Thematische Bibliographien / TGF alpha [Transforming Growth Factor]

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  4. Buchteile
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Auswahl der wissenschaftlichen Literatur zum Thema „TGF alpha [Transforming Growth Factor]“

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Veröffentlicht am 18. Mai 2024

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Zeitschriftenartikel zum Thema "TGF alpha [Transforming Growth Factor]"

1

Massagué, J. „Transforming growth factor-beta modulates the high-affinity receptors for epidermal growth factor and transforming growth factor-alpha.“ Journal of Cell Biology 100, Nr. 5 (01.05.1985): 1508–14. http://dx.doi.org/10.1083/jcb.100.5.1508.

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The epidermal growth factor (EGF) receptor mediates the induction of a transformed phenotype in normal rat kidney (NRK) cells by transforming growth factors (TGFs). The ability of EGF and its analogue TGF-alpha to induce the transformed phenotype in NRK cells is greatly potentiated by TGF-beta, a polypeptide that does not interact directly with binding sites for EGF or TGF-alpha. Our evidence indicates that TGF-beta purified from retrovirally transformed rat embryo cells and human platelets induces a rapid (t 1/2 = 0.3 h) decrease in the binding of EGF and TGF-alpha to high-affinity cell surface receptors in NRK cells. No change due to TGF-beta was observed in the binding of EGF or TGF-alpha to lower affinity sites also present in NRK cells. The effect of TGF-beta on EGF/TGF-alpha receptors was observed at concentrations (0.5-20 pM) similar to those at which TGF-beta is active in promoting proliferation of NRK cells in monolayer culture and semisolid medium. Affinity labeling of NRK cells and membranes by cross-linking with receptor-bound 125I-TGF-alpha and 125I-EGF indicated that both factors interact with a common 170-kD receptor structure. Treatment of cells with TGF-beta decreased the intensity of affinity-labeling of this receptor structure. These data suggest that the 170 kD high-affinity receptors for EGF and TGF-alpha in NRK cells are a target for rapid modulation by TGF-beta.
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2

Brown, P. I., R. Lam, J. Lakshmanan und D. A. Fisher. „Transforming growth factor alpha in developing rats“. American Journal of Physiology-Endocrinology and Metabolism 259, Nr. 2 (01.08.1990): E256—E260. http://dx.doi.org/10.1152/ajpendo.1990.259.2.e256.

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Transforming growth factor-alpha (TGF-alpha) concentrations were measured in lung, brain, liver, and kidney of rats at three different ages (20 days gestation and 9 and 50 days postnatal). TGF-alpha concentrations were maximal in the lung and brain by 20 days of gestation and showed minimal changes during nursing (day 9) and young adulthood (day 50). The liver, which also showed maximal TGF-alpha concentration by 20 days of gestation, demonstrated a progressive reduction with age to nadir values in the young adult. In contrast to the pattern in other tissues, kidney had the lowest concentration of TGF-alpha in late gestation and showed an increase by 50 days of age. As TGF-alpha acts via the epidermal growth factor (EGF) receptor, its function in development may be analogous to that of EGF. Thus TGF-alpha may have a role in lung maturation and postinjury repair, liver repair and regeneration, and neuronal cell growth.
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Wong, D. T., P. F. Weller, S. J. Galli, A. Elovic, T. H. Rand, G. T. Gallagher, T. Chiang, M. Y. Chou, K. Matossian und J. McBride. „Human eosinophils express transforming growth factor alpha.“ Journal of Experimental Medicine 172, Nr. 3 (01.09.1990): 673–81. http://dx.doi.org/10.1084/jem.172.3.673.

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Transforming growth factor alpha (TGF-alpha) is a pleuripotential cytokine with diverse biological effects, including the ability to influence the proliferation of normal cells or neoplastic epithelial cells. Eosinophils are a subset of granulocytes that normally enter the peripheral tissues, particularly those beneath gastrointestinal, respiratory, and urogenital epithelium, where they reside in close proximity to the epithelial elements. In this study, we demonstrate that the great majority of eosinophils infiltrating the interstitial tissues adjacent to two colonic adenocarcinomas and two oral squamous cell carcinomas labeled specifically by in situ hybridization with a 35S-riboprobe for human TGF-alpha (hTGF-alpha). No other identifiable leukocytes in these lesions contained detectable hTGF-alpha mRNA. We also examined leukocytes purified from a patient with the idiopathic hypereosinophilic syndrome. 80% of these eosinophils, but none of the patient's neutrophils or mononuclear cells, were positive for hTGF-alpha mRNA by in situ hybridization, and 55% of these eosinophils were positive by immunohistochemistry with a monoclonal antibody directed against the COOH terminus of the mature hTGF-alpha peptide. Finally, the identification of the purified eosinophil-associated transcript as hTGF-alpha was confirmed by polymerase chain reaction product restriction enzyme analysis followed by Southern blot hybridization. In contrast to eosinophils from the patient with hypereosinophilic syndrome, the peripheral blood eosinophils from only two of seven normal donors had detectable TGF-alpha mRNA and none of these eosinophils contained immunohistochemically detectable TGF-alpha product. Taken together, these findings establish that human eosinophils can express TGF-alpha, but suggest that the expression of TGF-alpha by eosinophils may be under microenvironmental regulation. Demonstration of TGF-alpha production by tissue-infiltrating eosinophils and the eosinophils in the hypereosinophilic syndrome identifies a novel mechanism by which eosinophils might contribute to physiological, immunological, and pathological responses.
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Lee, D. C., R. Rochford, G. J. Todaro und L. P. Villarreal. „Developmental expression of rat transforming growth factor-alpha mRNA“. Molecular and Cellular Biology 5, Nr. 12 (Dezember 1985): 3644–46. http://dx.doi.org/10.1128/mcb.5.12.3644-3646.1985.

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Expression of the gene encoding transforming growth factor-alpha (TGF alpha) was examined in developing rat embryos by using a cloned TGF alpha cDNA as a hybridization probe. Northern blot analysis of RNA isolated from whole fetuses revealed that TGF alpha mRNA was present at relatively high levels in 8- through 10-day-old embryos and then declined to the low or undetectable level, which is characteristic of adult tissues before birth. The level of TGF alpha mRNA present during early gestation was similar to that present in retrovirus-transformed cells in culture, suggesting that TGF alpha expression is not highly localized in the embryo. These observations are consistent with the hypothesis that TGF alpha plays a role in development, possibly as a fetal growth factor.
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Lee, D. C., R. Rochford, G. J. Todaro und L. P. Villarreal. „Developmental expression of rat transforming growth factor-alpha mRNA.“ Molecular and Cellular Biology 5, Nr. 12 (Dezember 1985): 3644–46. http://dx.doi.org/10.1128/mcb.5.12.3644.

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Expression of the gene encoding transforming growth factor-alpha (TGF alpha) was examined in developing rat embryos by using a cloned TGF alpha cDNA as a hybridization probe. Northern blot analysis of RNA isolated from whole fetuses revealed that TGF alpha mRNA was present at relatively high levels in 8- through 10-day-old embryos and then declined to the low or undetectable level, which is characteristic of adult tissues before birth. The level of TGF alpha mRNA present during early gestation was similar to that present in retrovirus-transformed cells in culture, suggesting that TGF alpha expression is not highly localized in the embryo. These observations are consistent with the hypothesis that TGF alpha plays a role in development, possibly as a fetal growth factor.
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Chen, M. C., A. T. Lee, W. E. Karnes, D. Avedian, M. Martin, J. M. Sorvillo und A. H. Soll. „Paracrine control of gastric epithelial cell growth in culture by transforming growth factor-alpha“. American Journal of Physiology-Gastrointestinal and Liver Physiology 264, Nr. 2 (01.02.1993): G390—G396. http://dx.doi.org/10.1152/ajpgi.1993.264.2.g390.

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Studying primary cultures of replicating canine oxyntic mucosal cells, we found evidence for modulation of cell growth by endogenous factors. [3H]thymidine incorporation into DNA was rapid with cells cultured in medium free of serum or added growth factors, and growth rates of these cultures were markedly dependent on plating density, indicating mitogenic control by soluble endogenous growth factors. Data indicated that endogenous transforming growth factor-alpha (TGF-alpha) exerted mitogenic control under the following conditions. 1) TGF-alpha was detected in the cultured cells by radioimmunoassay and immunohistochemistry. 2) TGF-alpha-like immunoreactivity and receptor reactivity were present in the medium in concentrations sufficient to exert mitogenic control. 3) Receptors for TGF-alpha and epidermal growth factor (EGF) were present in the cultures. 4) Immunoabsorption by a TGF-alpha-specific antisera reduced [3H]thymidine incorporation. TGF-alpha was localized to parietal cells by immunohistochemistry and cell separation. In contrast, combined [3H]thymidine autoradiography and immunohistochemistry with anti-TGF-alpha did not detect TGF-alpha in dividing cells. We conclude that parietal cell TGF-alpha exerts paracrine control of mucosal cell growth in vitro, and we speculate that this is an important paracrine mechanism in vivo.
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Ebner, R., und R. Derynck. „Epidermal growth factor and transforming growth factor-alpha: differential intracellular routing and processing of ligand-receptor complexes.“ Cell Regulation 2, Nr. 8 (August 1991): 599–612. http://dx.doi.org/10.1091/mbc.2.8.599.

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Two structurally related but different polypeptide growth factors, epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha), exert their activities after interaction with a common cell-surface EGF/TGF-alpha-receptor. Comparative studies of the effects of both ligands have established that TGF-alpha is more potent than EGF in a variety of biological systems. This observation is not explained by differences in affinities of the ligands for the receptor, because the affinity-constants of both factors are very similar. We have compared the intracellular processing of ligand-receptor complexes using either EGF or TGF-alpha in two different cell systems. We found that TGF-alpha dissociates from the EGF/TGF-alpha-receptor at much higher pH than EGF, which may reflect the substantial difference in the calculated isoelectric points. After internalization, the intracellular TGF-alpha is more rapidly cleared than EGF, and a substantial portion of the released TGF-alpha represents undegraded TGF-alpha in contrast to the mostly degraded EGF. In addition, TGF-alpha did not induce a complete down-regulation of cell surface receptors, as observed with EGF, which is at least in part responsible for a much sooner recovery of the ligand-binding ability after down-regulation, in the case of TGF-alpha. These differences in processing of the ligand-receptor complexes may explain why TGF-alpha exerts quantitatively higher activities than EGF.
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Han, V. K. M., A. J. D'Ercole und D. C. Lee. „Expression of transforming growth factor alpha during development“. Canadian Journal of Physiology and Pharmacology 66, Nr. 8 (01.08.1988): 1113–21. http://dx.doi.org/10.1139/y88-183.

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Transforming growth factors (TGFs) are polypeptides that are produced by transformed and tumour cells, and that can confer phenotypic properties associated with transformation on normal cells in culture. One of these growth-regulating molecules, transforming growth factor alpha (TGF-α), is a 50 amino acid polypeptide that is related to epidermal growth factor (EGF) and binds to the EGF receptor. Previous studies have shown that TGF-α is expressed during rodent embryogenesis between 7 and 14 days gestation. To investigate the cellular sites of TGF-α mRNA expression during development, we have performed Northern analyses and in situ hybridization histochemistry on the conceptus and maternal tissues at various gestational ages. Contrary to previous reports, both Northern analyses and in situ hybridization histochemistry indicate that TGF-α mRNA is predominantly expressed in the maternal decidua and not in the embryo. Decidual expression is induced following implantation, peaks at day 8, and declines through day 15 when the decidua is being resorbed. In situ hybridization revealed that expression of TGF-α mRNA is highest in the region of decidua adjacent to the embryo and is low or nondetectable in the uterus, placenta, and embryo. In addition, we could not detect TGF-α mRNA expression in other maternal tissues, indicating that the induction of TGF-α transcripts in the decidua is tissue specific, and not a pleiotropic response to changes in hormonal milieu that occur during pregnancy. The developmentally regulated expression of TGF-α mRNA in the decidua, together with the presence of EGF receptors in this tissue, suggests that this peptide may stimulate mitosis and angiogenesis locally by an autocrine mechanism. Because EGF receptors are also present in the embryo and placenta, TGF-α may act on these tissues by a paracrine or endocrine mechanism.
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Quigley, R., und M. Baum. „Effects of epidermal growth factor and transforming growth factor-alpha on rabbit proximal tubule solute transport“. American Journal of Physiology-Renal Physiology 266, Nr. 3 (01.03.1994): F459—F465. http://dx.doi.org/10.1152/ajprenal.1994.266.3.f459.

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The present in vitro microperfusion study examined the direct effects of epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha) on rabbit proximal convoluted tubule (PCT) solute transport. Tubules were perfused with an ultrafiltrate-like solution and bathed in an ultrafiltrate-like solution containing albumin. Albumin binding studies showed that both growth factors were highly protein bound with a free fraction of EGF of 0.31 +/- 0.04% and TGF-alpha of 1.08 +/- 0.15%. EGF at concentrations from 3 x 10(-11) M to 3 x 10(-8) M stimulated phosphate transport (JPhos) in a dose-dependent fashion but did not affect volume absorption (Jv) or bicarbonate transport (JtCO2). At 3 x 10(-7) M, EGF stimulated PCT Jv and JtCO2 in addition to the stimulation in JPhos. TGF-alpha stimulated Jv, JtCO2, and JPhos, but its effects were seen at a concentration that was 100-fold lower than that where EGF affected PCT transport. At 3 x 10(-13) M, TGF-alpha stimulated JtCO2, and at 3 x 10(-12) M, TGF-alpha also stimulated Jv and JPhos. EGF receptor downregulation with 3 x 10(-8) M EGF was able to block the effect of 3 x 10(-10) M TGF-alpha on Jv and JtCO2. Neither luminal EGF nor TGF-alpha had an effect on PCT transport. PCT bicarbonate and mannitol permeabilities were also not affected by either growth factor. These results demonstrate that EGF and TGF-alpha have direct effects on PCT solute transport.
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Ryan, R. M., M. M. Mineo-Kuhn, C. M. Kramer und J. N. Finkelstein. „Growth factors alter neonatal type II alveolar epithelial cell proliferation“. American Journal of Physiology-Lung Cellular and Molecular Physiology 266, Nr. 1 (01.01.1994): L17—L22. http://dx.doi.org/10.1152/ajplung.1994.266.1.l17.

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The type II alveolar epithelial cell plays a critical role in the repair of lung injury by repopulating the entire damaged alveolar epithelium. We report our studies of the effects of known growth factors on the in vitro proliferation of isolated neonatal rabbit type II cells. Transforming growth factor-alpha (TGF-alpha) and epidermal growth factor (EGF) increased [3H]thymidine incorporation, cell number, and labeling index above control. Transforming growth factor-beta (TGF-beta) decreased [3H]thymidine incorporation, cell number, and labeling index compared with control. When added simultaneously, TGF-beta blocked the stimulatory effect of TGF-alpha or EGF. If TGF-alpha is added before TGF-beta, the ability of TGF-beta to block the mitogenic effect of TGF-alpha was diminished the later in time TGF-beta was added. If TGF-beta was added first, later addition of TGF-alpha had no effect. The current work demonstrates that specific growth factors, including some known to be produced by other lung cells, alter the proliferation in vitro of isolated neonatal rabbit type II alveolar epithelial cells.
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Dissertationen zum Thema "TGF alpha [Transforming Growth Factor]"

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Chia, Choy May. „Epidermal growth factor (EGF) : transforming growth factor alpha (TGF-#alpha#) in human preimplantation development“. Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362631.

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Lau, Kwok-pui. „Clinicopathological roles of transforming growth factor alpha (TGF[alpha]) in papillary thyroid carcinoma /“. Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39558733.

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Lam, Sze-man Joyce. „Expression of transforming growth factors (TGF-alpha and TGF-beta 1) on postmortem skin wounds /“. View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38480566.

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Liu, Xiaoying. „Molecular mechanisms of myofibroblast differentiation and the role of TGF beta1, TNF alpha, and thrombin signal transduction“. Columbus, Ohio : Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1236711907.

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Glinsmann-Gibson, Betty Jean 1961. „Molecular mechanism of autocrine regulation by TGF-alpha in T(3)M(4) human pancreatic carcinoma cells“. Thesis, The University of Arizona, 1989. http://hdl.handle.net/10150/277113.

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The human pancreatic cancer cell line T3M4, is known to produce transforming growth factor-alpha (TGF-alpha); as well as overexpress the receptor for this ligand, epidermal growth factor (EGF) receptor. TGF-alpha messenger RNA (mRNA) levels were assayed using northern blot, after addition of epidermal growth factor or TGF-alpha. The level of TGF-alpha mRNA was found to increase 2-fold at 2 hours and then return to near basal levels at 10 hours, after treatment with either ligand. Both ligands were also equipotent in a 2 hour dose response assay, with half maximal stimulation seen at 1 nM and maximal stimulation reached at 4 nM. Furthermore, there appeared to be a 2-fold increase in TGF-alpha transcription as determined by nuclear runoff experiments. Induction of TGF-alpha mRNA coupled with the overexpression of the EGF receptor, may result in a potent autocrine cycle; which may be found in other cancers.
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Hallbeck, Anna-Lotta. „Studies of transforming growth factor alpha in normal and abnormal growth“. Doctoral thesis, Linköping : Univ, 2007. http://www.bibl.liu.se/liupubl/disp/disp2007/med1025s.pdf.

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林詩敏 und Sze-man Joyce Lam. „Expression of transforming growth factors (TGF-alpha and TGF-beta 1) on postmortem skin wounds“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011400.

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Kiesow, Claudia. „Pathogenese der equinen Endometrose: Bedeutung der Wachstumsfaktoren Transforming growth factor-alpha, -beta1, -beta2 und -beta3 sowie der Matrixmetalloproteinase-2“. Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-65079.

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Ziel der vorliegenden Arbeit war die immunhistologische Charakterisierung der Expression der profibrotischen Wachstumsfaktoren Transforming growth factor-beta-1, -beta2 und -beta3 und des Enzyms Matrixmetalloproteinase-2 (MMP-2) im equinen Endometrium während des Zyklus sowie innerhalb der verschiedenen Erscheinungsformen der equinen Endometrose. Zudem wurde der potentielle Einfluss einer gleichzeitig auftretenden Endometritis auf die glanduläre und stromale Wachstumsfaktor- und Enzym-Expression untersucht. Die Ergebnisse dieser Studie sollten klären, ob und inwieweit den untersuchten Wachstumsfaktoren unter Beteiligung von MMP-2 in der Pathogenese der equinen Endometrose eine mit anderen Organfibrosen vergleichbare Schlüsselrolle zukommt. Zu diesem Zweck standen an definierten Tagen entnommene Endometriumbioptate (n=21) von drei zyklisch aktiven, klinisch und gynäkologisch gesunden Maidenstuten sowie Endometriumbioptate von 60 Stuten mit graduell variabler Endometrose unterschiedlichen Charakters und Endometriumbioptate von 22 Stuten mit mittelgradiger Endometrose und gleichzeitiger mittelgradiger eitriger (n=16) bzw. nichteitriger (n=6) Endometritis aus dem Routineeinsendungsmaterial des Institutes für Veterinär-Pathologie der Universität Leipzig zur Verfügung. Die Wachstumsfaktoren TGF-beta1, -beta2 und -beta3 sowie das Enzym MMP-2 zeigen im Zyklus ein typisches, zellspezifisches Reaktionsmuster, das unterschiedlichen Regulations-mechanismen zu unterliegen scheint. Ein Maximum der TGF-beta1-Expression in den luminalen Epithelzellen, Stroma- und Drüsenzellen kann in der endometrialen Sekretionsphase mit Anstieg bzw. einem Maximum der Serumprogesteron-Konzentration beobachtet werden. Im Gegensatz dazu tritt eine Expression von MMP-2 in den Stromazellen in der Sekretionsphase mit Abfall der Progesteronkonzentration im Serum auf. Das luminale Epithel und die Stromazellen zeigen eine maximale Expression von TGF-beta2 beim Vorliegen hoher Progesteronspiegel im Serum bzw. mit Abfall der Serumprogesteron-Konzentration in der Sekretionsphase. TGF-beta3 weist im luminalen Epithel ein ähnliches Expressionsmuster auf, eine deutliche Abhängigkeit zu den Serumhormon-Konzentrationen lässt sich jedoch nicht feststellen. Die stromale Expression von TGF-alpha unterliegt im equinen Endometrium keinen zyklusabhängigen Variationen. Die Stromazellen innerhalb der verschiedenen Endometroseherde zeigen, im Vergleich zum unveränderten Endometrium, vor allem eine verminderte Expression von TGF-alpha. Das Expressionsmuster der TGF-beta-Wachstumsfaktoren ist grundsätzlich variabel, es fällt jedoch auf, dass die Stromazellen insbesondere in inaktiven Endometrosen eine geringere Expression der TGF-beta-Isoformen aufweisen. Ursache ist möglicherweise eine gestörte hormonelle Stimulation bzw. eine stromale Synthesestörung in Folge veränderter epithelial/stromaler Wechselwirkungen. Das Enzym MMP-2 wird dagegen in den Stromazellen aller Endometroseherde, unabhängig von deren Differenzierung und dem Auftreten glandulärer Alterationen, deutlich vermehrt nachgewiesen. Dies ist sehr wahrscheinlich Folge der Extra-zellularmatrix-Akkumulation innerhalb der Endometroseherde und für die fortschreitende Zerstörung der glandulären Basalmembranen verantwortlich. Die glanduläre Expression innerhalb der Endometroseherde gleicht weitgehend der der unveränderten Drüsenzellen, lediglich in destruierenden Endometrosen werden TGF-alpha, TGF-beta2 und MMP-2 in den involvierten Drüsenzellen vermehrt nachgewiesen. Mögliche Ursachen wären eine Diffusion durch die geschädigte glanduläre Basalmembran bzw. eine Anregung der Synthese im Rahmen der epithelialen Wundheilung. Eine Anregung der glandulären und stromalen Expression der untersuchten Wachstumsfaktoren und des Enzyms MMP-2 im Rahmen der Endometrose durch die Anwesenheit von Entzündungszellen konnte nicht nachgewiesen werden. Eine der Leber- und Lungenfibrose ähnelnde, überschießende Wundheilungsreaktion durch eine primär epithelial bedingte, vermehrte TGF-Wachstumsfaktorproduktion sowie direkte Zusammenhänge zwischen der MMP-2- und TGF-beta-Wachstumsfaktor-Expression waren in der equinen Endometrose nicht festzustellen. Da vor allem die Stromazellen in der Endometrose eine veränderte Expression der Wachstumsfaktoren aufwiesen, ist möglicherweise eine primäre stromale Fehldifferenzierung der Ausgangspunkt für die Entstehung der Endometrose. Eine mit der Leber- und Lungenfibrose vergleichbare Schlüsselrolle der TGF-Wachstumsfaktoren in der Pathogenese der equinen Endometrose konnte nicht eindeutig belegt werden.
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劉國培 und Kwok-pui Lau. „Clinicopathological roles of transforming growth factor alpha (TGFα) in papillary thyroid carcinoma“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39558733.

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Freese, Christiane. „Rolle der Plasmakonzentrationen von transforming growth factor-[beta]1 [factor-beta1] (TGF[beta]1) [TGF beta 1], Tumor necrosis factor [alpha] [Tumor necrosis factor alpha] (TNF [alpha]) [TNF alpha] und Plasminogen-Activator-Inhibitor-(PAI-)-Antigen bei Patienten mit Diabetes Mellitus Typ 2 und koronarer Herzkrankheit“. [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=97149200X.

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Bücher zum Thema "TGF alpha [Transforming Growth Factor]"

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Rik, Derynck, und Miyazono Kōhei 1956-, Hrsg. The TGF-[beta] family. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2008.

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Gregory, Bock, Marsh Joan und Symposium on Clinical Applications of TGF-[beta] (1990 : Ciba Foundation), Hrsg. Clinical applications of TGF-[beta]. Chichester: Wiley, 1991.

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Al-Maatouq, Mohamed A. Transforming growth factor-alpha gene expression in the pituitary gland. Ottawa: National Library of Canada, 1990.

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Lew, April May. Partial isolation of cDNA for the transforming growth factor-alpha message. Ottawa: National Library of Canada, 1990.

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Benson, John R. TGF [beta] and cancer. Austin: R.G. Landes, 1998.

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Cruz, Briolange Maria. Transforming growth factor beta (TGF-[beta]) regulates macrophage procoagulant activity (PCA) induction by murine hepatitis virus strain 3 (MHV-3). Ottawa: National Library of Canada, 1994.

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Triningsih, Ediati. Expression of transforming growth factor alpha and beta mRNA in cervical neoplasia by in situ hybridisation. Manchester: University of Manchester, 1993.

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Battaglini, Michelina. Determination of the transforming growth factor-B (TGF-B) receptor on the surface of interleukin-2 activated natural killer (IANK) cells. Sudbury, Ont: Laurentian University, 1992.

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Spudich, Rani Karina. Effect of phenobarbital on extracellular matrix production, cell replication, transforming growth factor-B1 binding, and TGF-B receptor profile in rat dermal fibroblast cultures. [New Haven, Conn: s.n.], 1997.

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Dworkin, Chaim R. The use of growth factors in cancer therapy. [Bethesda, Md.?]: U.S. DHHS, PHS, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1993.

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Buchteile zum Thema "TGF alpha [Transforming Growth Factor]"

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El-Youssef, M., A. Hughes, K. J. Bloch, S. R. Martin und P. R. Harmatz. „Identification of tumor necrosis factor alpha (TNF-α) and transforming growth factor beta (TGF-β) in murine milk“. In Advances in Mucosal Immunology, 537–38. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_162.

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Wilkinson, Deepti S., und Michelle Craig Barton. „Tumor Suppressors p53 and TGFβ Converge to Regulate the Alpha-Fetoprotein Oncodevelopmental Tumor Marker“. In Transforming Growth Factor-β in Cancer Therapy, Volume II, 309–20. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-293-9_20.

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Williams, R. S., G. S. Schultz, T. E. Geoghegan, M. C. Steffan und M. A. Yussman. „Variations in the Level of Transforming Growth Factor-Alpha (TGFα) mRNA During the Human Menstrual Cycle“. In Growth Factors and the Ovary, 205–8. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5688-2_20.

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Wang, D. Y., W. H. Harris, I. S. Fentiman, H. Hamed und W. R. Miller. „Insulin-Like (IGF-I, IGF-II), Epidermal (EGF) and Alpha Transforming (TGF-α) Growth Factors in Human Breast Cyst Fluid (BCF)“. In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury, 471–74. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_93.

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Heldin, Carl-Henrik. „Transforming Growth Factor-β Signaling“. In TGF-β in Human Disease, 3–32. Tokyo: Springer Japan, 2013. http://dx.doi.org/10.1007/978-4-431-54409-8_1.

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Todorovic, Vesna, und Daniel B. Rifkin. „TGF-β Availability: Latent TGF-β and Latent TGF-β Binding Proteins“. In Transforming Growth Factor-β in Cancer Therapy, Volume I, 37–55. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-292-2_3.

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Wang, Guiying Y., Xiaochua H. Hu, Rongmei M. Zhang, Lindsey J. Leach und Zewei W. Luo. „TGF-β Ligands, TGF-β Receptors, and Lung Cancer“. In Transforming Growth Factor-β in Cancer Therapy, Volume II, 79–93. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-293-9_6.

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Gamble, Jennifer R., Pu Xia und Mathew A. Vadas. „The transforming growth factor family and the endothelium“. In TGF-β and Related Cytokines in Inflammation, 41–64. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8354-2_3.

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Salajegheh, Ali. „Transforming Growth Factor α and β (TGF-α and TGF-β)“. In Angiogenesis in Health, Disease and Malignancy, 331–37. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_53.

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Ebina, Masahito. „TGF-β in Pulmonary Fibrosis“. In Transforming Growth Factor-β in Cancer Therapy, Volume I, 569–80. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-292-2_35.

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Konferenzberichte zum Thema "TGF alpha [Transforming Growth Factor]"

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Gould, Russell, Karen Chin, Puifai Santisakultam, Amanda Dropkin, Jennifer Richards, Yung-Nung Chiu, Chris Schaffer und Jonathan Butcher. „Anisotropic Strain Fields Enhance Matrix Remodeling Through Elevated TGF-β Signaling“. In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53805.

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In this work, we demonstrate the unique effect of controlled anisotropic strain on fibroblast behavior in 3D engineered tissue environments. Anisotropy of biaxial strain resulted in increased cellular orientation and collagen fiber alignment. Transforming growth factor beta-1 (TGFβ1) gene expression and pSmad2 nuclear translocation increased with biaxial directionality. Myofibroblastic alpha-smooth muscle actin (α-SMA) decreased with applied strain similar to mechanically unloaded hydrogels. Collectively, these results demonstrate a novel mechanobiological mechanism by which fibroblasts develop rapid anisotropic matrix striation while maintaining phenotype quiescence.
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Lecras, TD, TR Korfhagen, CR Davidson, SM Schmidt, M. Ikegami, JA Whitsett und WD Hardie. „Inhibition of PI3K Prevents Transforming Growth Factor-alpha Induced Pulmonary Fibrosis.“ In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2727.

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Wang, Kimberley, Timothy Le Cras, Alexander Larcombe, Graeme Zosky, Alan James und Peter Noble. „Transforming growth factor alpha produces airway remodelling and reduces airway distensibility“. In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa386.

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Hardie, William, Timothy LeCras, Tom Korfhagen, Cindy Davidson, Stephanie Schmidt, Machiko Ikegami und Jeffrey A. Whitsett. „Inhibition Of PI3K Reverses Transforming Growth Factor-alpha Induced Pulmonary Fibrosis“. In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1058.

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Javle, Milind M., Xiaoqun Dong, Dongfeng Tan, Yanan Li, Siddhartha P. Kar, Veera Baladandayuthapani, Jacqueline Weatherly et al. „Abstract 4491: Transforming growth factor (TGF) ≤ pathway and clinical outcome of pancreatic cancer“. In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4491.

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Jaschinski, Frank, Hanna Korhonen, Stephan Braun, Katja Wosikowski und Michel Janicot. „Abstract 717: Novel potent antisense oligonucleotides targeting transforming growth factor beta1 (TGF-β1)“. In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-717.

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Madala, Satish, Cindy Davidson, Stephanie Schmidt, Tim LeCras, Tom Korfhagen, Machiko Ikegami und William Hardie. „Pharmacologic Inhibition Of MEK Reverses Transforming Growth Factor-Alpha Induced Pulmonary Fibrosis“. 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.a5979.

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Palumbo, F., T. Likhoshvay, M. Gunjak, W. Seeger und R. E. Morty. „Development and Characterization of Reporter Mice for Canonical Transforming Growth Factor (TGF)-β Signaling“. In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6044.

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Pertseva, Tetyana, und Daria Koval. „Transforming growth factor beta 1 (TGF-ß1) level as a marker of COPD severity“. In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2472.

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Yazisiz, V., S. Oygen, M. Çavuşoğlu, M. Kahraman, EG Gök, S. Karahan, I. Uçar und ME Terzioğlu. „AB0057 The role of growth differentiation factor (GDF)-15 and transforming growth factor (TGF)-β in the development of pulmonary fibrosis“. In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.1586.

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Berichte der Organisationen zum Thema "TGF alpha [Transforming Growth Factor]"

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Chung, Lee. Expression of Transforming Growth Factor-Beta (TGF-B) in Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada405312.

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Lee, Chung. Expression of Transforming Growth Factor-Beta (TGF-Beta) in Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada419151.

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Chung, Lee. Expression of Transforming Growth Factor-Beta (TGF-B) in Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, März 2000. http://dx.doi.org/10.21236/ada391531.

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Lee, Chung. Expression of Transforming Growth Factor-Beta (TGF-Beta) in Prostate Cancer Cell Progression. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412198.

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Dumont, Nancy, und C. L. Arteaga. Temporal Control of Transforming Growth Factor (TGF) - Betal Expression on Mammary Cell Multistep Transformation. Fort Belvoir, VA: Defense Technical Information Center, Oktober 2000. http://dx.doi.org/10.21236/ada394049.

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Dumont, Nancy, und Carlos L. Arteaga. Temporal Control of Transforming Growth Factor (TGF) - Betal Expression on Mammary Cell Multistep Transformation. Fort Belvoir, VA: Defense Technical Information Center, Oktober 1999. http://dx.doi.org/10.21236/ada391622.

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Funkenstein, Bruria, und Shaojun (Jim) Du. Interactions Between the GH-IGF axis and Myostatin in Regulating Muscle Growth in Sparus aurata. United States Department of Agriculture, März 2009. http://dx.doi.org/10.32747/2009.7696530.bard.

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Growth rate of cultured fish from hatching to commercial size is a major factor in the success of aquaculture. The normal stimulus for muscle growth in growing fish is not well understood and understanding the regulation of muscle growth in fish is of particular importance for aquaculture. Fish meat constitutes mostly of skeletal muscles and provides high value proteins in most people's diet. Unlike mammals, fish continue to grow throughout their lives, although the size fish attain, as adults, is species specific. Evidence indicates that muscle growth is regulated positively and negatively by a variety of growth and transcription factors that control both muscle cell proliferation and differentiation. In particular, growth hormone (GH), fibroblast growth factors (FGFs), insulin-like growth factors (IGFs) and transforming growth factor-13 (TGF-13) play critical roles in myogenesis during animal growth. An important advance in our understanding of muscle growth was provided by the recent discovery of the crucial functions of myostatin (MSTN) in controlling muscle growth. MSTN is a member of the TGF-13 superfamily and functions as a negative regulator of skeletal muscle growth in mammals. Studies in mammals also provided evidence for possible interactions between GH, IGFs, MSTN and the musclespecific transcription factor My oD with regards to muscle development and growth. The goal of our project was to try to clarify the role of MSTNs in Sparus aurata muscle growth and in particular determine the possible interaction between the GH-IGFaxis and MSTN in regulating muscle growth in fish. The steps to achieve this goal included: i) Determining possible relationship between changes in the expression of growth-related genes, MSTN and MyoD in muscle from slow and fast growing sea bream progeny of full-sib families and that of growth rate; ii) Testing the possible effect of over-expressing GH, IGF-I and IGF-Il on the expression of MSTN and MyoD in skeletal muscle both in vivo and in vitro; iii) Studying the regulation of the two S. aurata MSTN promoters and investigating the possible role of MyoD in this regulation. The major findings of our research can be summarized as follows: 1) Two MSTN promoters (saMSTN-1 and saMSTN-2) were isolated and characterized from S. aurata and were found to direct reporter gene activity in A204 cells. Studies were initiated to decipher the regulation of fish MSTN expression in vitro using the cloned promoters; 2) The gene coding for saMSTN-2 was cloned. Both the promoter and the first intron were found to be polymorphic. The first intron zygosity appears to be associated with growth rate; 3) Full length cDNA coding for S. aurata growth differentiation factor-l I (GDF-II), a closely related growth factor to MSTN, was cloned from S. aurata brain, and the mature peptide (C-terminal) was found to be highly conserved throughout evolution. GDF-II transcript was detected by RT -PCR analysis throughout development in S. aurata embryos and larvae, suggesting that this mRNA is the product of the embryonic genome. Transcripts for GDF-Il were detected by RT-PCR in brain, eye and spleen with highest level found in brain; 4) A novel member of the TGF-Bsuperfamily was partially cloned from S. aurata. It is highly homologous to an unidentified protein (TGF-B-like) from Tetraodon nigroviridisand is expressed in various tissues, including muscle; 5) Recombinant S. aurata GH was produced in bacteria, refolded and purified and was used in in vitro and in vivo experiments. Generally, the results of gene expression in response to GH administration in vivo depended on the nutritional state (starvation or feeding) and the time at which the fish were sacrificed after GH administration. In vitro, recombinantsaGH activated signal transduction in two fish cell lines: RTHI49 and SAFI; 6) A fibroblastic-like cell line from S. aurata (SAF-I) was characterized for its gene expression and was found to be a suitable experimental system for studies on GH-IGF and MSTN interactions; 7) The gene of the muscle-specific transcription factor Myogenin was cloned from S. aurata, its expression and promoter activity were characterized; 8) Three genes important to myofibrillogenesis were cloned from zebrafish: SmyDl, Hsp90al and skNAC. Our data suggests the existence of an interaction between the GH-IGFaxis and MSTN. This project yielded a great number of experimental tools, both DNA constructs and in vitro systems that will enable further studies on the regulation of MSTN expression and on the interactions between members of the GHIGFaxis and MSTN in regulating muscle growth in S. aurata.
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