, EGFR1, SPP1, and TGM2) within these important pat
102 In MCF-7 and ZR75.1 breast cancer cells, IGF-1 induces peroxisome proliferator-activated receptor
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
109 -type HNPCs, RIT1 (-/-) HNPCs show deficient IGF-1-dependent Akt signaling and neuronal differentiati
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
117 t exogenous DHEA significantly downregulated IGF-1 and its receptor in both HCFs and HKCs with HKCs s
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
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)
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
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
140 omal biogenesis response is not required for IGF-1-mediated hypertrophy of human primary myotubes.
144 his study, we investigated the levels of GH, IGF-1 and IGF-binding protein 2 (IGFBP-2) after gastric
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
154 that mutagenesis and skin carcinogenesis in IGF-1-deficient geriatric skin may be caused by defects
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;
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
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
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
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
180 The Flot-1 pathway is more responsive to low IGF-1 concentrations, whereas the AP2A1/2 pathway predom
184 therapy inhibiting (anti-IL-6) or mimicking (IGF-1) the cardiac hMSC secretome can rescue arrhythmia
186 We investigated serum concentrations of IGF-1 and IGFBP-3 and their molar ratio in relation to T
189 a and PRC with siRNA reverses the effects of IGF-1 and disrupts mitochondrial morphology and membrane
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
197 Experiments using several inhibitors of IGF-1 receptor signaling revealed that inhibiting the Ra
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
202 Monocytes/macrophages express high levels of IGF-1 receptor (IGF1R) and play a pivotal role in athero
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
208 sting findings included a protective role of IGF-1 (insulin-like growth factor 1) in systolic blood p
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
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
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
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
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
233 lin/insulin-like growth factor-1 signalling (IGF-1) and insulin resistance (i.e. decreased insulin/IG
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
241 , but not early, infarct size by suppressing IGF-1 degradation and, consequently, diminished cardiac
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
246 ll bodies following depolarization, and that IGF-1 controls release of dopamine in the ventral midbra
249 nal precursor cells (HNPCs) demonstrate that IGF-1 stimulates a RIT1-dependent increase in Sox2 level
259 vate insulin receptors (IR-A and -B) and the IGF-1 receptor (IGF-1R) is crucial for understanding the
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
266 of the insulin receptor (M-IR-/- mice), the IGF-1 receptor (M-IGF1R-/- mice), or both (MIGIRKO mice)
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
272 pertrophy has primarily been ascribed to the IGF-1 and its receptor, IGF-1 receptor (IGF-1R), and sub
275 rst demonstration to our knowledge of tissue IGF-1 regulation through proteolytic degradation and sug
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
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
283 do not confirm an association between total IGF-1 concentrations and risk of T2DM in the general stu
285 ich entails the solid-phase synthesis of two IGF-1 precursor chains that is followed by the Cu(I)-cat
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
294 eased in normal preterm infants, but whether IGF-1 treatment can prevent BPD or PH is unknown.Objecti
297 s was increased after both AE and NMES, with IGF-1 being a signaling molecule that correlated with MC
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