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Academic literature on the topic 'IGFBP1'

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Published: 6 September 2023

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Journal articles on the topic "IGFBP1"

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Czogała, Wojciech, Wojciech Strojny, Przemysław Tomasik, Mirosław Bik Multanowski, Małgorzata Wójcik, Klaudia Miklusiak, Emil Krzysztofik, Albert Wróbel, Karol Miklusiak, and Szymon Skoczeń. "The Insight into Insulin-Like Growth Factors and Insulin-Like Growth-Factor-Binding Proteins and Metabolic Profile in Pediatric Obesity." Nutrients 13, no. 7 (July 15, 2021): 2432. http://dx.doi.org/10.3390/nu13072432.

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Insulin-like growth factors (IGFs) and insulin-like growth-factor-binding proteins (IGFBPs) regulate cell proliferation and differentiation and may be of importance in obesity development. The aim of the study was to analyze the expression of chosen IGF-axis genes and the concentration of their protein products in 28 obese children (OB) and 34 healthy control (HC), and their correlation with essential parameters associated with childhood obesity. The gene expression of IGFBP7 was higher, and the expression of IGF2 and IGFBP1 genes was lower in the OB. The expression of IGFBP6 tended to be lower in OB. IGFBP4 concentration was significantly higher, and IGFBP3 tended to be higher in the OB compared to the HC, while IGFBP1, IGFBP2, and IGFBP6 were significantly lower, and IGFBP7 tended to be lower in OB. We found numerous correlations between IGFs and IGFBP concentration and obesity metabolic parameters. IGFBP6 correlated positively with apelin, cholecystokinin, glucagone-like peptide-1, and leptin receptor. These peptides were also significantly lower in obese children in our study. The biological role of decreased levels of IGFBP6 in obese children needs further investigation.
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Zhong, Zhenglan, Xiaoping Xu, Shiguo Han, Yongxiang Shao, and Yong Yi. "Comprehensive Analysis of Prognostic Value and Immune Infiltration of IGFBP Family Members in Glioblastoma." Journal of Healthcare Engineering 2022 (July 4, 2022): 1–13. http://dx.doi.org/10.1155/2022/2929695.

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Glioblastoma (GBM) is the most common primary malignant brain tumor in adults. The insulin-like growth factor-binding protein (IGFBP) family is involved in tumorigenesis and the development of multiple cancers. However, little is known about the prognostic value and regulatory mechanisms of IGFBPs in GBM. Oncomine, Gene Expression Profiling Interactive Analysis, PrognoScan, cBioPortal, LinkedOmics, TIMER, and TISIDB were used to analyze the differential expression, prognostic value, genetic alteration, biological function, and immune cell infiltration of IGFBPs in GBM. We observed that IGFBP1, IGFBP2, IGFBP3, IGFBP4, and IGFBP5 mRNA expression was significantly upregulated in patients with GBM, whereas IGFBP6 was downregulated; this difference in mRNA expression was statistically insignificant. Subsequent investigations showed that IGFBP4 and IGFBP6 mRNA levels were significantly associated with overall survival in patients with GBM. Functional Gene Ontology Annotation and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis revealed that genes coexpressed with IGFBP4 and IGFBP6 were mainly enriched in immune-related pathways. These results were validated using the TIMER and TSMIDB databases. This study demonstrated that the IGFBP family has prognostic value in patients with GBM. IGFBP4 and IGFBP6 are two members of the IGFBP family that had the highest prognostic value; thus, they have the potential to serve as survival predictors and immunotherapeutic targets in GBM.
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Zheng, Ruoyi, Wenming Chen, Weiting Xia, Jingyu Zheng, and Qing Zhou. "The Prognostic Values of the Insulin-Like Growth Factor Binding Protein Family in Ovarian Cancer." BioMed Research International 2020 (November 16, 2020): 1–15. http://dx.doi.org/10.1155/2020/7658782.

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Purpose. To assess the expression of insulin-like growth factor binding protein (IGFBP) family and its prognostic impact in ovarian cancer (OC) patients. Materials and Methods. The mRNA expression and protein expression of individual IGFBPs in healthy ovarian samples and OC tissues were explored through Oncomine, Gene Expression Profiling Interactive Analysis, and Human Protein Atlas database. Additionally, the prognostic values of the six IGFBP members in patients with OC were evaluated by Kaplan-Meier plotter. Results. IGFBP2 and IGFBP4 mRNA expression were remarkably upregulated in patients with OC. To be specific, the mRNA expression of IGFBP2 was upregulated in patients with serous ovarian cancer (SOC), while IGFBP1/3/4/5/6 mRNA levels were downregulated. In addition, the IGFBP4 protein expression was upregulated in SOC, and the IGFBP6 protein expression was upregulated in both of SOC and endometrioid ovarian cancer (EOC) tissues. High IGFBP1 mRNA levels showed favorable overall survival (OS) and progression-free survival (PFS) in all OC. Meanwhile, increased IGFBP5/6 mRNA levels revealed worsen OS and PFS in all OC patients. IGFBP4/6 mRNA levels predicted unfavorable OS and PFS only in SOC patients. Moreover, the aberrant mRNA expression of IGFBP1/2/4/5/6 was correlated with significantly prognosis in patients receiving different chemotherapeutic regimens. Conclusion. This study indicates that the IGFBP family reveals distinct prognosis in patients with OC. IGFBP1/2/4/5/6 are useful prognostic predictors for chemotherapeutic effect in OC patients, and IGFBP2/4 are potential tumor markers for the diagnosis of OC.
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Minchenko, Dmytro O., D. O. Tsymbal, O. P. Yavorovsky, N. V. Solokha, and O. H. Minchenko. "Expression of genes encoding IGFBPs, SNARK, CD36, and PECAM1 in the liver of mice treated with chromium disilicide and titanium nitride nanoparticles." Endocrine Regulations 51, no. 2 (April 25, 2017): 84–95. http://dx.doi.org/10.1515/enr-2017-0008.

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AbstractObjective. The aim of the present study was to examine the effect of chromium disilicide and titanium nitride nanoparticles on the expression level of genes encoding important regulatory factors (IGFBP1, IGFBP2, IGFBP3, IGFBP4, IGFBP5, SNARK/NUAK2, CD36, and PECAM1/CD31) in mouse liver for evaluation of possible toxic effects of these nanoparticles.Methods. Male mice received 20 mg chromium disilicide nanoparticles (45 nm) and titanium nitride nanoparticles (20 nm) with food every working day for 2 months. The expression of IGFBP1, IGFBP2, IGFBP3, IGFBP4, IGFBP5, SNARK, CD36, and PECAM1 genes in mouse liver was studied by quantitative polymerase chain reaction.Results. Treatment of mice with chromium disilicide nanoparticles led to down-regulation of the expression of IGFBP2, IGFBP5, PECAM1, and SNARK genes in the liver in comparison with control mice, with more prominent changes for SNARK gene. At the same time, the expression of IGFBP3 and CD36 genes was increased in mouse liver upon treatment with chromium disilicide nanoparticles. We have also shown that treatment with titanium nitride nanoparticles resulted in down-regulation of the expression of IGFBP2 and SNARK genes in the liver with more prominent changes for SNARK gene. At the same time, the expression of IGFBP3, IGFBP4, and CD36 genes was increased in the liver of mice treated with titanium nitride nanoparticles. Furthermore, the effect of chromium disilicide nanoparticles on IGFBP2 and CD36 genes expression was significantly stronger as compared to titanium nitride nanoparticles.Conclusions. The results of this study demonstrate that chromium disilicide and titanium nitride nanoparticles have variable effects on the expression of IGFBP2, IGFBP3, IGFBP4, IGFBP5, SNARK, CD36, and PECAM1 genes in mouse liver, which may reflect the genotoxic activities of the studied nanoparticles.
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Rehman, Muhammad Saif-ur, Muqeet Mushtaq, Faiz-ul Hassan, Zia-ur Rehman, Muhammad Mushahid, and Borhan Shokrollahi. "Comparative Genomic Characterization of Insulin-Like Growth Factor Binding Proteins in Cattle and Buffalo." BioMed Research International 2022 (July 25, 2022): 1–15. http://dx.doi.org/10.1155/2022/5893825.

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The somatotropic axis consists of genes associated with economic traits like muscle growth and carcass traits in livestock. Insulin-like growth factor binding proteins (IGFBPs) are the major proteins that play a vital role in the somatotropic axis. The present study performed a genome-wide characterization of IGFBP genes in cattle. Genomic sequences of the IGFBP gene family for different mammals (cattle, buffalo, goat, and sheep) were recovered from the NCBI database. Sequence analyses were performed to investigate cattle’s genomic variations in the IGFBP gene family. Phylogenetic analysis, gene structure, motif patterns, and conserved domain analysis (CDA) of the IGFBP family revealed the evolutionarily conserved nature of the IGFBP genes in cattle and other studied species. Physicochemical properties of IGFBP proteins in cattle revealed that most of these proteins are unstable, hydrophilic, thermostable, and acidic. Comparative amino acid analysis revealed variations in all protein sequences with single indels in IGFBP3 and IGFBP6. Mutation analysis revealed only one nonsynonymous mutation D212 > E in the IGFBP6 protein of cattle. A total of 245 nuclear hormone receptor (NHRs) sites were detected, including 139 direct repeats (DR), 65 everted repeats (ER), and 41 inverted repeats (IR). Out of 133 transcription factors (TFs), 10 TFs (AHR, AHRARNT, AP4, CMYB, E47, EGR2, GATA, SP1, and SRF) had differential distribution ( P value < 0.05) of putative transcriptional binding sites (TFBS) in cattle compared to buffalo. Synteny analysis revealed the conserved nature of genes between cattle and buffalo. Two gene pairs (IGFBP1/IGFBP3 and IGFBP2/IGFBP5) showed tandem duplication events in cattle and buffalo. This study highlights the functional importance of genomic variation in IGFBP genes and necessitates further investigations better to understand the role and mechanisms of IGFBPs in bovines.
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Simmons, Rebecca M., David W. Erikson, Jinyoung Kim, Robert C. Burghardt, Fuller W. Bazer, Greg A. Johnson, and Thomas E. Spencer. "Insulin-Like Growth Factor Binding Protein-1 in the Ruminant Uterus: Potential Endometrial Marker and Regulator of Conceptus Elongation." Endocrinology 150, no. 9 (June 4, 2009): 4295–305. http://dx.doi.org/10.1210/en.2009-0060.

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Abstract Establishment of pregnancy in ruminants requires conceptus elongation and production of interferon-τ (IFNT), the pregnancy recognition signal that maintains ovarian progesterone (P4) production. These studies determined temporal and spatial alterations in IGF binding protein (IGFBP)-1 and IGFBP3 in the ovine and bovine uterus; effects of P4 and IFNT on their expression in the ovine uterus; and effects of IGFBP1 on ovine trophectoderm cell proliferation, migration, and attachment. IGFBP1 and IGFBP3 were studied because they are the only IGFBPs specifically expressed by the endometrial luminal epithelia in sheep. In sheep, IGFBP1 and IGFBP3 expression was coordinate with the period of conceptus elongation, whereas only IGFBP1 expression was coordinate with conceptus elongation in cattle. IGFBP1 mRNA in the ovine endometria was between 5- and 29-fold more abundant between d 12 and 16 of pregnancy compared with the estrous cycle and greater on d 16 of pregnancy than nonpregnancy in the bovine uterus. In sheep, P4 induced and IFNT stimulated expression of IGFBP1 but not IGFBP3; however, the effect of IFNT did not mimic the abundant increase observed in pregnant ewes. Therefore, IGFBP1 expression in the endometrium is regulated by another factor from the conceptus. IGFBP1 did not affect the proliferation of ovine trophectoderm cells in vitro but did stimulate their migration and mediate their attachment. These studies reveal that IGFBP1 is a common endometrial marker of conceptus elongation in sheep and cattle and most likely regulates conceptus elongation by stimulating migration and attachment of the trophectoderm.
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Fouque, D., Y. Le Bouc, M. Laville, F. Combarnous, M. O. Joly, P. Raton, and P. Zech. "Insulin-like growth factor-1 and its binding proteins during a low-protein diet in chronic renal failure." Journal of the American Society of Nephrology 6, no. 5 (November 1995): 1427–33. http://dx.doi.org/10.1681/asn.v651427.

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The effects of a low-protein diet on the serum insulin-like growth factor (IGF)-1 and IGF binding proteins (IGFBP) were investigated during a 3-month controlled study in 12 adult chronic renal failure patients. Six patients were randomly supplemented with keto acids (Cetolog, Clintec, Velizy, France). Protein intake was prescribed so that both groups were isonitrogenous. Dietary survey included a monthly 3-day food record and a 24-h urinary urea measurement. After a 4- to 6-wk equilibrium period (1.11 g of protein, 32 kcal/kg body wt per day), patients reduced their protein intake to 0.71 g protein/kg body wt per day. Energy intake was kept constant (31 kcal/kg body wt per day) during the 3-month period. Serum IGF-1 levels were in normal range and, for 11 of the 12 patients, were correlated with the GFR (P = 0.01). These serum IGF-1 values did not decrease after reducing the protein intake. By Western ligand blotting, serum IGFBP1, IGFBP2, and IGFBP4 levels were significantly higher than normal adults, whereas the IGFBP3 level was not increased. IGFBP were not modified when protein intake was reduced. The IGFBP1 level was elevated despite a normal insulin level. IGFBP4 changes were inversely correlated with IGF-1 variations. There was no difference between groups receiving or not receiving the keto acids. Thus, in adult chronic renal failure, reducing protein intake by 40% did not modify the growth hormone/IGF-1/IGFBP axis.
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Alterki, Abdulmohsen, Eman Al Shawaf, Irina Al-Khairi, Preethi Cherian, Devarajan Sriraman, Maha Hammad, Thangavel A. Thanaraj, et al. "The Rise of IGFBP4 in People with Obstructive Sleep Apnea and Multilevel Sleep Surgery Recovers Its Basal Levels." Disease Markers 2021 (October 4, 2021): 1–9. http://dx.doi.org/10.1155/2021/1219593.

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IGFBP4 is the smallest member of the insulin-like growth factor binding protein family (IGFBP). It is a hepatic protein that plays a role in modulating the activity and bioavailability of IGF-I. The expression of IGFBP4 was found to increase under conditions of hypoxia. Obstructive sleep apnea (OSA) is a common disorder, characterized by cyclic episodes of intermittent hypoxia and fragmented sleep. Our aim was to quantify levels of circulating IGFBP1, IGFBP2, IGFBP3, IGFBP4, and IGFBP7 in fasting plasma samples of 69 Kuwaiti participants and explore its correlation with indices of OSA. The quantification was performed using multiplexing assay. The study involved 28 controls and 41 patients with OSA. Levels of circulating IGFBP4 were significantly higher in people with OSA ( 289.74 ± 23.30 ng/ml) compared to the control group ( 217.60 ± 21.74 ng/ml, p = 0.028 ). The increase in IGFBP4 correlated significantly and positively with AHI ( r = .574 , p = .01 ) and AI ( r = .794 , p = .001 ) in people with moderate and severe OSA. There was a significant decline in circulating IGFBP4 after 3 months of surgery ( 225.89 ± 18.16 ng/ml, p = 0.012 ). This was accompanied by a prominent improvement in OSA (AHI 8.97 ± 2.37 events/h, p = 0.001 ). In this study, our data showed a significant increase in circulating IGFBP4 in people with OSA. We also report a significant positive correlation between IGFBP4 and indices of OSA at baseline, which suggests IGFBP4 as a potential diagnostic biomarker for OSA. There was a significant improvement in OSA after 3 months of surgical intervention, which concurred with a significant decline in IGFBP4 levels. Altogether, the detected change suggests a potential link between IGFBP4 and OSA or an OSA-related factor, whereby OSA might play a role in triggering the induction of IGFBP4 expression.
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Alterki, Abdulmohsen, Eman Al Shawaf, Irina Al-Khairi, Preethi Cherian, Devarajan Sriraman, Maha Hammad, Thangavel A. Thanaraj, et al. "The Rise of IGFBP4 in People with Obstructive Sleep Apnea and Multilevel Sleep Surgery Recovers Its Basal Levels." Disease Markers 2021 (October 4, 2021): 1–9. http://dx.doi.org/10.1155/2021/1219593.

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IGFBP4 is the smallest member of the insulin-like growth factor binding protein family (IGFBP). It is a hepatic protein that plays a role in modulating the activity and bioavailability of IGF-I. The expression of IGFBP4 was found to increase under conditions of hypoxia. Obstructive sleep apnea (OSA) is a common disorder, characterized by cyclic episodes of intermittent hypoxia and fragmented sleep. Our aim was to quantify levels of circulating IGFBP1, IGFBP2, IGFBP3, IGFBP4, and IGFBP7 in fasting plasma samples of 69 Kuwaiti participants and explore its correlation with indices of OSA. The quantification was performed using multiplexing assay. The study involved 28 controls and 41 patients with OSA. Levels of circulating IGFBP4 were significantly higher in people with OSA ( 289.74 ± 23.30 ng/ml) compared to the control group ( 217.60 ± 21.74 ng/ml, p = 0.028 ). The increase in IGFBP4 correlated significantly and positively with AHI ( r = .574 , p = .01 ) and AI ( r = .794 , p = .001 ) in people with moderate and severe OSA. There was a significant decline in circulating IGFBP4 after 3 months of surgery ( 225.89 ± 18.16 ng/ml, p = 0.012 ). This was accompanied by a prominent improvement in OSA (AHI 8.97 ± 2.37 events/h, p = 0.001 ). In this study, our data showed a significant increase in circulating IGFBP4 in people with OSA. We also report a significant positive correlation between IGFBP4 and indices of OSA at baseline, which suggests IGFBP4 as a potential diagnostic biomarker for OSA. There was a significant improvement in OSA after 3 months of surgical intervention, which concurred with a significant decline in IGFBP4 levels. Altogether, the detected change suggests a potential link between IGFBP4 and OSA or an OSA-related factor, whereby OSA might play a role in triggering the induction of IGFBP4 expression.
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Kharkova, A., D. Minchenko, D. Tsymbal, and O. Minchenko. "Expression of IGFBP1, IGFBP2 and IGF2BP3 genes in U87 glioma cells with suppressed ERN1 signaling enzyme function in glutamine and glucose deprivation conditions." Bulletin of Taras Shevchenko National University of Kyiv. Series: Biology 68, no. 3 (2014): 24–29. http://dx.doi.org/10.17721/1728_2748.2014.68.24-29.

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Insulin-like growth factor binding proteins play an important role in the regulation of cell proliferation and malignant tumor growth. It was shown that blockade of both enzymatic functions of sensor and signaling enzyme ERN1 (from endoplasmic reticulum to nuclei-1), the major component of endoplasmic reticulum stress signaling, decreases the expression level of IGFBP1, IGFBP2 and IGF2BP3 genes in U87 glioma cell. The decreased level of these gene expressions in glioma cells with ERN1 signaling enzyme loss of function correlates with suppression of cell proliferation. It was shown that glutamine deprivation condition leads to enhance the expression of IGFBP1 gene, but did not change significantly the expression of IGFBP2 and IGF2BP3 genes in both types of glioma cells. Moreover, this effect of glutamine deprivation did not depend from suppression of ERN1 enzyme function. At the same time, the expression of IGFBP2 and IGF2BP3 genes is decreased in glucose deprivation condition in both types of glioma cells and blockade of ERN1 signaling enzyme enhanced this effect. Thus, results of this investigation demonstrated that the expression of IGFBP1, IGFBP2 and IGF2BP3 genes in U87 glioma cells is dependent from signaling enzyme ERN1 and is changed in glutamine and glucose deprivation conditions, but only effect of glucose deprivation was depended of ERN1 signaling enzyme function. Moreover, the decreasing of IGFBP1, IGFBP2 and IGF2BP3 gene expressions in glioma cells with blockade of both enzymatic activities of ERN1 is possibly related to suppression of these cells proliferation.
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Dissertations / Theses on the topic "IGFBP1"

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Matz-Soja, Madlen, and Rolf Gebhardt. "Hepatic Hedgehog signaling contributes to the regulation of IGF1 and IGFBP1 serum levels." Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-142560.

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Background Hedgehog signaling plays an important role in embryonic development, organogenesis and cancer. In the adult liver, Hedgehog signaling in non-parenchymal cells has been found to play a role in certain disease states such as fibrosis and cirrhosis. However, whether the Hedgehog pathway is active in mature healthy hepatocytes and is of significance to liver function are controversial. Findings Two types of mice with distinct conditional hepatic deletion of the Smoothened gene, an essential co-receptor protein of the Hedgehog pathway, were generated for investigating the role of Hedgehog signaling in mature hepatocytes. The knockout animals (KO) were inconspicuous and healthy with no changes in serum transaminases, but showed a slower weight gain. The liver was smaller, but presented a normal architecture and cellular composition. By quantitative RT-PCR the downregulation of the expression of Indian hedgehog (Ihh) and the Gli3 transcription factor could be demonstrated in healthy mature hepatocytes from these mice, whereas Patched1 was upregulated. Strong alterations in gene expression were also observed for the IGF axis. While expression of Igf1 was downregulated, that of Igfbp1 was upregulated in the livers of both genders. Corresponding changes in the serum levels of both proteins could be detected by ELISA. By activating and inhibiting the transcriptional output of Hedgehog signaling in cultured hepatocytes through siRNAs against Ptch1 and Gli3, respectively, in combination with a ChIP assay evidence was collected indicating that Igf1 expression is directly dependent on the activator function of Gli3. In contrast, the mRNA level of Igfbp1 appears to be controlled through the repressor function of Gli3, while that of Igfbp2 and Igfbp3 did not change. Interestingly, body weight of the transgenic mice correlated well with IGF-I levels in both genders and also with IGFBP-1 levels in females, whereas it did not correlate with serum growth hormone levels. Conclusions Our results demonstrate for the first time that Hedgehog signaling is active in healthy mature mouse hepatocytes and that it has considerable importance for IGF-I homeostasis in the circulation. These findings may have various implications for mouse physiology including the regulation of body weight and size, glucose homeostasis and reproductive capacity.
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Green, Charmaine. "THE ROLE OF INSULIN-LIKE GROWTH FACTOR 1 RECEPTOR SIGNALLING IN THE MOUSE EMBRYO DURING PREIMPLANTATION DEVELOPMENT AND EARLY IMPLANTATION." Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/17684.

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The use of assisted reproductive technologies (ART) such as in vitro fertilisation (IVF) is increasing and today close to 4 percent of babies born in Australia, are as a result of ART. IVF procedures involve the culture of resultant embryos in medium that routinely lacks the growth factors that are present in the reproductive tract. Cultured embryos develop at a slower rate and have higher levels of developmental arrest, with fewer than 50% of embryos reaching the blastocyst stage. Furthermore, once an embryo is transferred back into the uterus, it faces the hurdle of implantation, with implantation failure being a major cause of IVF failure. This thesis examines whether the addition of growth factors to the embryo culture medium can increase blastocyst development and adhesion competency, using mouse embryos as a model system. In particular, the effect of insulin-like growth factor 1(IGF1) and insulin-like binding protein 3 (IGFBP3) on preimplantation mouse embryo development in vitro and the role of IGF1 on implantation in vitro was examined. In the present study, the culture of preimplantation embryos in the presence of a physiological concentration of IGF1 improved development from compaction onwards, resulting in improved blastocyst development. Conversely, high levels of IGF1 negatively impacted on development by decreasing hatching probably due to these high levels of IGF1 causing IGF1 receptor (IGF1R) down-regulation and apoptosis in the mouse embryo, as shown previously. Blocking the IGF1R with a neutralising antibody was shown to decrease blastocyst development, hatching and cell numbers and to increase apoptosis. Furthermore, treatment of blastocysts with IGF1 caused phosphorylation of Akt, which regulates cell survival by activating anti-apoptotic pathways. Therefore, IGF1 may act as a survival factor in the preimplantation embryo. During early implantation integrins accumulate on the surface of the blastocyst and endometrium and these interact with each other via extracellular matrix proteins such as fibronectin. These interactions are important for the attachment of blastocysts to the endometrium. In the present study treatment of blastocysts with IGF1 increased fibronectin on the surface of the blastocyst via activation of the Phosphoinositide 3 Kinase (PI3K) pathway. As a result, blastocysts had increased attachment to cultured uterine epithelial cells and increased outgrowth. In addition to IGF1, the reproductive tract produces IGFBP3, which is also thought to improve development of the embryo. However, to the best of our knowledge this is the first study to examine the effect of exogenous IGFBP3 on embryo development in vitro. IGFBP3 caused an increase rate of progression of embryos through the early stages of division (5-8cells) and activation of Akt and ribosomal protein S6 (rpS6) proteins as well as induction of calcium signalling. In the present study, it appears that IGFBP3 signalling in the embryo requires the IGF1R, as the use of an IGF1R neutralising antibody blocked IGFBP3 from enhancing early stages of division and the induction of calcium signalling. In other cell types, IGFBP3 signals through the IGF1R following a transactivation event involving the Sphingosine 1-Phosphate (S1P) pathway. The complex interactions and signalling of IGFBP3 are beginning to emerge in a number of different cell types and further investigation of IGFBP3 function is required in the embryo. As growth factors are generally absent from embryo culture media there is a potential avenue for the improvement of embryo culture and ART outcomes by addition of IGF1 and or IGFBP3 to the culture medium. The requirements of the embryo are complex and understanding the role of growth factors in embryo development is essential in order to optimise embryo culture and develop culture media for use in ART.
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Lin, Wan-Jung. "The nuclear actions of IGFBP-3." Online access for everyone, 2006. http://www.dissertations.wsu.edu/Thesis/Summer2006/w%5Flin%5F072606.pdf.

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Eddiry, Sanaa. "Rôle du SNORD116 et de l'IGFBP7 dans la réponse à l'IGF1 dans le syndrome de Prader-Willi." Toulouse 3, 2013. http://www.theses.fr/2013TOU30215.

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Le syndrome de Prader-Willi (SPW) est une maladie génétique complexe du développement qui résulte de l'absence d'expression de gènes sur le chromosome15q11-q13 paternel. Les patients SPW présentent des taux de GH diminués et des taux de ghréline élevés. Ils sont traités précocement par GH. La région du chromosome 15q11-q13 responsable du SPW est soumise au phénomène d'empreinte génétique, des études récentes la limitent à une région minimale incluant un cluster de small nucleolar RNA (snoARN): le SNORD116. Nos résultats montrent une sensibilité accrue à l'IGF1 et à l'insuline dans les fibroblastes de patients SPW. Ces cellules montrent également un taux augmenté de la prolifération et une diminution de la sénescence. Des études par microarrays, RT-qPCR, ainsi que du sécrétome montrent que l'expression de l'IGFBP7, un important facteur anti-prolifératif, a été considérablement abaissée chez ces patients. IGFBP7 est connu pour interagir avec les récepteurs de l'IGF1 et de l'insuline en modulant négativement leur action. Ces résultats étaient identiques chez la patiente SD. Notre hypothèse a été que l'augmentation de la prolifération et de la sensibilité aux facteurs de croissance est due à l'absence de l'expression du SNORD116. Nous avons démontré que le défaut du SNORD116 entraîne des taux de prolifération élevés et une diminution de la sénescence chez les patients SPW, avec une diminution de la sécrétion de l'IGFBP7. Les taux d'IGFBP7 in vitro décroissent sous l'effet de l'IGF1. De plus nous avons constaté que l'augmentation des taux d'IGF1 était corrélée significativement avec la diminution des taux de l'IGFBP7 chez des enfants SPW traités par GH pendant un an. Ces études soulignent fortement l'importance du SNORD116 pour contrôler la production de l'IGFBP7 en présence d'IGF1 et de facteurs de croissance et donc la sensibilité au traitement à l'hormone de croissance
Prader-willi syndrome (PWS) is a complex genetic disease of neurodevelopment that arises from lack of expression of paternally imprinted genes on chromosome 15q11-q13. GH levels are low in PWS, and GH treatment is recommended. The current management of PWS patients includes early treatment by growth hormone (GH). We demonstrated that GH treatment of PWS patients is associated with elevated IGF1 levels. Human chromosome 15q11-q13 contains an imprinting control region, which when deleted is sufficient to cause PWS. In addition, human genetic studies have defined a minimal PWS gene locus including a cluster of paternally expressed small nucleolar RNA (snoRNA), within the SNORD116. This makes PWS the first human disease found to be caused by loss of non-coding RNA. Our results showed increased sensitivity to IGF1 and Insulin in PWS cells. These cells demonstrate also increased proliferation rate and decreased senescence. From multi-array and RT-qPCR analysis, expression of IGFBP7, an important antiproliferative factor, was dramatically decreased in those patients. IGFBP7 is known to interact with IGF1 and Insulin receptors to decrease their action. We demonstrated that the lack of expression of SNORD116 in this patient results in increased response to IGF1 and Insulin and highly decreased secretion of IGFBP7. Therefore lack of SNORD116 results in high proliferation rate and decreased senescence in PWS, with decreased IGFBP7 secretion. Finally, we found that the increase of IGF1 level was significantly correlated with the decrease of IGFBP7 level in the serum of PWS children treated one year with GH. These data suggest that the lack of SNORD116 expression results in increased responsiveness to growth factors due to a low level of IGFBP7 in cells of PWS patients. They highlight a new phenotype of PWS, modified IGFBP7 levels, which, given the properties of IGFBP7 as a strong regulator of IGF1 effect, has potential consequences on the management of PWS patients treated by GH
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Grosse, Christina Maria. "Knochenalterassozierte IGF-I und IGFBP-3 Befunde." Diss., lmu, 2008. http://nbn-resolving.de/urn:nbn:de:bvb:19-93014.

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HO, Penny Pei-Ying. "NOVEL IGF-INDEPENDENT MECHANISMS OF IGFBP-5." Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/10010.

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Insulin-like growth factor binding proteins (IGFBPs) are a group of six structurally similar proteins that modulates the mitogenic actions of IGFs through high binding affinity. IGFBP-5 and -3 has been reported to function independently of their IGF-binding ability and this involves interaction with several non-IGF proteins. Yeast two-hybrid and co immunoprecipitation (co-IP) assays identified SPRY2 and GADD34 as novel IGFBP-5-interacting partners. In MCF 10A cells, IGFBP 5:SPRY2 interaction potentiated SPRY2-mediated inhibition to EGF-stimulated DNA synthesis while IGFBP-5 expression alone had no effect. Under EGF-stimulation, cell numbers was decreased in SPRY2 and IGFBP 5 transfected cells to 24 % and 52 %, respectively, and a further reduction to 80 % was observed when cells co-expressed SPRY2 and IGFBP-5. These findings suggest a synergistic effect of the IGFBP-5:SPRY2 interaction. Biochemical analysis demonstrated that GADD34 binds to IGFBP 5 and -3, but not -1, -2, -4 and -6, and that amino acids between 320 and 400 were required for the interaction. Further co-IP showed that IGFBP-5 forms a complex with GADD34 and protein phosphate 1 alpha and in return, accelerate the survival of breast cancer MCF-7 cells from stress stimuli. In summary, we have characterised two novel mechanisms and expanded the current understanding of IGF-independent functions of IGFBP-5.
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TROTTA, ROSA. "A novel biomarker for cancer and autoimmune diseases: IGFBP6." Doctoral thesis, Università degli Studi di Foggia, 2019. http://hdl.handle.net/11369/382356.

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La temperatura corporea costituisce un importante meccanismo di difesa ed è il risultato di una complessa interazione che coinvolge numerosi fattori. Nell'uomo sano, la temperatura corporea è finemente regolata; deviazioni di 0.5°C oltre il limite superiore possono indicare una condizione patologica. Numerosi agenti possono indurre ipertermia, tra cui, insufficienza cardiaca acuta/cardiomiopatia acuta da stress [1] e infarto miocardico acuto [2] sindrome neurolettica maligna [3], endocrinopatie [4, 5], disturbi del sistema nervoso centrale (SNC) [6] e patologie oncologiche [7]. Le temperature febbrili aumentano l'efficacia della risposta immunitaria durante le infezioni stimolando il sistema immunitario innato e adattativo. Questo studio ha come obiettivo quello di dimostrare come l'ipertermia possa indurre modifiche del profilo di espressione genica e di evidenziare nuovi marker precoci di prognosi/diagnosi in patologie autoimmuni e/o tumorali. Nelle cellule dendritiche, alcuni tra i geni up-regolati codificano per proteine secrete, come IGFBP6 [8]. In condizioni ipertermiche, questa proteina induce chemiotassi dei monociti, dei linfociti T, ma non dei linfociti B. Inoltre, IGFBP6 è un agonista selettivo nei neutrofili poiché aumenta sia il burst ossidativo che la degranulazione e agisce come fattore chemotattico.
Body temperature is an important defense mechanism and is the result of a complex interaction of many factors. In healthy human, the body temperature is regulated very carefully; deviations of 0.5°C above the upper limit of normal are considered to be significant indications of disease. Numerous elements may induce febrile conditions, including acute heart failure/stress cardiomyopathy [1] and acute myocardial infarction [2] neuroleptic malignant syndrome [3], endocrinopathies [4, 5], central nervous system (CNS) disorders [6] and oncological diseases [7]. Febrile temperatures increase the effectiveness of the immune response during infections by stimulating both the innate and adaptive arms of the immune system. The aim of this study is to demonstrate how hyperthermia can induce changes in the gene expression profile and highlight new early markers of prognosis/diagnosis in autoimmune and/or tumor pathologies. Among the up-regulated genes in dendritic cells, some encode secreted proteins, such as IGFBP6 [8]. This protein may have a functional role in the hyperthermic conditions as chemoattractant factor in monocytes and T cells, but not in B cells. Moreover, IGFBP6 is a selective neutrophil agonist, increasing oxidative burst and degranulation, as well as functioning as a chemotactic factor.
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8

Pillai, Chitra Claire. "IGFPBp1 : a multifunctional role in implantation, embryonic and fetal development." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271064.

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Paula, Mariana Teresa Alves Sarti de. "Estudo da expressão do IGF1R mRNA em meninas com puberdade precoce central antes e durante o tratamento com análogos do GnRH." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/17/17144/tde-20072016-142344/.

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INTRODUÇÃO Na puberdade, tanto fisiológica quanto precoce, um dos eventos marcantes é o estirão de crescimento. Análogos do GnRH tem sido utilizado como tratamento da puberdade precoce central (PPC) tendo como consequência o bloqueio do eixo gonadal e diminuição da velocidade de crescimento, porém mantém níveis séricos elevados de IGF-I e IGFBP-3. Não existem relatos sobre a expressão do IGF1R durante a puberdade. Considerando-se que este poderia ser um ponto de regulação da velocidade de crescimento, o presente estudo propõe avaliar a expressão do IGF1R em meninas com PPC antes e durante o tratamento. MÉTODOS: Avaliamos meninas com PPC que foram divididas em dois grupos: Grupo A foi constituído por 16 meninas avaliadas antes do início do tratamento com idade média de 8,0+-0,7anos e o Grupo B constituído por 16 pacientes em uso regular do análogo do GnRH com idade média de 9,4+-0,8 anos. O grupo controle foi composto por 18 crianças saudáveis, pré-púberes com idade média 7,1+-1,3 anos. RESULTADOS: A expressão do mRNA do gene do IGF1R foi maior no grupo B quando comparado ao grupo A (p= 0,04) e ao grupo controle (p=0,004). Não foi observado diferença estatística entre o Grupo A e o grupo controle (p=0,17). Os níveis séricos de IGF-I e IGFBP3 assim como a relação molar IGF-I/IGFBP3 foram significativamente maiores no grupo A em relação ao grupo controle. (p<0,0001). Não encontramos diferença nas concentrações de IGF-I, IGFBP3 ou na relação molar entre os grupos A e B. O grupo controle apresentou níveis mais elevados de IGFBP1 quando comparado com os grupos A e B (p<0,001). Ao compararmos somente os grupos A e B, o grupo B apresentou número estatisticamente maior de valores indetectáveis de IGFBP1 quando comparado com o grupo A (p=0,01) mostrando uma tendência a valores menores no grupo B. A dosagem de insulina foi significativamente menor no grupo controle quando comparado ao grupo A (p<0,001) e não apresentou diferença entre os grupos A e B. Ao analisarmos os 3 grupos (controle, A e B) não encontramos a correlação negativa entre insulina e IGFBP-1. Essa correlação aparece quando avaliamos somente o grupo controle e o grupo A (r= - 0,5; p=0,007) e desaparece quando acrescentamos o grupo B na análise. CONCLUSÃO: As variações nas concentrações séricas de IGF-I, IGFBP-3, IGFBP-1 e insulina não explicam a desaceleração da velocidade de crescimento durante o tratamento de meninas com puberdade precoce central com análogos do GnRH. O aumento da expressão do IGF1R parece refletir uma redução da sinalização intracelular do IGF1R com consequente diminuição da bioatividade do IGF-I em um mecanismo de feedback de alça ultra curta. O aumento da secreção do hormônio de crescimento devido a redução do feedback negativo na hipófise, explica as concentrações encontradas de IGF-I, IGFBP3 e IGFBP1.Estudos outros serão necessários para confirmar esta hipótese, avaliando diferentes pontos de sinalização na cascata pós-receptor
BACKGROUND: Growth spurt is a major event in central precocious puberty (CPP). GnRH analogues (GnRHa) treatment inhibit gonadal axis and decrease height velocity. However, serum IGF-I and IGFBP-3 remain high as before treatment. No reports regarding IGF type 1 receptor (IGF1R) in CPP is available. Considering that this could be a point of regulation of height velocity, the present study aims to study IGF1R mRNA expression in girls with CPP before and during GnRHa treatment. MÉTHODS: Sixteen girls with CPP (8.0±0.7yr) were evaluated before treatment (Group A) and sixteen (9.4±0.8yr) in use of GnRHa (Group B). Age-matched pre pubertal children were studied as controls (n=18). Fasting blood sample were collect for IGF1R mRNA expression analysis in peripheral lymphocytes (RT-PCR) and serum IGF-I, IGFBP-3, IGFBP-1 and insulin determination. RESULTS: The expression of IGF1R mRNA was higher in Group B than in Group A (p=0.04) and Controls (p=0.004). No difference was observed between Groups A and Controls. IGF-I, IGFBP-3 and IGF-I/IGFBP3 molar ratio were similar in Group A and B but higher than in Controls (p<0.0001). IGFBP-1 was higher (p<0.0001) in Controls than in Groups A and B. When we compare only Groups A and B, group B showed more IGFBP1 undetectable values than group A (p = 0.01) showing a tendency to lower values in group B. Insulin levels were lower in Controls than in Group A (p<0.001), but no difference were observed between Groups B and A. Negative correlation was found between insulin and IGFBP-1 when controls and Group A were put together (r= -0.5; p=0.007). This correlation disappear if Group B is included in the analysis. CONCLUSION: Serum concentrations of IGF-I, IGFBP-3, IGFBP-1 and insulin do not explain the decrease in height velocity during CPP treatment with GnRH analogue. The increase in IGF1R mRNA expression suggest impairment of IGF-I signaling and compensatory up regulation of the IGF1R. Increased GH concentrations due to reduction of IGF-I feedback could explain the IGF-I, IGFBP-3 and IGFBP-1 findings. Other studies are necessary to confirm this hypothesis by studying different signaling points in post-receptor cascade
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Wilhelm, Franziska Katharina. "Der PI3K/AKT/mTOR-Signalweg und die Produktion des Insulinähnlichen Wachstumsfaktorbindungsproteins-2 (IGFBP-2) in humanen Adipozyten." Doctoral thesis, Universitätsbibliothek Leipzig, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-219991.

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In den letzten Jahren wurde gezeigt, dass die Serumkonzentration des insulinähnlichen Wachstumsfaktorbindungsproteins-2 (IGFBP-2) bei Krebserkrankungen, die mit dem Verlust des Tumorsuppressorgens PTEN einhergehen, erhöht ist und daher möglicherweise einen Marker für den PTEN-Status und die Aktivität des PI3K/AKT/mTOR-Signalweges darstellt. Schmid et al. haben 2014 einen Patienten mit PTEN-Hamartom-Tumor-Syndrom (PHTS) mit einer heterozygoten PTEN-Keimbahndeletion und massiver Lipomatose beschrieben, bei dem erhöhte IGFBP-2 Serumspiegel gemessen wurden. Ziel dieser Arbeit war es zu analysieren, ob PTEN-defiziente Lipomzellen des Patienten im Vergleich zu Kontrollfettzellen mehr IGFBP-2 produzieren, sowie den Einfluss verschiedener pharmakologischer Inhibitoren des AKT/PI3K/mTOR - und des MAPK- Signalwegs auf die IGFBP-2 Produktion zu untersuchen. In der PTEN-defizienten Lipomzellkultur, gewonnen aus reseziertem Lipomgewebe des Patienten, wurden vergleichbare Mengen an IGFBP-2 wie in den nicht PTEN-defizienten Kontrollzellen gefunden. Die pharmakologische Hemmung der PI3K und AKT bewirkten eine signifikante Senkung der IGFBP-2 Expression und Sekretion, wohingegen sich bei Hemmung der MEK und des mTORC1 keine Effekte zeigten. Diese Ergebnisse weisen darauf hin, dass eine heterozygote PTEN-Deletion in Lipomzellen nicht zu einer erhöhten IGFBP-2 Produktion führt und daher die erhöhten Serumspiegel des Patienten nicht darauf zurückzuführen sind. Des Weiteren bestätigen die in vitro Ergebnisse die klinische Beobachtung, dass unter der Therapie mit dem mTORC1-Inhibitor Rapamycin die IGFBP-2 Serumspiegel des Patienten nicht zurückgingen. Möglicherweise stellt IGFBP-2 jedoch einen geeigneten Verlaufsmarker für eine Therapie mit PI3K- oder AKT-Inhibitoren dar.
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Books on the topic "IGFBP1"

1

Lai, Joe Heng. A polymorphic locus in the promoter region of the IGFBP3 gene is associated with mammographic breast density. Ottawa: National Library of Canada, 2003.

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Rauschnabel, Uta. RGD-spezifische Bindung von Insulin-ähnlichen Wachstumsfaktor Bindungsprotein 2 (IGFBP-2) an [alpha]5[beta]1-Integrinrezeptoren [alpha beta-Integrinrezeptoren] auf der Oberfläche von Ewingsarkom Zellen und IGF-unabhängige Effekte. Stuttgart, Augustenstr. 97: U. Rauschnabel, 2000.

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Hoeflich, Andreas, John Pintar, and Briony Forbes, eds. Current Perspectives on Insulin-like Growth Factor Binding Protein (IGFBP) Research. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-718-2.

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Perks, Claire, and Shin-Ichiro Takahashi, eds. The Role of the IGF/Insulin-IGFBP Axis in Normal Physiology and Disease. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-142-5.

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F. Moosavinasab, J. Ghiasi Ghalehkand, O. Ghanbari, and S. Hassanpour. In ovo injection of IGF1 improves intestinal enzyme activity in broilers. Verlag Eugen Ulmer, 2015. http://dx.doi.org/10.1399/eps.2015.94.

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Book chapters on the topic "IGFBP1"

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CCN3: NOV, IGFBP9, IGFBP-rP3." In Encyclopedia of Signaling Molecules, 282. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100183.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CCN1: Cyr61, CEF10, ßIG-M1, IGFBP10, IGFBP-rP4." In Encyclopedia of Signaling Molecules, 282. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100181.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CCN2: CTGF, FISP12, HCS24, ßIG-M2, HBGF-0.8, Ecogenin, IGFBP8, IGFBP-rP2." In Encyclopedia of Signaling Molecules, 282. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100182.

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Fang, Peng, Vivian Hwa, and Ron Rosenfeld. "IGFBPs and Cancer." In Biology of IGF-1: Its Interaction with Insulin in Health and Malignant States, 215–34. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470869976.ch14.

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Savage, M. O., J. C. Blair, A. J. Jorge, M. E. Street, M. B. Ranke, and C. Camacho-Hübner. "IGFs and IGFBPs in GH Insensitivity." In IGF-I and IGF Binding Proteins, 100–106. Basel: KARGER, 2005. http://dx.doi.org/10.1159/000085760.

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Powell, David R., Phillip D. K. Lee, and Adisak Suwanichkul. "Multihormonal Regulation of IGFBP-1 Promoter Activity." In Advances in Experimental Medicine and Biology, 205–14. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2988-0_20.

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Aimaretti, Gianluca, Roberto Baldelli, Ginevra Corneli, Chiara Croce,, Silvia Rovere, Claudia Baffoni, Simonetta Bellone, et al. "IGFs and IGFBPs in Adult Growth Hormone Deficiency." In IGF-I and IGF Binding Proteins, 76–88. Basel: KARGER, 2005. http://dx.doi.org/10.1159/000085758.

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Huynh, HoangDinh, Megan Kaba, Sonali Rudra, Junke Zheng, Catherine J. Wu, Harvey F. Lodish, and Cheng Cheng Zhang. "IGFBP2 Supports ex vivo Expansion of Hematopoietic Stem Cells." In Research and Perspectives in Endocrine Interactions, 21–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-04302-4_3.

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Holly, Jeff M. P., and Janet K. Fernihough. "The Insulin-Like Growth Factor (IGF) Binding Proteins (IGFBPS)." In Growth Hormone, 77–96. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5163-8_5.

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Mesotten, Dieter, and Greet Van den Berghe. "Changes Within the GH/IGF-I/IGFBP Axis in Critical Illness." In Acute Endocrinology, 181–98. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-177-6_9.

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Conference papers on the topic "IGFBP1"

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Slater, Tom, Alexander-Francisco Bruns, and Stephen Wheatcroft. "117 The divergent effects of IGFBP1 and IGFBP2 on vascular endothelial function." In British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.116.

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LeRoy, Elizabeth C., Elizabeth T. Jacobs, Erin L. Ashbeck, María Elena Martínez, Loic Le Marchand, Peter Lance, David Duggan, and Patricia A. Thompson. "Abstract 2853: Genetic variation in IGF1, GHR, and IGFBP1 is associated with colorectal cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2853.

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Kim, Jin Cheon, Ye Jin Ha, Ka Hee Tak, Seon Ae Roh, Chan Wook Kim, Tae Won Kim, Dong-Hyung Cho, Seon-Kyu Kim, Seon-Young Kim, and Yong Sung Kim. "Abstract 1641: Complex behavior of ALDH1A1 and IGFBP1 in liver metastasis of colorectal cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1641.

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Ungurs, O., M. Vetter, N. Pazaitis, J. Beer, C. Thomssen, and C. Wickenhauser. "Expression von IGF2BP1 in Ovarialkarzinomen." In 12. Jahrestagung der Mitteldeutschen Gesellschaft für Frauenheilkunde und Geburtshilfe e.V. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1645902.

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Backu, E., E. Aschenbrenner, K. Pollinger, S. Schlosser, K. Gülow, C. Kunst, and M. Müller-Schilling. "Relevanz von IGFBP2 im hepatozellulären Karzinom." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695235.

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Ahasic, Amy M., Rihong Zhai, Li Su, Konstantinos Aronis, Christos S. Mantzoros, B. T. Thompson, and David C. Christiani. "IGFBP3 Polymorphism Is Associated With Plasma Insulin-Like Growth Factor (IGF)-1 And Insulin-Like Growth Factor Binding Protein (IGFBP-3) In An Intensive Care Unit (ICU) Cohort." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3545.

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Lohse, M., D. Gschwind, E. Aschenbrenner, K. Pollinger, S. Schlosser, C. Kunst, and M. Müller-Schilling. "Die p53-Familie reguliert IGFBP2 beim hepatozellulären Karzinom." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1605129.

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Fathy, A., M. Habeb, S. Embarak, M. M. Zalat, and N. A. A. Oweedah. "Non-Invasive IGFBP 1 and IGFBP 2 Biomarkers as Predictors of Therapy and Outcomes in Usual Interstitial Pneumonia." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3079.

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Guiot, Julien, Monique Henket, Jean-Louis Corhay, and Renaud Louis. "Serum IGFBP2 as a marker of idiopathic pulmonary fibrosis." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3840.

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Kolligs, F., E. Backu, D. Gschwind, E. Aschenbrenner, K. Pollinger, K. Gülow, C. Kunst, and M. Müller-Schilling. "Dosisabhängige Effekte von IGFBP2 auf die Viabilität von Hepatomzellen." In Viszeralmedizin 2021 Gemeinsame Jahrestagung Deutsche Gesellschaft für Gastroenterologie, Verdauungs- und Stoffwechselkrankheiten (DGVS), Sektion Endoskopie der DGVS, Deutsche Gesellschaft für Allgemein und Viszeralchirurgie (DGAV). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1733618.

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Reports on the topic "IGFBP1"

1

Schoen, Timothy J. Expression and Characterization of Insulin-Like Growth Factor Binding Proteins (IGFBPs) and IGFBP-2 mRNA in the Developing Chicken Eye. Fort Belvoir, VA: Defense Technical Information Center, March 1995. http://dx.doi.org/10.21236/ad1011459.

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Funkenstein, Bruria, and Cunming Duan. GH-IGF Axis in Sparus aurata: Possible Applications to Genetic Selection. United States Department of Agriculture, November 2000. http://dx.doi.org/10.32747/2000.7580665.bard.

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Many factors affect growth rate in fish: environmental, nutritional, genetics and endogenous (physiological) factors. Endogenous control of growth is very complex and many hormone systems are involved. Nevertheless, it is well accepted that growth hormone (GH) plays a major role in stimulating somatic growth. Although it is now clear that most, if not all, components of the GH-IGF axis exist in fish, we are still far from understanding how fish grow. In our project we used as the experimental system a marine fish, the gilthead sea bream (Sparus aurata), which inhabits lagoons along the Mediterranean and Atlantic coasts of Europe, and represents one of the most important fish species used in the mariculture industry in the Mediterranean region, including Israel. Production of Sparus is rapidly growing, however, in order for this production to stay competitive, the farming of this fish species has to intensify and become more efficient. One drawback, still, in Sparus extensive culture is that it grows relatively slow. In addition, it is now clear that growth and reproduction are physiological interrelated processes that affect each other. In particular sexual maturation (puberty) is known to be closely related to growth rate in fish as it is in mammals, indicating interactions between the somatotropic and gonadotropic axes. The goal of our project was to try to identify the rate-limiting components(s) in Sparus aurata GH-IGF system which might explain its slow growth by studying the ontogeny of growth-related genes: GH, GH receptor, IGF-I, IGF-II, IGF receptor, IGF-binding proteins (IGFBPs) and Pit-1 during early stages of development of Sparus aurata larvae from slow and fast growing lines. Our project was a continuation of a previous BARD project and could be divided into five major parts: i) obtaining additional tools to those obtained in the previous project that are necessary to carry out the developmental study; ii) the developmental expression of growth-related genes and their cellular localization; iii) tissue-specific expression and effect of GH on expression of growth-related genes; iv) possible relationship between GH gene structure, growth rate and genetic selection; v) the possible role of the IGF system in gonadal development. The major findings of our research can be summarized as follows: 1) The cDNAs (complete or partial) coding for Sparus IGFBP-2, GH receptor and Pit-1 were cloned. Sequence comparison reveals that the primary structure of IGFBP-2 protein is 43-49% identical to that of zebrafish and other vertebrates. Intensive efforts resulted in cloning a fragment of 138 nucleotides, coding for 46 amino acids in the proximal end of the intracellular domain of GH receptor. This is the first fish GH receptor cDNA that had been cloned to date. The cloned fragment will enable us to complete the GH - receptor cloning. 2) IGF-I, IGF-II, IGFBP-2, and IGF receptor transcripts were detected by RT-PCR method throughout development in unfertilized eggs, embryos, and larvae suggesting that these mRNAs are products of both the maternal and the embryonic genomes. Preliminary RT-PCR analysis suggest that GH receptor transcript is present in post-hatching larvae already on day 1. 3) IGF-1R transcripts were detected in all tissues tested by RT-PCR with highest levels in gill cartilage, skin, kidney, heart, pyloric caeca, and brain. Northern blot analysis detected IGF receptor only in gonads, brain and gill cartilage but not in muscle; GH increased slightly brain and gill cartilage IGF-1R mRNA levels. 4) IGFBP-2 transcript were detected only in liver and gonads, when analyzed by Northern blots; RT-PCR analysis revealed expression in all tissues studied, with the highest levels found in liver, skin, gonad and pyloric caeca. 5) Expression of IGF-I, IGF-II, IGF-1R and IGFBP-2 was analyzed during gonadal development. High levels of IGF-I and IGFBP-2 expression were found in bisexual young gonads, which decreased during gonadal development. Regardless of maturational stage, IGF-II levels were higher than those of IGF-L 6) The GH gene was cloned and its structure was characterized. It contains minisatellites of tandem repeats in the first and third introns that result in high level of genetic polymorphism. 7) Analysis of the presence of IGF-I and two types of IGF receptor by immunohistochemistry revealed tissue- and stage-specific expression during larval development. Immunohistochemistry also showed that IGF-I and its receptors are present in both testicular and ovarian cells. Although at this stage we are not able to pinpoint which is the rate-limiting step causing the slow growth of Sparus aurata, our project (together with the previous BARD) yielded a great number of experimental tools both DNA probes and antibodies that will enable further studies on the factors regulating growth in Sparus aurata. Our expression studies and cellular localization shed new light on the tissue and developmental expression of growth-related genes in fish.
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3

Yee, Douglas A. Prevention of Breast Cancer by IGFBP. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada405491.

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Yee, Douglas A. Prevention of Breast Cancer in IGFBP. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada431788.

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Yee, Douglas. Prevention of Breast Cancer in IGFBP. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada421773.

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Chen, Xiaole, Peng Wang, Yunquan Luo, Yi-Yu Lu, Wenjun Zhou, Mengdie Yang, Jian Chen, Zhi-Qiang Meng, and Shi-Bing Su. Therapeutic Efficacy Evaluation and Underlying Mechanisms Prediction of Jianpi Liqi Decoction for Hepatocellular Carcinoma. Science Repository, September 2021. http://dx.doi.org/10.31487/j.jso.2021.02.04.sup.

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Abstract:
Objective: The aim of this study was to assess the therapeutic effects of Jianpi Liqi decoction (JPLQD) in hepatocellular carcinoma (HCC) and explore its underlying mechanisms. Methods: The characteristics and outcomes of HCC patients with intermediate stage B who underwent sequential conventional transcatheter arterial chemoembolization (cTACE) and radiofrequency ablation (RFA) only or in conjunction with JPLQD were analysed retrospectively. The plasma proteins were screened using label-free quantitative proteomics analysis. The effective mechanisms of JPLQD were predicted through network pharmacology approach and partially verified by ELISA. Results: Clinical research demonstrated that the Karnofsky Performance Status (KPS), traditional Chinese medicine (TCM) syndrome scores, neutropenia and bilirubin, median progression-free survival (PFS), and median overall survival (OS) in HCC patients treated with JPLQD were superior to those in patients not treated with JPLQD (all P<0.05). The analysis of network pharmacology, combined with proteomics, suggested that 52 compounds targeted 80 potential targets, which were involved in the regulation of multiple signaling pathways, especially affecting the apoptosis-related pathways including TNF, p53, PI3K-AKT, and MAPK. Plasma IGFBP3 and CA2 were significantly up-regulated in HCC patients with sequential cTACE and RFA therapy treated with JPLQD than those in patients not treated with JPLQD (P<0.001). The AUC of the IGFBP3 and CA2 panel, estimated using ROC analysis for JPLQD efficacy evaluation, was 0.867. Conclusion: These data suggested that JPLQD improves the quality of life, prolongs the overall survival, protects liver function in HCC patients, and exhibits an anticancer activity against HCC. IGFBP3 and CA2 panels may be potential therapeutic targets and indicators in the efficacy evaluation for JPLQD treatment, and the effective mechanisms involved in the regulation of multiple signaling pathways, possibly affected the regulation of apoptosis.
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Cobb, Laura. Understanding the Apoptotic Functions of IGFBP-3 in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2007. http://dx.doi.org/10.21236/ada593327.

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Cobb, Laura, and Pinchas Cohen. Understanding the Apoptotic Functions of IGFBP-3 in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada464008.

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Oh, Youngman. Role of IGFBP-3/IGFBP-3 Receptor Interaction in Normal and Malignant Mammary Growth: A Potential Diagnostic Parameter and New Strategy for Endocrine Therapy. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada392333.

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Zhang, Wei. The Cellular Localization of IGFBP5 Determines its Oncogenic Functions in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada457676.

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