Добірка наукової літератури з теми "Somatomedin"

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Статті в журналах з теми "Somatomedin":

1
&NA;. "Somatomedin-1." Reactions Weekly &NA;, no. 566 (September 1995): 11. http://dx.doi.org/10.2165/00128415-199505660-00040.
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&NA;. "Somatomedin 1." Reactions Weekly &NA;, no. 528 (November 1994): 12. http://dx.doi.org/10.2165/00128415-199405280-00048.
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&NA;. "Somatomedin 1." Reactions Weekly &NA;, no. 529 (November 1994): 9. http://dx.doi.org/10.2165/00128415-199405290-00034.
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&NA;. "Somatomedin-1." Reactions Weekly &NA;, no. 768 (September 1999): 11. http://dx.doi.org/10.2165/00128415-199907680-00037.
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Goldstein, Steven, Terry G. Unterman, and Lawrence S. Phillips. "Nutrition and Somatomedin." Annals of Nutrition and Metabolism 31, no. 6 (1987): 367–77. http://dx.doi.org/10.1159/000177296.
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6
Huybrechts, L. M., D. B. King, T. J. Lauterio, J. Marsh, and C. G. Scanes. "Plasma concentrations of somatomedin-C in hypophysectomized, dwarf and intact growing domestic fowl as determined by heterologous radioimmunoassay." Journal of Endocrinology 104, no. 2 (February 1985): 233–39. http://dx.doi.org/10.1677/joe.0.1040233.
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ABSTRACT The application of a human somatomedin-C radioimmunoassay for the determination of somatomedin-C in chicken plasma has been examined. Parallel inhibition of binding of 125I-labelled somatomedin-C to antisera raised against somatomedin-C was observed with acid-treated human and chicken plasma. The concentration of immunoreactive (IR)-somatomedin-C in the plasma of the domestic fowl appears to be GH dependent. Plasma concentrations of IR-somatomedin-C were reduced after hypophysectomy and partially restored by replacement therapy with chicken GH. The age/development pattern of circulating concentrations of IR-somatomedin-C has been determined in normal and dwarf strains of domestic fowl. Increases in the plasma concentration of IR-somatomedin-C were observed between 1 and 6 weeks of age in control male domestic fowl of either heavy (broiler type) or light (White Leghorn) strains. Thereafter, the plasma concentrations of IR-somatomedin-C remained constant in the heavy strain birds but declined in White Leghorn chicks. Plasma concentrations of IR-somatomedin-C were reduced in sex-linked dwarf chickens, in both light and heavy strains of fowl, but were unaffected in autosomal dwarf chickens. J. Endocr. (1985) 104, 233–239
7
Unterman, Terry G., Richard M. Vazquez, Anthony J. Slas, Pamela A. Martyn, and Lawrence S. Phillips. "Nutrition and somatomedin. XIII. Usefulness of somatomedin-C in nutritional assessment." American Journal of Medicine 78, no. 2 (February 1985): 228–34. http://dx.doi.org/10.1016/0002-9343(85)90431-0.
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8
Pavelić, K., D. Vrbanec, S. Marušić, S. Levanat, and T. Čabrijan. "Autocrine tumour growth regulation by somatomedin C: an in-vitro model." Journal of Endocrinology 109, no. 2 (May 1986): 233–38. http://dx.doi.org/10.1677/joe.0.1090233.
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ABSTRACT A human primary haemangiosarcoma was derived from a patient with severe hypoglycaemia. Cell line established from that tumour secreted somatomedin C in serum-free culture media. Immunoreactive somatomedin from the media eluted from Sephacryl S-200 in two peaks of 160 000 and 8000 molecular weights. Similar results were obtained when medium was acidified and chromatographed on Sephadex G-50. Binding of tracer concentrations of 125I-labelled somatomedin C to human haemangiosarcoma cells was much higher than that of 125I-labelled insulin. Half-maximal displacement of 125I-labelled somatomedin C binding occurred at an unlabelled somatomedin C concentration of 0·7 nmol/l. Insulin competed with 125I-labelled somatomedin for binding to this receptor, but 150-fold more insulin was required for half-maximal displacement. Somatomedin secreted by human haemangiosarcoma cells and purified from serum-free media strongly stimulated [methyl-3H]thymidine incorporation into the DNA of these cells. Inhibition of somatomedin C secretion by cortisol resulted in the inhibition of tumour cell proliferation but stimulation of somatomedin secretion by human GH stimulated the cell proliferation rate. It appears that production of somatomedin C in human haemangiosarcoma cells plays a part in the regulation of tumour growth by an autocrine mechanism. J. Endocr. (1986) 109, 233–238
9
Sifianou, P. "Somatomedin C: In Memoriam." Hormone and Metabolic Research 24, no. 08 (August 1992): 403. http://dx.doi.org/10.1055/s-2007-1003345.
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10
Le Roith, Derek, Carolyn Bondy, Shoshana Yakar, Jun-Li Liu, and Andrew Butler. "The Somatomedin Hypothesis: 2001." Endocrine Reviews 22, no. 1 (February 2001): 53–74. http://dx.doi.org/10.1210/edrv.22.1.0419.
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Abstract Since the original somatomedin hypothesis was conceived, a number of important discoveries have allowed investigators to modify the concept. Originally somatic growth was thought to be controlled by pituitary GH and mediated by circulating insulin-like growth factor-I (IGF-I, somatomedin C) expressed exclusively by the liver. With the discovery that IGF-I is produced by most, if not all, tissues, the role of autocrine/paracrine IGF-I vs. the circulating form has been hotly debated. Recent experiments using transgenic and gene-deletion technologies have attempted to answer these questions. In the liver-specific igf-1 gene-deleted mouse model, postnatal growth and development are normal despite the marked reduction in circulating IGF-I and IGF-binding protein levels; free IGF-I levels are normal. Thus, the normal postnatal growth and development in these animals may be due to normal free IGF-I levels (from as yet unidentified sources), although the role of autocrine/paracrine IGF-I has yet to be determined.

Дисертації з теми "Somatomedin":

1
Dodson, Michael Verne. "EFFECTS OF INSULIN AND INSULIN-LIKE GROWTH FACTORS ON SATELLITE CELL PROLIFERATION IN VITRO (SOMATOMEDINS, RECEPTORS)." Dissertation-Reproduction (electronic), The University of Arizona, 1985. http://hdl.handle.net/10150/188065.
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Primary cultures of skeletal muscle satellite cells were induced to proliferate by exposure to physiologic levels of somatomedins and pharmacologic levels of insulin. Dexamethasone inclusion in serum containing medium facilitated the ovine somatomedin (oSm) (P < 0.05), but that both were different than the proliferation induced by MSA/rIGF-II (P < 0.05). In the presence of insulin concentrations that promote maximum proliferation, addition of oSm did not produce an additive effect, whereas the addition of MSA/rIGF-II did produce a significant increase in satellite cell proliferation above that induced by insulin. A more, in depth, analysis of the interaction of MSA/rIGF-II with its satellite cell receptor under a variety of experimental conditions revealed that binding of ¹²⁵I-MSA/rIGF-II was inhibited by oSm and MSA/rIGF-II, but not by insulin. Migration, and localization of ¹²⁵I-MSA/rIGF-II-receptor complexes in 7% sodium dodecyl sulfate polyacrylamide gels suggest that these complexes are Type II IGF receptors. In addition, this receptor system of satellite cells was shown to be modulated by other hormones; notably, pre-exposure of cells with insulin increased ¹²⁵I-MSA/rIGF-II binding, while oSm, or MSA/rIGF-II preincubation decreased the binding of ¹²⁵I-MSA/rIGF-II. Therefore, the proliferative effects of MSA/rIGF-II appeared not as a consequence of MSA/rIGF-II induction of other receptor types such as the insulin, or Type I IGF receptor systems. Concommitant to the previous experimentation, oSm was further examined in an initial attempt to elucidate its biologic binding mechanism in myogenic satellite cells. Binding of ¹²⁵I-oSm was inhibited by MSA/rIGF-II, insulin and IGF-I; thus these data suggest that oSm may be the ovine analog to human IGF-I. In addition, pre-exposure of cells to MSA/rIGF-II and oSm down-regulated the ability of satellite cells to bind oSm, while only concentrations of insulin greater than 550 ng insulin had this ability. Collectively, these data support the hypothesis that somatomedins play an important role in the control of postnatal muscle growth by providing a link between these hormones and satellite cells, one of the significant target cells involved in the growth process.
2
涂文偉 and Wenwei Tu. "Effects of insulin-like growth factor 1 on cord blood T cell development." PG_Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31239377.
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3
Joseph, Suman C. "Allelic variations in the chicken insulin-like growth factor-I gene : effects on traits of economic importance in poultry." Electronic Thesis or Dissertation, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35902.
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Due to the importance of insulin-like growth factor-I (IGF-I) in regulating many physiological and metabolic processes, the IGF-I gene was chosen as a candidate gene to study trait associated polymorphisms in chickens. A PstI restriction fragment length polymorphism (RFLP) was detected at the 5' region of the gene and mapped to about 7 Kb upstream of the published promoter sequence. Analysis for association of the marker with traits of economic importance in an unselected, random-bred population of 359 White Leghorns revealed a significant association with egg weight (P ≤ 0.05) and specific gravity (P ≤ 0.05). There was also a trend for association with juvenile body weight (P = 0.08) but not adult body weight. For egg weight the PstI (-/-) genotype was associated with lower egg weight as compared to the heterozygote or the PstI (+/+) genotype. The PstI marker also was found to be significantly associated with differences in trait correlations. A regulatory loop that co-ordinated feed consumption, body weight, egg weight and rate of egg laying was detected, and this regulatory loop differed among the IGF-I genotypic classes. In the PstI (+/-) genotype, the degree of correlation between some of the traits was time dependent, while in the PstI (+/+) genotype it remained constant through the different periods of measurement. Since IGF-I is known to play an important role in immune functions, the association of the IGF-I genotypes with immune traits was also investigated. A significant association was found for delayed type hypersensitivity, interferon production and T-cell count (P ≤ 0.05). Individuals belonging to the PstI (+/-) genotypic class exhibited higher immune response, reflected by the delayed type hypersensitivity reaction and antibody the interactive effects of marker genotypes in the GH, GH-receptor and IGF-I genes on traits and trait correlations indicated that the three are part of an epistatic pathway, wherein the phenotypic consequences of
4
Brice, Amy L. "Growth factors and lipid transport in early mammalian development." Electronic Thesis or Dissertation, University of Oxford, 1990. http://ora.ox.ac.uk/objects/uuid:63dddafd-edd7-4c90-8b22-17b9ef81f96f.
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5
Ryder, Jeffrey W. "The effects of fasting and refeeding on insulin-like growth factor-I stimulated glucose transport." Virtual Press, 1996. http://liblink.bsu.edu/uhtbin/catkey/1020146.
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Insulin-like growth factor-I (IGF-I) is a known stimulator of glucose transport. IGF binding protein 1 (IGFBP1) is a protein that regulates the actions of IGF-I by binding to IGF-I which alters it's ability to bind to the IGF-I receptor. Diet and exercise may influence this system. While IGFBP1 levels increase with fasting or prolonged exercise, feeding will reverse this elevation. The intent of this study was to determine if an in vivo manipulation of IGFBP1 affects in vitro glucose transport in the rat soleus. Sixteen male Spaque Dawley rats were fasted for 12 hours. Half of the animals were then allowed a two hour ad libitum refeeding period. Animals were anesthetized and had their soleus muscles removed. Muscles were then randomly assigned to one of four treatment groups. Treatments involved an incubation in either 4 or 8 mM glucose in either the presence or absence of IGF-I (75 ng x ml"'). Final incubation for all treatment groups included [3H]-3-O-methylglucose (437 µCi x mM-) for the measurement of glucose transport. Following incubation, muscles were weighed, homogenized in 1 ml of 10% trichloroacetic acid, and centrifuged to precipitate out protein. 100 µl of the supernatant was added to 3 ml of scintillation fluid and analyzed in a scintillation counter. Glucose transport was determined by 3H activity. A statistical analysis of the various groups shows that there is no significant difference between fasted and refed animal for any specific treatment. However, when all the fasted and refed animals area grouped, glucose transport rate is significantly greater (p<0.05) in fasted (3.59 ± 0.44 µM x ml"' x hr) animals than in refed animals (2.56 ± 0.27 µM x ml"' x hr'). Additionally, muscles that were treated with IGF-I in 8 mM glucose demonstrated a greater rate of glucose transport (5.12 ± 0.68 µM x ml-1 x hr') than all other treatments (2.13 ± 0.39 to 2.90 ± .33 µM x ml-' x hr'). This study showed that IGF-I is a stimulator of glucose transport in an 8 mM glucose media. Additionally, the results show that glucose transport is greater if the animals are fasted. The differences between fasted and refed animals demonstrated in this study supports the hypothesis that diet manipulated IGFBP1 levels are able to alter the biological effects of IGF-I.
School of Physical Education
6
沈維華 and Weihua Shen. "Stability and absorption of milk-borne growth factors in the gastrointestinal tract of neonatal pigs." PG_Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31237642.
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Gao, Shan. "Screen for proteins that regulate sensitivity to inhibition of the insulin-like growth factor 1 receptor." Electronic Thesis or Dissertation, University of Oxford, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.565965.
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The type 1 insulin-like growth factor receptor (lGF-1 R) plays a significant role in tumor growth and spread, and IGF-1 R inhibitors and antibodies are now undergoing clinical testing. However, factors that regulate sensitivity to IGF-1 R inhibition remain unclear. The aim of this project is to identify proteins whose depletion regulates sensitivity to IGF-1 R inhibition, in order to design effective combination treatments to benefit patients. An IGF-1 R kinase inhibitor, AZ12253801 (provided by AstraZeneca) was able to block IGF-induced phosphorylation of IGF-1 R in DU145 prostate cancer and MCF-7 breast cancer cells, inhibited downstream signalling in DU145 cells, and also inhibited proliferation and cell survival of both cell lines. AZ12253801 was used in an unbiased siRNA screen in both cell lines, using two s'iRNA libraries (779 kinase-related Kinome and 230 DNA repair-associated siRNAs). Eight Kinome and five DNA repair-associated hits have been identified after primary and second round screens, and further validated. The strongest hit was dishevelled homolog 3 (DVL3), a member of the WNT signalling pathway, which is highly expressed in both cell lines. DVL3 silencing caused reduction in active l3-catenin and inactivated the mTOR pathway, consistent with previous studies, and did not affect IGF-1 Rand AKT activity. However, DVL3 silencing led to activation of MEK1/2-ERK1/2 in serum-starved cells and sensitized this pathway to IGF-1 stimulation, with translocation of ERK1/2 into the nucleus and increased expression of ERK1/2 target genes. A DVL PDZ domain inhibitor (DVLi) showed similar effects on active l3-catenin, mTOR signalling and ERK1/2 signalling activity. The administration of DVLi increased sensitivity to AZ12253801 in cell lines with detectable ERK1/2 activation, but not prostate cancer cells in which ERK signalling was suppressed and AKT was activated in the context of loss of functional PTEN. Furthermore, DVL3 regulated activation of ERKs by influencing signaling downstream of the IGF-1 R and upstream of RAS, and DVL3 was found in a complex with the adaptor proteins GRB2 and DAB2. GRB2 knockdown was capable of abolishing ERK1/2 activation induced by DVLi, further implicating involvement of GRB2, and DAB2 silencing sensitized to IGF-1 R inhibition, mimicking effects of DVL3 depletion. Taken together, DVL3 silencing or inhibition enhances sensitivity to IGF-1 R inhibition by negatively regulating the ERK1/2 signaling pathway. These investigations shed new light on the factors that regulate IGF signaling, and provide a rational basis for design of clinical trials of IGF-1 R inhibitors.
8
Chui, Shiu Hon. "Biochemical and pharmacological effects of Chinese medicines on homocysteine and insulin-like growth factor-1 in health and in disease." Text, HKBU Institutional Repository, 2001. http://repository.hkbu.edu.hk/etd_ra/539.
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Woll, Steven Cody. "Insulin-like Growth Factor Pathway Described in Austrofundulus limnaeus Diapause and Escape Embryos." Text, PDXScholar, 2008. https://pdxscholar.library.pdx.edu/open_access_etds/3207.
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Development in the annual killifish Austrofundulus limnaeus can follow two distinct developmental trajectories. Typical development includes the entrance of embryos into a state of metabolic and developmental arrest termed diapause. Alternately, embryos can escape diapause and develop directly without pause. These two trajectories are characterized by differences in the rate and timing of developmental, morphological, and physiological traits. Insulin and Insulin-like growth factor (IGF) signaling (IIS) is known to regulate entrance into diapause in a variety of invertebrates. In this thesis I explore the possible role of IGFs in the regulation of development and diapause in embryos of A. limnaeus. Here I report stage-specific expression of IGF-I and II proteins and their associated mRNA transcripts. Patterns of IGF-I protein expression are consistent with IGF signaling playing a major role in supporting the escape trajectory. In addition, treatment of embryos with a potent inhibitor of the IGF-I receptor (IGF1R) mimics the diapause developmental pattern even under conditions that should favor direct development. Evaluation of mRNA gene expression patterns in the two developmental trajectories suggests a role for IGF-I signaling through the RAS-MAPK-ERK pathway, which may be promoting the escape phenotype. Additionally, IGF-I activity may be enhanced in escape trajectory embryos though upregulation of IGF binding protein 2 (IGFBP-2) mRNA. These data suggest a major role for IGF signaling in the promotion of the escape trajectory, and thus we predict that specific mechanisms are in place in diapause-bound embryos that block IGF signaling and thus promote entrance into diapause. The data presented here suggest that blocking IGF signaling is critical for induction of diapause, but also suggests that other signaling pathways are likely also at play. Other pathways such at the TGF-beta signaling molecules and SMAD pathway, may also be involved in the direct regulation of the diapause phenotype, as has been shown for other animal models of developmental arrest.
10
Durrer, Katherine Elaine. "Impact of a Genetically Engineered Probiotic Therapy and IGF-1 Genomics in the PAHenu2 Mouse Model of PKU." Thesis or Dissertation, University of North Texas, 2012. https://digital.library.unt.edu/ark:/67531/metadc822730/.
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Absence of functional phenylalanine hydroxylase results in phenylketonuria (PKU). Viable treatments remain few, expensive and secondary conditions such as osteopenia occur in most PKU patients. Objective 1: Given the recently described roles of gut microbes to aid host digestion, an orally administered genetically engineered probiotic as the delivery vehicle for enzyme replacement therapy was created. The engineered probiotic, pHENOMMenal, produced phenylalanine ammonia lyase with significant production of trans-cinnamate (phenylalanine cleavage product) in vitro and resulted in a reduction of 515 μM in blood phenylalanine when fed to PKU animals for 14 days (from 2307µM ± 264µM to 1792µM ± 261µM, n = 6, P < 0.05). The control probiotic produced no change in blood phenylalanine. Thus, pHENOMMenal treatment in PKU mice demonstrated engineered microbes could compensate for a metabolic deficiency of the host. Objective 2: Evaluate the PAHenu2 mouse model of PKU for a genetic discrepancy causing ocular enlargement and delayed development observed only after the PAHenu2 mutation was crossed to the C57BL/6J mouse. When compared to healthy littermates, ELISA indicated a consistent but insignificant decrease in plasma IGF-1 and an increase in ocular IGF-1 in PKU animals. SNP screening demonstrated a differential inheritance of IGF-1 alleles in healthy and PKU animals based on PAH allele inheritance. Ocular and developmental phenotypes in the PAHenu2 colony match those described in previous IGF-1 studies. Understanding the IGF-1 inheritance discrepancy will enable better osteopenia research using PAHenu2 mice and allow breeding of a healthier mouse colony for continued research. Collectively the results from this work describe a new therapeutic approach for treatment of PKU as well as a better understanding of the PAHenu2 mouse model to study this disease.

Книги з теми "Somatomedin":

1
Litwack, Gerald. Insulin and IGFs. Amsterdam: Academic Press, 2009.
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2
Hildahl, Jon. Endocrine regulation of flatfish metamorphosis: Growth hormone, insulin-like growth factor-I and their receptors in Atlantic halibut. [Gothenburg]: Göteborg University, Department of Zoology/Zoophysiology, 2007.
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3
Hildahl, Jon. Endocrine regulation of flatfish metamorphosis: Growth hormone, insulin-like growth factor-I and their receptors in Atlantic halibut. [Gothenburg]: Göteborg University, Department of Zoology/Zoophysiology, 2007.
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4
Ross, Conference on Pediatric Research (89th 1984 Carefree Ariz ). Somatomedins and other peptide growth factors--relevance to pediatrics: Report of the Eighty-ninth Ross Conference on Pediatric Research. Columbus, Ohio: Ross Laboratories, 1985.
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5
Lawlor, Margaret Ann. The role of the insulin-like growth factor-II/mannose-6-phosphate receptor in embryonic development. Dublin: University College Dublin, 1998.
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6
Novo, Nordisk International Conference on Growth (1992 Sydney N. S. W. ). Growth and sexual development. Chur, Switzerland: Harwood Academic Publishers, 1993.
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7
Hooghe-Peters, Elisabeth L. Growth hormone, prolactin, and IGF-1 as lymphohemopoietic cytokines. Austin: R.G. Landes, 1995.
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8
International, Symposium on Insulin-Like Growth Factors/Somatomedins (2nd 1991 San Francisco Calif ). Modern concepts of insulin-like growth factors: Proceedings of the Second International Symposium on Insulin-Like Growth Factors/Somatomedins held January 12-16, 1991 in San Francisco, California. New York: Elsevier, 1991.
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9
Colloque, médecine et recherche (8th :. 2008 Paris France). IGFs: Local repair and survival factors throughout life span. Heidelberg: Springer, 2010.
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10
International, Symposium on Insulin-Like Growth Factors (4th 1997 Tokyo Japan). Molecular mechanisms to regulate the activities of insulin-like growth factors: Proceedings of the 4th International Symposium on Insulin-like Growth Factors, at Tokyo International Forum, Tokyo, Japan, 21-24 October 1997. Amsterdam: Elsevier, 1998.
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Частини книг з теми "Somatomedin":

1
Kaplowitz, Paul B., and Steven D. Chernausek. "Somatomedin Receptors." In Peptide Hormone Receptors, edited by M. Y. Kalimi and J. R. Hubbard, 519–60. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110850246-011.
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2
Phillips, L. S., S. Goldstein, and J. D. Klein. "Somatomedin Inhibitors." In Molecular and Cellular Biology of Insulin-like Growth Factors and Their Receptors, 81–95. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5685-1_7.
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3
Hoffman, Andrew R., Susan N. Perkins, Ines Zangger, James Eberwine, Jack D. Barchas, Phillip James, Ron G. Rosenfeld, and Raymond L. Hintz. "Somatomedin Gene Expression." In Acromegaly, 45–53. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1913-9_6.
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4
Hintz, Raymond L. "The Somatomedin Binding Proteins." In Human Growth Hormone, 553–61. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-7201-5_44.
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5
Pòvoa, G., K. Hall, and V. P. Collins. "Studies on somatomedin binding protein." In Advances in Growth Hormone and Growth Factor Research, 121–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-11054-6_8.
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6
Phillips, L. S., and T. G. Unterman. "Increased Somatomedin Inhibitors in Renal Failure." In Human Growth Hormone, 575–84. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-7201-5_46.
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7
Underwood, Louis E., Eric P. Smith, Judson J. Van Wyk, David R. Clemmons, A. Joseph D’Ercole, M. R. Pandian, Michael A. Preece, and Wayne V. Moore. "Somatomedin C/Insulinlike Growth Factor I." In Human Growth Hormone, 609–19. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-7201-5_49.
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8
Li, Choh Hao. "Synthetic Somatomedin C/Insulinlike Growth Factor I." In Human Growth Hormone, 521–27. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-7201-5_41.
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9
Rosenfeld, Ron G., Gian Paolo Ceda, Darrell M. Wilson, and Andrew R. Hoffman. "Somatomedin Action and Tissue Growth Factor Receptors." In Acromegaly, 55–63. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1913-9_7.
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10
Nissley, S. Peter, Lynne A. Gaynes, and Robert M. White. "Somatomedin/Insulinlike Growth Factor in the Human Fetus." In Human Growth Hormone, 621–34. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-7201-5_50.
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Тези доповідей конференцій з теми "Somatomedin":

1
Wasi, S., P. Alles, D. Gauthier, U. Bhargava, J. Farsi, J. E. Aubin, and J. Sodeki. "STUDIES ON SMALL MOLECULAR WEIGHT ADHESION PROTEINS (SAPs) FROM CONNECTIVE TISSUES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643556.
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Анотація:
We have identified a family of low molecular weight proteins with cell attachment properties in a variety of soft and mineralised connective tissues (Wong et al., Biochem. J. 232, 119, 1985). For further characterisation of these proteins we extracted porcine bones with 4 M guanidine hydrochloride and purified the proteins on a series of gel filtration columns The purifed SAPs comprise three bands with Mr -14 000 -17 000. All three proteins bound to heparin-sepahrose in both the presence and absence of 4M urea, and when eluted with 2 M NaCl they retained their cell binding capacity. These proteins promoted the adhesion and spreading of a variety of cell types, including normal fibroblasts, osteoblasts, and epithelial cells, and tumour (osteosarcoma) cells. On Western blotting SAPs did not cross-react with antibodies against fibronectin, laminin or type I collagen; however, they were recognised by a monoclonal antibody to human vitronectin, a polyclonal antibody to bovine vitronectin and polyclonal antibody to human somatomedin B. Dose response experiments indicated that maximum attachment of human gingival fibroblasts occurred in the presence or absence of fetal bovine serum on wells precoated with 2.5 μg/cm2 of SAPs. Attachment of cells to these proteins was partially inhibited by the synthetic pentapeptide Gly-Arg-Gly-Asp-Ser. Utilising the nitrocellulose cell binding assay of Hayman et al (J. Cell. Biol. 95, 20, 1982), the cell attachment to these proteins could be completely inhibited by heparin (100 units/mL) whereas up to 1000 units/mL of heparin had no inhibitory effect on cell attachment to fibronectin and vitronectin. The occurrence of these proteins in a variety of connective tissues and their recognition by different cell types may reflect their general biological role in adhesive mechanisms in both hard and soft connective tissues. Currently, we are investigating the relationship between SAPs and vitronectin, since it is possible that SAPs represent a tissue-processed form of vitronectin or may be novel attachment proteins with regions of homology with vitronectin

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