| 26568417 | We also demonstrate that oxidative stress promoted the expression of Btg2, and that FGF2 and IGF1 which are survival signals for embryonic limb mesenchyme inhibited Btg2 expression |
| 26467393 | In conclusion, we demonstrated that high extracellular concentration of phosphate induced senescence in cultured smooth muscle through the activation of IGF-1 receptor and ILK overexpression and provided solid evidences for the in vivo relevance of these results since aged animals showed high levels of serum phosphate linked to increased expression of ILK and senescence genes |
| 26448623 | Accelerated Telomere Shortening in Acromegaly; IGF-I Induces Telomere Shortening and Cellular Senescence |
| 26448623 | The effect of GH and IGF-I on telomere length and cellular senescence was examined in human skin fibroblasts |
| 26448623 | In vitro analysis revealed that not GH but IGF-I induced telomere shortening in human skin fibroblasts |
| 26448623 | CONCLUSION: Shortened telomeres in acromegaly and cellular senescence induced by IGF-I can explain, in part, the underlying mechanisms by which acromegaly exhibits an increased morbidity and mortality in association with the excess secretion of IGF-I |
| 26372907 | The similar abundance of WAT senescent cells in GHA and control mice suggests that any protection against generation of senescent cells afforded by decreased GH action, low insulin-like growth factor 1 and/or improved insulin sensitivity in the GHA mice may be offset by their severe adiposity, since obesity is known to increase senescence |
| 26033200 | Such events are controls by a family of small, non-coding RNAs (miRNAs) that interact with component of cellular senescence pathway; mitochondrial biogenesis/removal, DNA damage response machinery and IGF-1 signaling pathway |
| 25989853 | Functionally, impaired actin dynamics resulted in reduced NO secretion and reduced release of TNFalpha and IL-6 from LPS-stimulated microglia and of IGF-1 from IL-4 stimulated microglia |
| 25343365 | 3) with values for two anabolic hormones (serum dehydroepiandrosterone sulfate [DHEAS] and insulin growth factor [IGF]-1), four catabolic hormones (cortisol, epinephrine, norepinephrine, and interleukin-6 [IL-6]), and LTL were examined |
| 25274775 | Finally, the accelerated cellular senescence was also observed at the organismal level as shown by down-regulation of insulin-like growth factor 1 (IGF-1), a hallmark of premature ageing |
| 25148910 | Exercise training enhanced SIRT1 longevity signaling replaces the IGF1 survival pathway to attenuate aging-induced rat heart apoptosis |
| 25148910 | In our previous studies, rats with obesity, high blood pressure, and diabetes exhibiting slowed myocardial performance and induced cell apoptosis were reversed via sports training through IGF1 survival signaling compensation |
| 25148910 | As rats age, this pathway loses its original function, even with increasing upstream IGF1 |
| 25148910 | Moreover, exercise training enhanced the SIRT longevity pathway compensation instead of IGF1 survival signaling to improve cardiomyocyte survival |
| 25070626 | In this study, we demonstrate that IGF-1 exerts a dual function in promoting cell proliferation as well as cellular senescence |
| 25070626 | While acute IGF-1 exposure promotes cell proliferation and is opposed by p53, prolonged IGF-1 treatment induces premature cellular senescence in a p53-dependent manner |
| 25070626 | We show that prolonged IGF-1 treatment inhibits SIRT1 deacetylase activity, resulting in increased p53 acetylation as well as p53 stabilization and activation, thus leading to premature cellular senescence |
| 24937130 | We demonstrate that ATM plays an important role in insulin-like growth factor 1 (IGF-1) expression, that in turn, regulates downstream sCLU induction during senescence |
| 24937130 | In contrast, administration of an IGF-1 inhibitor caused apoptosis of senescent cells |
| 24937130 | Thus, IGF-1 signaling is required for survival, whereas sCLU appears to protect cells from premature senescence, as IMR-90 cells with sCLU knockdown undergo senescence faster than control cells |
| 24659628 | With aging, p85alpha, IGF-1 and B-myb muscle levels were lower while the expression of certain cell arrest proteins (p53, p16 and pRB) increased |
| 24659628 | Impaired MPC proliferation resulted from interactions between miR-29 and the 3'-UTR of p85a, IGF-1 and B-myb, suppressing the translation of these mediators of myoblast proliferation |
| 24659628 | Thus, aging-induced muscle senescence results from activation of miR-29 by Wnt-3a leading to suppressed expression of several signaling proteins (p85alpha, IGF-1 and B-myb) that act coordinately to impair the proliferation of MPCs contributing to muscle atrophy |
| 24269635 | FOXO1 and FOXO3 phosphorylation was increased by IL-1beta, PDGF, bFGF, IGF-1, and the oxidant t-BHP |
| 24205274 | Pathway-directed microarrays revealed increased transcription of insulin-like growth factor I (IGF-1), a modulator of cell growth and proliferation upstream of mTOR |
| 24205274 | Consistent with upregulation of these ligands, we found that X-ray exposure led to hyperphosphorylation of IGF-1R, the receptor for IGF-1 and -2 |
| 24063161 | At 24 hours, 72 hours, and 6 days after culture, the cell morphology and density were observed by inverted microscope; the cell proliferation was assessed by MTT; after 6 days of culture, the cell cycle by propidium iodide staining and flow cytometry, the apoptosis by acridine orange/ ethidium bromide staining, and the cell senescence by beta-galactosidase staining; the levels of tumor necrosis factor alpha (TNF-alpha), interleukin 1 (IL-1), platelet-derived growth factor (PDGF), and insulin-like growth factor 1 (IGF-1) in serum were detected by a double-antibody sandwich ELISA kit |
| 24063161 | The levels of TNF-alpha, IL-1, PDGF, and IGF-1 in group C were significantly higher than those in group B (P < 0 |
| 24055032 | Clinical significance of proliferation, apoptosis and senescence of nasopharyngeal cells by the simultaneously blocking EGF, IGF-1 receptors and Bcl-xl genes |
| 24055032 | BACKGROUND: In previous work, we constructed short hairpin RNA (shRNA) expression plasmids that targeted human EGF and IGF-1 receptors messenger RNA, respectively, and demonstrated that these vectors could induce apoptosis of human nasopharyngeal cell lines (CNE2) and inhibit ligand-induced pAkt and pErk activation |
| 23953979 | Possible mechanisms that mediate the consequences of genomic instability at the local vascular and at the systemic level, such as cell senescence, mutations, mitochondrial damage, and sirtuin 1 and IGF-1 decrease, are discussed and important goals for future research are set |
| 23940366 | Growth hormone (GH) elicits direct peripheral metabolic actions as well as growth effects mediated by insulin-like growth factor 1 (IGF1) |
| 23826727 | Tissue regeneration diminishes with age, concurrent with declining hormone levels including growth factors such as insulin-like growth factor-1 (IGF-1) |
| 23579096 | We hypothesize that Amadori products induce senescence in primary human mesangial cells through the activation of IGF-1 receptor and investigate, in the present work, the intracellular mechanism involved after this activation |
| 23579096 | We demonstrated that prolonged exposition (more than 24h) to glycated albumin induced senescence and, in parallel, incremented the release of IGF-1 and the activation of the IGF-1 receptor |
| 23579096 | Inhibition of the IGF-1 activation prevented the GA induced senescence |
| 23579096 | In conclusion, we propose that the Amadori product, glycated albumin, promotes premature cell senescence in mesangial cells through the activation of the IGF-1 receptor and the subsequent reduction in the antioxidant enzyme catalase |
| 23406856 | OBJECTIVE: To investigate the relationship between insulin-like growth factor-1 (IGF-1) in the serum and the vascular endothelial function in patients with hypercholesterolemia and the underlying mechanism |
| 23406856 | Cells were treated with IGF-1 30 min before ox-LDL treatment |
| 23406856 | The effect of ox-LDL on HUVECs was significantly attenuated at the presence of IGF-1 |
| 23406856 | CONCLUSION: The decrease in IGF-1 in the peripheral blood may contribute to vascular endothelial dysfunction in patients with hypercholesterolemia |
| 23362143 | An integrated miRNA and gene profiling approach revealed that hsa-miR-299-3p is upregulated in senescent HUVECs compared with the young cells, and one of its target genes could be IGF1 |
| 23362143 | IGF1 was upregulated in senescent compared with young HUVECs, and knockdown of hsa-miR-299-3p dose-dependently increased the mRNA expression of IGF1, more significantly observed in the presenescent cells (passage 19) compared with the senescent cells (passage 25) |
| 24579735 | Recent studies suggest that oncogenic pathways, such as the insulin-like growth factor-1 (IGF-I), Ras, and Akt/PKB, can contribute to both aging and cancer not only by promoting growth and preventing apoptosis, but also by promoting DNA damage and genomic instability |
| 23261989 | To investigate potential antioxidant effects of IGF-1 we treated human aortic endothelial cells (hAECs) with 0-100ng/mL IGF-1 prior to exposure to native or oxidized low-density lipoprotein (oxLDL) |
| 23261989 | IGF-1 dose- and time- dependently reduced basal- and oxLDL-induced ROS generation |
| 23261989 | IGF-1 did not alter superoxide dismutase or catalase activity but markedly increased activity of glutathione peroxidase (GPX), a crucial antioxidant enzyme, via a phosphoinositide-3 kinase dependent pathway |
| 23261989 | IGF-1 did not increase GPX1 mRNA levels but increased GPX1 protein levels by 2 |
| 23261989 | Furthermore, IGF-1 blocked hydrogen peroxide induced premature cell senescence in hAECs |
| 23261989 | In conclusion, IGF-1 upregulates GPX1 expression in hAECs via a translational mechanism, which may play an important role in the ability of IGF-1 to reduce endothelial cell oxidative stress and premature senescence |
| 23261989 | Our findings have major implications for understanding vasculoprotective effects of IGF-1 |
| 23251848 | Compared to early passage normal fibroblasts, DC fibroblasts express significantly lower transcript levels of several genes that code for secreted proteins, including Insulin-like Growth Factor 1 (IGF1) and Hepatocyte Growth Factor (HGF) |
| 23251848 | Aged normal fibroblasts with short telomeres also had reduced levels of IGF1 and HGF, similar to early passage DC fibroblasts |
| 23251848 | Knockdown of IGF1 or HGF in normal fibroblasts caused a reduction in the capacity of conditioned media from these fibroblasts to support keratinocyte clonogenic growth |
| 23251848 | Surprisingly, reconstitution of telomerase in DC fibroblasts did not significantly increase transcript levels of IGF1 or HGF or substantially increase the ability of the fibroblasts to support keratinocyte growth, indicating that the gene expression defect is not readily reversible |
| 23251848 | Our results suggest that telomere shortening in dermal fibroblasts leads to reduction in expression of genes such as IGF1 and HGF and that this may cause a defect in supporting normal epidermal proliferation |
| 23152410 | IGF-I receptor phosphorylation is impaired in cathepsin X-deficient prostate cancer cells |
| 23041151 | Furthermore, transgenic overexpression of klotho in mice extends their life span through inhibition of insulin and IGF1 signaling |
| 22877754 | Insulin-like growth factor-I (IGF-I) plays a critical role in cellular growth, proliferation, tumorigenesis, and regulation of aging |
| 22877754 | IGF-I induced expression of a DNA damage marker, gammaH2AX, the increased levels of p53 and p21 proteins, and activated SA-beta-gal |
| 22877754 | In the confluent state, an altered downstream signaling of IGF-I receptor was observed |
| 22877754 | In p53-null mouse embryonic fibroblasts, the IGF-I-induced augmentation of SA-beta-gal and p21 was inhibited, demonstrating that p53 is required for cellular senescence induced by IGF-I |
| 22877754 | Thus, these data reveal a novel pathway whereby IGF-I enhances cellular senescence in the ROS and p53-dependent manner and may explain the underlying mechanisms of IGF-I involvement in tumorigenesis and in regulation of aging |
| 22733568 | An increase in insulin-like growth factor (IGF)-1 was observed in Grn(-/-) brains, and increased IGF-1 signalling has been associated with decreased longevity |
| 22391413 | AIMS: Insulin/insulin-like growth factor-1 (IGF-1) signaling plays an important role in many biological processes |
| 21965376 | Young-to-old mice also exhibited higher expression of the anti-aging gene Klotho and less phosphorylation of IGF-1 receptor beta |
| 20890120 | In this Extra View we discuss the interactive role of three molecules, PPARgamma, nocturnin and IGF-I in regulating stem cell fate in the marrow and the potential implications of this network for understanding cellular aging |
| 20830296 | Long-term IGF-I exposure decreases autophagy and cell viability |
| 20830296 | A reduction in IGF-I signaling has been found to increase lifespan in multiple organisms despite the fact that IGF-I is a trophic factor for many cell types and has been found to have protective effects against multiple forms of damage in acute settings |
| 20830296 | The increase in longevity seen in response to reduced IGF-I signaling suggests that there may be differences between the acute and chronic impact of IGF-I signaling |
| 20830296 | We have examined the possibility that long-term stimulation with IGF-I may have a negative impact at the cellular level using quiescent human fibroblasts |
| 20830296 | We find that fibroblast cells exposed to IGF-I for 14 days have reduced long-term viability as judged by colony forming assays, which is accompanied by an accumulation of senescent cells |
| 20830296 | In addition we observe an accumulation of cells with depolarized mitochondria and a reduction in autophagy in the long-term IGF-I treated cultures |
| 20830296 | An examination of mice with reduced IGF-I levels reveals evidence of enhanced autophagy and fibroblast cells derived from these mice have a larger mitochondrial mass relative to controls indicating that changes in mitochondrial turnover occurs in animals with reduced IGF-I |
| 20830296 | The results indicate that chronic IGF-I stimulation leads to mitochondrial dysfunction and reduced cell viability |
| 20627123 | Dynamic SUMO regulation controls the biological outcomes initiated by various growth factors involved in cartilage homeostasis, including basic fibroblast growth factors (bFGF or FGF-2), transforming growth factor-beta (TGF-beta) and insulin-like growth factor-1 (IGF-1) |
| 20591642 | Hormones such as leptin, ghrelin, insulin-like growth factor 1, IGFBP3, and cytokines, including IL-7, regulate both thymopoiesis and maintenance of naive T cells in the periphery |
| 20080172 | Additionally, (iv) they act as inhibitors of proteins mediating the insulin/IGF1 and target of rapamycin (TOR) signalling, both of which are conserved modulators of organism life span |
| 19580824 | We review these findings with reference to pathways linked to ageing, including cell cycle control or cell senescence, oxidative stress, insulin, IGF1 and other endocrine signalling, and inflammation |
| 19021034 | IGF-1 rescues human intervertebral annulus cells from in vitro stress-induced premature senescence |
| 19021034 | The objectives of the present work were: (1) to develop a reliable in vitro model for stress-induced premature senescence in human annulus cells, and (2) to investigate the potential for insulin-like growth factor-1 (IGF-1) to prevent or ameliorate senescence in vitro |
| 19021034 | Nine sets of annulus cells were obtained from eight human surgical disc specimens; cells were tested with 0, 50, 100 or 500 ng/ml IGF-1 |
| 19021034 | Although 50 or 100 ng/ml IGF-1 did not significantly alter the percentage of senescent cells, a significant reduction was present following exposure to 500 ng/ml IGF-1 (control, 56 |
| 18938767 | Elevated insulin-like growth factor 1 receptor, hepatocyte growth factor receptor and telomerase protein expression in mild ulcerative colitis |
| 18672169 | Running increased cardiac expression of insulin-like growth factor (IGF)-1 |
| 18672169 | Treatment with IGF-1 up-regulated myocardial telomerase activity >14-fold and increased the expression of phosphorylated Akt protein kinase and phosphorylated eNOS |
| 18672169 | These beneficial cardiac effects are mediated by TERT, eNOS, and IGF-1 |
| 18638538 | Linking sirtuins, IGF-I signaling, and starvation |
| 18638538 | Here, I review the studies linking SirT1, IGF-I signaling and starvation in various model organisms with a focus on the post-mitotic cells, which indicate that sirtuins can play both protective and pro-aging roles |
| 18451178 | Insulin-like growth factor-I (IGF-I) is a polypeptide hormone that can influence growth, differentiation, and survival of cells expressing the cognate type 1 receptor (IGF-IR) |
| 18451178 | In contrast to epidemiologic studies that established a correlation between elevated serum IGF-I and the risk of developing prostate cancer, we show that abrogation of IGF-IR expression in the dorsal and lateral prostate could activate extracellular signal-regulated kinase 1/2 signaling and cause cell autonomous proliferation and hyperplasia |
| 17234973 | We hypothesized that decreased levels of insulin-like growth factor-1 (IGF-1) during age contribute to dysfunctional EPC |
| 17234973 | We measured the effect of growth hormone (GH), which increases endogenous IGF-1 levels, on EPC in mice and human subjects |
| 17234973 | GH treatment in middle-aged subjects elevated IGF-1 levels (126 |
| 17234973 | Treatment of aged mice with GH (7 days) or IGF-1 increased IGF-1 and EPC levels and improved EPC function, whereas a two day GH treatment did not alter IGF-1 or EPC levels |
| 17234973 | Ex vivo treatment of EPC from elderly individuals with IGF-1 improved function and attenuated cellular senescence |
| 17234973 | IGF-1 stimulated EPC differentiation, migratory capacity and the ability to incorporate into forming vascular networks in vitro via the IGF-1 receptor |
| 17234973 | IGF-1 increased telomerase activity, endothelial nitric oxide synthase expression, phosphorylation and activity in EPC in a phosphoinositide-3-kinase/Akt dependent manner |
| 17234973 | Small interference RNA-mediated knockdown of endothelial nitric oxide synthase in EPC abolished the IGF-1 effects |
| 17234973 | Growth hormone-mediated increase in IGF-1 reverses age-related EPC dysfunction and may be a novel therapeutic strategy against vascular disorders with impairment of EPC |
| 17173483 | However, despite persistent cachectic dwarfism, blood glucose and serum insulin-like growth factor 1 levels returned to normal by 10 wk, with hypoglycemia reappearing near premature death at 5 mo of age |
| 16263123 | The PDGF beta-receptor and insulin-like growth factor 1 receptor at the protein level also decreased but remained readily detectable |
| 16170353 | However, tyrosine phosphorylation of the receptors for EGF and IGF-I and Akt/PKB activation were unaltered by Sirtinol treatment |
| 15140969 | Concomitantly, these late-passage cervical cells exhibit an increase in sensitivity to IGF-1, including enhanced phosphorylation of the IGF receptor (IGF-R) and insulin receptor substrate as well as increased DNA synthesis (5-fold) and cell proliferation (3 |
| 15140969 | However, there was no change in the level of IGF-R in these cells (surface or total), and the cells did not synthesize IGF-1, indicating that these arms of the IGF pathway were independently regulated and not responsible for the augmented signaling |
| 15140969 | Consistent with a causal relationship between IGFBP-3 expression and enhanced IGF-1 responses, we found that early-passage cells could be converted to the late-passage, IGF-1-responsive phenotype by preincubation with IGFBP-3 |
| 15140969 | Thus, in contrast to findings with some cell types, IGFBP-3 expression in cervical cells is associated with augmented IGF-1 signaling and cell proliferation and correlates with the timing of cellular immortalization |
| 14726476 | These parameters were similarly studied in insulin-like growth factor-1 (IGF-1) transgenic mice (TG) because IGF-1 promotes cell growth and survival and may delay cellular aging |
| 14726476 | IGF-1 attenuated the levels of these proteins at all ages |
| 14726476 | IGF-1 enhanced nuclear phospho-Akt and telomerase delaying cellular aging and death |
| 11855685 | The role of insulin-like growth factor 1 and insulin in ageing and atherosclerosis |
| 11855685 | With advancing age insulin-like growth factor (IGF)1 blood levels decrease continuously, but with great interindividual differences |
| 11855685 | There is a relationship between the IGF1 serum concentration and biomarker behaviour, indicating that growth hormone (GH) secretion is a determinant of organismic well being and surviving in advanced age |
| 11855685 | When insulin or IGF1 is added, there is no reversibility, so that there is no recovery to the values of SMCs from young donors |
| 11855685 | The blockade of Ca2+ channels by diltiazem inhibits the in vitro stimulation by IGF1 and insulin on SMC proliferation and migration |
| 11855685 | We conclude that the acceleration of ageing is related to the decline of IGF1 in such a manner that ageing rates progress as GH secretion diminishes |
| 10962000 | Using the insulin-like growth factor I (IGF-I) transgenic mouse in which the IGF-I transgene is expressed during skeletal muscle development and maturation prior to isolation and during culture of satellite cells (the myogenic stem cells of mature skeletal muscle fibers) as a model system, we elucidated the underlying molecular mechanisms of IGF-I-mediated enhancement of proliferative potential of these cells |
| 10962000 | Satellite cells from IGF-I transgenic muscles achieved at least five additional population doublings above the maximum that was attained by wild type satellite cells |
| 10962000 | Adenovirally mediated ectopic overexpression of p27(Kip1) in exponentially growing IGF-I transgenic satellite cells reversed the increase in cyclin E-cdk2 kinase activity, pRb phosphorylation, and cyclin A protein abundance, thereby implicating an important role for p27(Kip1) in promoting satellite cell senescence |
| 9808148 | Thus, dex may act at multiple levels to enhance cellular proliferation in WI-38 cells: first, to decrease the level of an inhibitor of cell-cycle progression, and second, to increase the sensitivity of WI-38 cells to the proliferative effects of IGF-1 |
| 7688732 | In this paper we show, by a very sensitive technique (reverse transcriptase-polymerase chain reaction), that senescent cells fail to express insulin-like growth factor-1 (IGF-1) mRNA, which is expressed in moderate amounts by young cells |
| 7688732 | Human fibroblasts immortalized by transfection with a temperature-sensitive SV40 T antigen gene regain the ability to express IGF-1 mRNA, but only at the permissive temperature of 34 degrees C |
| 7688732 | At the restrictive temperature of 39 degrees C, the temperature-sensitive T antigen is nonfunctional, IGF-1 RNA is not detectable, and the cells fail to grow even in 10% serum |
| 7688732 | The failure to express IGF-1 mRNA in postsenescent cells can be ascribed, at least in part, to a transcriptional mechanism |
| 7688732 | Despite the correlation among immortalization by SV40 T antigen, expression of IGF-1, and growth, it seems unlikely that the failure to express IGF-1 is the sole cause of cellular senescence; other requirements must be postulated |
| 8376318 | These cells respond to the combination of epidermal growth factor (EGF), insulin-like growth factor-I (IGF-I), and dexamethasone by DNA synthesis at a rate and extent equivalent to serum-stimulated cells |
| 7687431 | IGF-1 receptor levels and the proliferation of young and senescent human fibroblasts |
| 7687431 | We have investigated the role of the IGF-1 receptor in the proliferation of young and senescent human diploid fibroblasts |
| 7687431 | Using WI-38 cells, we have established the following: 1) both young and senescent cells have IGF-1 receptors, which can be autophosphorylated by IGF-1, the intensity of the autophosphorylation being roughly the same in both types of cells; 2) the levels of IGF-1 receptor mRNA are also similar in young and senescent cells; 3) both young and senescent cells have an absolute requirement for the IGF-1 receptor in order to be stimulated by either serum or SV40, respectively; 4) despite these similarities, young cells respond to IGF-1 (in combination with other growth factors) with DNA synthesis and mitosis, and senescent cells do not |
| 7687431 | We conclude that, although the IGF-1 receptor is still needed by senescent cells for a growth response to SV40, it is not, by itself, the determinant of senescence, at least in WI-38 cells |
| 2365743 | Human diploid fibroblasts (HDF) were used to study aging-related changes in the proliferative response to platelet-derived growth factor (PDGF), epidermal growth factor (EGF), and insulin-like growth factor I (IGF-I, somatomedin-C) in serum-free, chemically defined culture medium |
| 2365743 | In contrast, IGF-I primarily affects the rate of transition of cells from G1 into S phase, and the dose of IGF-I which produced a half-maximal rate of G1 exit increased up to 130-fold in older-passage cells |
| 2365743 | Unexpectedly, supraphysiologic concentrations of IGF-I were found to increase the G1 exit rate of the dividing subpopulation of cells in older-passage cultures to rates higher than those seen in young cultures |
| 2365743 | In summary, among cells capable of cycling in aging cultures, there were few changes in the regulation of the growth fraction by PDGF and EGF, but there was a greatly increased dependence on IGF-I for regulation of the rate of entry into S phase |
| 2365743 | The slower growth of the dividing population of cells in aging cultures may be related to a requirement for IGF-I at levels which are greatly above those usually supplied |
| 2959670 | Insulin-like growth factor-I (IGF-I) (13 nM) can replace insulin (0 |
| 2959670 | The effect of IGF-I, EGF, and DEX is synergistic in stimulating multiple rounds of low density cell division |
| 2959670 | Binding to the alpha subunit of the IGF-I transmembrane receptor may increase slightly with age while the 50% displacement remains unchanged |
| 2959670 | The remainder of the IGF-I specific binding (five- to thirty-fold more) is to a low molecular weight, cell-associated binding protein whose 50% displacement is 10 times higher, but also remains unchanged with age |
| 2959670 | IGF-I binding to the alpha subunit of the transmembrane receptor is independent of cell density, while binding to the low molecular weight binding protein is inversely proportional to cell density and may vary by as much as tenfold |
