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Relevant bibliographies by topics / Leukaemia Inhibitory Factor Receptor

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Academic literature on the topic 'Leukaemia Inhibitory Factor Receptor'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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Journal articles on the topic "Leukaemia Inhibitory Factor Receptor"

1

CICHY, Joanna, Stefan ROSE-JOHN, and James TRAVIS. "Oncostatin M, leukaemia-inhibitory factor and interleukin 6 trigger different effects on α1-proteinase inhibitor synthesis in human lung-derived epithelial cells." Biochemical Journal 329, no. 2 (January 15, 1998): 335–39. http://dx.doi.org/10.1042/bj3290335.

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Interleukin 6 (IL-6), oncostatin M (OSM) and leukaemia-inhibitory factor (LIF) share a common signal-transducing subunit in each of their receptors and thus mediate an overlapping spectrum of biological activities. Although all of these cytokines stimulate the production of α1-proteinase inhibitor (α1-PI) in hepatocyte-derived cells, only OSM is able to up-regulate levels of this inhibitor in epithelial cells originating from the lung. In this study we characterized human lung-derived epithelial-like HTB58 cells for their ability to synthesize α1-PI after treatment with IL-6, OSM and LIF. The results demonstrate that the resistance of HTB58 cells to the effects of IL-6 and LIF was not because of a lack of their individual functional receptors and suggest that OSM utilizes two different receptors, gp130/LIF receptor and gp130/OSM receptor, in lung-derived epithelial cells.

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2

Schäfer-Somi, S., D. Klein, HB Beceriklisoy, S. Sabitzer, SS Ay, AR Agaoglu, I. Kücükaslan, D. Kaya, OA Aksoy, and S. Aslan. "Uterine Progesterone Receptor and Leukaemia Inhibitory Factor mRNA Expression in Canine Pregnancy." Reproduction in Domestic Animals 44 (July 2009): 109–14. http://dx.doi.org/10.1111/j.1439-0531.2009.01390.x.

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Fry, RC. "The effect of leukaemia inhibitory factor (LIF) on embryogenesis." Reproduction, Fertility and Development 4, no. 4 (1992): 449. http://dx.doi.org/10.1071/rd9920449.

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Leukaemia inhibitory factor (LIF) was originally identified as a haemopoetic factor that induced the differentiation of certain myeloid leukaemia cell lines. In contrast to this action, LIF was subsequently shown to inhibit the spontaneous differentiation of murine embryonic stem cells in culture, thus maintaining their pluripotency and ability to contribute to the germline of chimaeric mice. In the mouse, mRNA for LIF is expressed by the endometrial glands of the uterus coincident with the time of blastocyst implantation and receptors have been found on the preimplantation blastocyst. The signal for LIF expression appears to be of maternal origin, perhaps regulated by oestradiol. Recombinant LIF improves the development of murine and ovine blastocysts in culture although there is some species specificity with respect to the type of LIF that is bioactive. It is proposed here that LIF acts on the trophectoderm of the rapidly expanding blastocyst and improves the implantation rate of otherwise compromised embryos. Further studies in livestock should elicit therapeutic uses for LIF in embryo culture, embryo transfer and embryo survival in vivo.

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THIEL, Stefan, Iris BEHRMANN, Andreas TIMMERMANN, Heike DAHMEN, Gerhard MÜLLER-NEWEN, Fred SCHAPER, Jan TAVERNIER, Vincent PITARD, Peter C. HEINRICH, and Lutz GRAEVE. "Identification of a Leu-Ile internalization motif within the cytoplasmic domain of the leukaemia inhibitory factor receptor." Biochemical Journal 339, no. 1 (March 25, 1999): 15–19. http://dx.doi.org/10.1042/bj3390015.

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Leukaemia inhibitory factor (LIF) signals via a heterodimeric receptor complex comprised of the LIF receptor (LIFR) and the interleukin (IL)-6 signal transducer gp130. Upon binding to its cognate receptor LIF is internalized. In this study, we show that the LIFR is endocytosed independently of gp130. By using a heterochimaeric receptor system we identified a dileucine-based internalization motif within the cytoplasmic domain of the LIFR. Our findings suggest that a heterodimeric LIFR/gp130 complex and homodimeric gp130/gp130 complex are endocytosed via distinct internalization signals.

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Hirai, Hiroyuki, Peter Karian, and Nobuaki Kikyo. "Regulation of embryonic stem cell self-renewal and pluripotency by leukaemia inhibitory factor." Biochemical Journal 438, no. 1 (July 27, 2011): 11–23. http://dx.doi.org/10.1042/bj20102152.

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LIF (leukaemia inhibitory factor) is a key cytokine for maintaining self-renewal and pluripotency of mESCs (mouse embryonic stem cells). Upon binding to the LIF receptor, LIF activates three major intracellular signalling pathways: the JAK (Janus kinase)/STAT3 (signal transducer and activator of transcription 3), PI3K (phosphoinositide 3-kinase)/AKT and SHP2 [SH2 (Src homology 2) domain-containing tyrosine phosphatase 2]/MAPK (mitogen-activated protein kinase) pathways. These pathways converge to orchestrate the gene expression pattern specific to mESCs. Among the many signalling events downstream of the LIF receptor, activation and DNA binding of the transcription factor STAT3 plays a central role in transducing LIF's functions. The fundamental role of LIF for pluripotency was highlighted further by the discovery that LIF accelerates the conversion of epiblast-derived stem cells into a more fully pluripotent state. In the present review, we provide an overview of the three major LIF signalling pathways, the molecules that interact with STAT3 and the current interpretations of the roles of LIF in pluripotency.

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KASZA, Aneta, Krzysztof ROGOWSKI, Witold KILARSKI, Radoslaw SOBOTA, Tytus BERNAS, Jurek DOBRUCKI, James TRAVIS, Aleksander KOJ, Marcin BUGNO, and Tomasz KORDULA. "Differential effects of oncostatin M and leukaemia inhibitory factor expression in astrocytoma cells." Biochemical Journal 355, no. 2 (April 6, 2001): 307–14. http://dx.doi.org/10.1042/bj3550307.

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The effects of the production of two closely related cytokines, oncostatin M (OSM) and leukaemia inhibitory factor (LIF), by astrocytoma cells were investigated using the stable cell line human U373-MG, which expressed and secreted both biologically active polypeptides. The expression of LIF by these cells caused resistance to this cytokine due to loss of the LIF receptor (LIFR), from the cell surface, suggesting its retention. In contrast, cells expressing OSM were stimulated by this cytokine, utilizing an autocrine mechanism, and possessed receptors for OSM, but not LIF, on the cell surface. In these cells the continuous up-regulation of OSM-induced gene expression was found even though the Janus kinase-signal transducer and activator of transcription (‘JAK/STAT’) pathway was almost exhausted due to long-term autocrine stimulation of the cells by OSM. The amount of LIFR was down-regulated in both LIF- and OSM-producing cells and this effect was not found in wild-type U373-MG cells treated with externally added cytokines. To investigate the mechanism of autocrine stimulation by OSM we constructed a stable cell line expressing a form of OSM that is retained in the endoplasmic reticulum (ER). This biologically active cytokine was not secreted, but was localized in the ER. In addition, it did not stimulate the astrocytoma cells in an autocrine manner. We conclude that expression of LIF causes resistance of astrocytoma cells to this cytokine, whereas expression of OSM leads to autocrine stimulation.

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Owczarek, C. M., M. J. Layton, D. Metcalf, P. Lock, T. A. Willson, N. M. Gough, and N. A. Nicola. "Inter-species chimeras of leukaemia inhibitory factor define a major human receptor-binding determinant." EMBO Journal 12, no. 9 (September 1993): 3487–95. http://dx.doi.org/10.1002/j.1460-2075.1993.tb06023.x.

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ZHANG, Jian-Guo, Catherine M. OWCZAREK, Larry D. WARD, Geoffrey J. HOWLETT, Louis J. FABRI, Bronwyn A. ROBERTS, and Nicos A. NICOLA. "Evidence for the formation of a heterotrimeric complex of leukaemia inhibitory factor with its receptor subunits in solution." Biochemical Journal 325, no. 3 (August 1, 1997): 693–700. http://dx.doi.org/10.1042/bj3250693.

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Leukaemia inhibitory factor (LIF) is a polyfunctional cytokine that is known to require at least two distinct receptor components (LIF receptor α-chain and gp130) in order to form a high-affinity, functional, receptor complex. Human LIF binds with unusually high affinity to a naturally occurring mouse soluble LIF receptor α-chain, and this property was used to purify a stable complex of human LIF and mouse LIF receptor α-chain from pregnant-mouse serum. Recombinant soluble human gp130 was expressed, with a FLAG® epitope (DYKDDDDK) at the N-terminus, in the methylotropic yeast Pichia pastoris and purified using affinity chromatography. The formation of a trimeric complex in solution was established by native gel electrophoresis, gel-filtration chromatography, sedimentation equilibrium analysis, surface plasmon resonance spectroscopy and chemical cross-linking. The stoichiometry of this solution complex was 1:1:1, in contrast with that of the complex of interleukin-6, the interleukin-6-specific low-affinity receptor subunit and gp130, which is 2:2:2.

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Harvey, M. B., K. J. Leco, M. Y. Arcellana-Panlilio, X. Zhang, D. R. Edwards, and G. A. Schultz. "Proteinase expression in early mouse embryos is regulated by leukaemia inhibitory factor and epidermal growth factor." Development 121, no. 4 (April 1, 1995): 1005–14. http://dx.doi.org/10.1242/dev.121.4.1005.

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Several proteinases from different multigene families have been implicated in the uterine invasion required for establishment of pregnancy in some mammals. In this study, the expression of matrix metalloproteinase gelatinase B (MMP-9), urokinase-type plasminogen activator (uPA) and their inhibitors was investigated during early mouse embryo development. Transcripts for tissue inhibitors of metalloproteinases (TIMP-1,-2,-3) and uPA receptor were detected throughout pre- and peri-implantation development whilst MMP-9 and uPA mRNAs were first detected in peri-implantation blastocysts associated with the invasive phase of implantation. Through use of in situ hybridization, it was shown that MMP-9 transcripts were strongly expressed in the network of trophoblast giant cells at the periphery of implanting 7.5 day embryos and TIMP-3 transcripts were strongly expressed in the decidua immediately adjacent to the implanting embryo. uPA transcripts were preferentially expressed in the ectoplacental cone and its derivatives. Because these proteinases are regulated by growth factors and cytokines in other tissues, the effect of leukaemia inhibitory factor (LIF) and epidermal growth factor (EGF) on their activity was investigated. Both LIF and EGF, like the proteinases, have been implicated in peri-implantation development. Blastocysts collected on day 4 of pregnancy were cultured 2 days in TCM 199 + 10% fetal bovine serum to allow outgrowth followed by 24 hour culture in defined media containing either LIF or EGF. Conditioned media were assayed for uPA activity by a chromogenic assay and MMP activity by gelatin zymography. Both LIF and EGF stimulated uPA and MMP-9 activity in blastocyst outgrowths after 3 days of culture (day 7). Proteinase activity was assayed again at the 5th to 6th day of culture (day 9 to 10). EGF was found to have no effect whereas LIF decreased production of both proteinases. These results demonstrate that proteinase activity in early embryos can be regulated by growth factors and cytokines during the implantation process and, in particular, they demonstrate the possible involvement of LIF in establishment of the correct temporal programme of proteinase expression.

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CHAMBERS, Ian, Alison COZENS, Joanne BROADBENT, Morag ROBERTSON, Muriel LEE, Meng LI, and Austin SMITH. "Structure of the mouse leukaemia inhibitory factor receptor gene: regulated expression of mRNA encoding a soluble receptor isoform from an alternative 5′ untranslated region." Biochemical Journal 328, no. 3 (December 15, 1997): 879–88. http://dx.doi.org/10.1042/bj3280879.

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The low-affinity leukaemia inhibitory factor receptor (LIF-R) is a component of cell-surface receptor complexes for the multifunctional cytokines leukaemia inhibitory factor, ciliary neurotrophic factor, oncostatin M and cardiotrophin-1. Both soluble and transmembrane forms of the protein have been described and several LIF-R mRNAs have been reported previously. In order to determine the coding potential of LIF-R mRNAs we have isolated and characterized the mouse LIF-R gene. mRNA encoding soluble LIF-R (sLIF-R) is formed by inclusion of an exon in which polyadenylation signals are provided by a B2 repeat. This exon is located centrally within the LIF-R gene but is excluded from the transmembrane LIF-R mRNA by alternative splicing. The transmembrane receptor is encoded by 19 exons distributed over 38 kb. Two distinct 5ʹ non-coding exons have been identified, indicating the existence of alternative promoters. One of these is G/C rich and possesses a consensus initiator sequence as well as potential Sp1 binding sites. Expression of exon 1 from this promoter occurs in a wide variety of tissues, whereas expression of the alternative 5ʹ untranslated region (exon 1a) is normally restricted to liver, the principal source of sLIF-R. During pregnancy expression of exon 1a becomes detectable also in the uterus. Expression of exon 1a increases dramatically during gestation and is accompanied by a similar quantitative rise in expression of sLIF-R mRNA. These findings establish that expression of LIF-R is under complex transcriptional control and indicate that regulated expression of the soluble cytokine receptor isoform may be due principally to an increase in the activity of a dedicated promoter.

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Dissertations / Theses on the topic "Leukaemia Inhibitory Factor Receptor"

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Chobotova, Katya. "Ligand binding determinants of LIF receptor." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244596.

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Hill, Eric J. "Polarised secretion of leukaemia inhibitory factor." Thesis, Aston University, 2004. http://publications.aston.ac.uk/11019/.

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Leukaemia inhibitory factor (LIF) is a cytokine that is active on a wide variety of cells. Multiple LIF transcripts have been described. The transcripts LIF-D and LIF-M encode different signal peptides, which in mouse have been associated with differential localisation of the mature protein. LIF-D is associated with a freely diffusible protein, whereas the LIF-M is associated with the extracellular matrix. The polarity of LIF secretion has yet to be described and could illuminate the mechanisms of LIF localisation. Here the polarised endogenous secretion of human LIF and IL-6 in Caco-2 cells was characterised under normal culture conditions and following induction with IL-1b. Whether the apical or basolateral membrane was stimulated influenced the pattern of secretion (LIF: Unstimulated, 59% basolateral. Dual stimulation, 68% basolateral. Basolateral stimulation, 79% basolateral. Apical stimulation, 53% basolateral). IL-6 displayed a similar dependence on the site of stimulation but was predominantly secreted at the membrane that was stimulated. To determine the effect of the alternate signal peptides on the polarity of LIF secretion, LIF was epitope tagged with FLAG. Epitope-tagging with FLAG was used to separate endogenous from exogenous protein expression. However, despite the normal biological activity of LIF-FLAG and detection of the FLAG in a western blot, detection of the LIF-FLAG under non-reducing conditions was not observed, and therefore it was unsuitable for secretion studies. Untagged LIF was expressed exogenously in Madin-Darby canine kidney (MDCK) cells under the control of a tetracycline response promoter that allowed a variety of LIF expression levels to be tested. Exogenous murine LIF was secreted predominantly from the apical (60%) membrane of MDCK cells irrespective of the signal peptide expressed.

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Grey, Laura M. "Structure and function of leukaemia inhibitory factor." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359460.

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Sherwin, James Robert Alexander. "The role of leukaemia inhibitory factor in endometrial receptivity." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619897.

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Muthukumarana, Poorni Apsara de Silva. "Stem cell factors, axotrophin and leukaemia inhibitory factor in immune regulation." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611884.

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Voyle, Roger Bruce. "Mechanisms of intracellular and extracellular cytokine production from the human leukaemia inhibitory factor gene." Title page, contents and summary only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phv975.pdf.

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Addendum attached to back facing leaves. Includes bibliographical references (leaves 172-199). The findings establish leukemia inhibitory factor, and possibly oncostatin M, as new members of a small but growing class of cytokines produced in an intracellularly active form and also suggest that the production of alternate transcripts and intercellularly-retained proteins may be a common and important feature of cytokines of the IL-6 and other families.

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Wiest, Stephanie. "Mutationen im Leukaemia-inhibitory-factor-(LIF)-Gen bei wiederholtem Implantationsversagen nach extrakorporaler Befruchtung." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=975102621.

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Segrave, Alicia Maree. "An investigation of the pharmacokinetics and lymphatic transport of recombinant human leukaemia inhibitory factor." Monash University, Dept. of Pharmaceutics, 2004. http://arrow.monash.edu.au/hdl/1959.1/9389.

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Schiemann, William Paul. "Determination and characterization of leukemia inhibitory factor receptor signal transduction systems /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/6277.

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West, Peter William. "The regulation of Toll-like receptor signalling by macrophage migration inhibitory factor." Thesis, University of Sheffield, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505343.

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Toll-like receptors (TLRs) fonn a vital part of the innate immune response to infection through the recognition of diverse molecular patterns leading to the generation of an inflammatory reaction. The resulting cytokines act on both tissue and immune cells to coordinate the response to infection. Cytokine networks also play an important role in the modulation of an increasing number of diseases which we now understand to have an inflammatory basis. TLR activation has been implicated in both chronic and acute diseases, and understanding and modulation of these responses may be central to th'e manageinent of inflammatory disease. This thesis investigates the impact of an enigmatic early response cytokine macrophage migration inhibitory factor on the TLR response of human cells. I have shown that the role ofMIF as an inflammatory cytokine is not clear-cut. Recombinant MIF failed to induce a significant inflammatory response from either a monocytic THP-l cell line or primary human monocytes. Furthennore, it failed to modulate the dexamethasone induced suppression of TLR induced cytokine release, a classically described activity of MIF. In keeping with these observations, anti-MIF antibodies did not modulate the LPS induced cytokine release of monocytes or monocytelHUVEC cocultures, which suggests that MIF may not act as a classical autocrine cytokine. I have demonstrated using a specific, cell-penneable MIF antagonist, known as ISO-I, and MIF siRNA, that MIF modulated specific arms of the TLR response leading to the activation of mitogen activated protein kinases (MAPKs) in monocytic cells. Cell-type spe~ific downstream effects on cytokine production were also seen. ISO-l potentiated LPS induced p38 phosphorylation and TNFa release from THP-I cells. Conversely, in primary monocytes, TNFa and CXCL8 production in response to LPS was significantly inhibited by both ISO-I and MIF siRNA, whilst TNFa but not CXCL8 production was maintained in response to TLR2 activation. LPS induced cytokine release from MDMs was unaffected by :NIIF inhibition. During the course of this thesis I have also observed differences in TLR2 induced inflammatory reactions in primary monocytes. This observation was explored further. These data suggest that whilst targeting MIF may be a useful therapeutic axis in disease, the roles of MIF are not straightforward. Further work will be needed to fully address the roles of this molecule in human biology.

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Books on the topic "Leukaemia Inhibitory Factor Receptor"

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Gregory, Bock, Marsh Joan, and Widdows Kate, eds. Polyfunctional cytokines: IL-6 and LIF. Chichester, Eng: Wiley, 1992.

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Book chapters on the topic "Leukaemia Inhibitory Factor Receptor"

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Hilton, Douglas J., Nicos A. Nicola, and Donald Metcalf. "Distribution and Binding Properties of Receptors for Leukaemia Inhibitory Factor." In Novartis Foundation Symposia, 227–44. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514269.ch14.

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Gearing, David P., Tim VandenBos, M. Patricia Beckmann, Catherine J. Thut, Michael R. Comeau, Bruce Mosley, and Steven F. Ziegler. "Reconstitution of High Affinity Leukaemia Inhibitory Factor (LIF) Receptors in Haemopoietic Cells Transfected with the Cloned Human LIF Receptor." In Novartis Foundation Symposia, 245–66. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514269.ch15.

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Martin, T. J., E. H. Allan, R. S. Evely, and I. R. Reid. "Leukaemia Inhibitory Factor and Bone Cell Function." In Novartis Foundation Symposia, 141–59. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514269.ch9.

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Gough, Nicholas M., Tracy A. Willson, Jürgen Stahl, and Melissa A. Brown. "Molecular Biology of the Leukaemia Inhibitory Factor Gene." In Novartis Foundation Symposia, 24–46. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514269.ch3.

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Stewart, Colin L. "Leukaemia Inhibitory Factor and the Regulation of Blastocyst Implantation." In Endocrinology of Embryo—Endometrium Interactions, 269–78. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-1881-5_22.

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Graham, Amanda, and Warren B. Nothnick. "Concurrent Immunohistochemical Localization and Western Blot Analysis of the MIF Receptor, CD74, in Formalin-Fixed, Paraffin-Embedded Tissue." In Macrophage Migration Inhibitory Factor, 123–34. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9936-1_11.

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Metcalf, D., P. Waring, and N. A. Nicola. "Actions of Leukaemia Inhibitory Factor on Megakaryocyte and Platelet Formation." In Novartis Foundation Symposia, 174–87. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514269.ch11.

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Lotem, Joseph, and Leo Sachs. "Regulation of Leukaemic Cells by Interleukin 6 and Leukaemia Inhibitory Factor." In Novartis Foundation Symposia, 80–99. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514269.ch6.

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Baumann, H., S. Marinkovic-Pajovic, K. A. Won, V. E. Jones, S. P. Campos, G. P. Jahreis, and K. K. Morella. "The Action of Interleukin 6 and Leukaemia Inhibitory Factor on Liver Cells." In Novartis Foundation Symposia, 100–124. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514269.ch7.

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Hunt, Liam C., and Jason White. "The Role of Leukemia Inhibitory Factor Receptor Signaling in Skeletal Muscle Growth, Injury and Disease." In Growth Factors and Cytokines in Skeletal Muscle Development, Growth, Regeneration and Disease, 45–59. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27511-6_3.

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Conference papers on the topic "Leukaemia Inhibitory Factor Receptor"

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Heinrichs, D., TH Wirtz, A. Saal, I. Bergmann, P. Fischer, EF Brandt, J. Bernhagen, C. Trautwein, and ML Berres. "Macrophage Migration Inhibitory Factor promotes HCC progression in vivo via the receptor CD74." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402219.

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Chang, Xiaofei, Yong G. Cho, Il-Seok Park, Chunbo Shao, Patrick Ha, Sara I. Pai, David Sidransky, and Myoung S. Kim. "Abstract 4799: Promoter methylation of leukemia inhibitory factor receptor gene in colorectal carcinoma." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4799.

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Bell, H., S. Lalnunhlimi, M. Green, F. Van Delft, and A. Krippner-Heidenreich. "Tumour Necrosis Factor receptor (TNFR)-signalling dependent killing in T-cell acute lymphoblastic leukaemia (T-ALL)." In 32. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1687172.

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Zhu, Y. M., and P. S. Daugherty. "Identification of potential inhibitory peptide drugs for vascular endothelial growth factor receptor 2 (VEGFR2, KDR) using bacteria display methods." In 2009 IEEE 35th Annual Northeast Bioengineering Conference. IEEE, 2009. http://dx.doi.org/10.1109/nebc.2009.4967802.

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Iorns, Elizabeth J., Toby M. Ward, Sonja Dean, Anna Jegg, Nirupa Murugaesu, David Sims, Christopher Lord, et al. "Abstract 4979: Whole genome in vivo RNA interference screening identifies the leukemia inhibitory factor receptor as a novel breast tumor suppressor." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4979.

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Iorns, E., T. Ward, S. Dean, A. Jegg, C. Lord, N. Murugaesu, D. Sims, et al. "Abstract P5-05-02: Whole Genome In Vivo RNA Interference Screening Identifies the Leukemia Inhibitory Factor Receptor as a Novel Breast Tumor Suppressor." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p5-05-02.

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Simmons, Andrew D., Sarah Jaw-Tsai, Henry J. Haringsma, Andrew Allen, and Thomas C. Harding. "Abstract 793: Insulin-like growth factor 1 (IGF1R)/insulin receptor (INSR) inhibitory activity of rociletinib (CO-1686) and its metabolites in nonclinical models." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-793.

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Saksela, O., D. Moscatelli, and D. B. Rifkin. "THE OPPOSING OF BASIC FIBROBLAST GROWTH FACTOR AND TRANSFORMING GROWTH FACTOR BETA ON THE REGULATION OF PLASMINOGEN ACTIVATOR ACTIVITY IN CAPILLARY ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644660.

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Basic fibroblast growth factor (bFGF), a potent inducer of angio-genesis in vivo, stimulates the production of both the cell-associated and the secreted forms of urokinase-and tissue-type plasminogen activators (PA) in cultured bovine capillary endothelial cells. This stimulation was counteracted by picogram amounts of transforming growth factor beta The stimulatory effect of bFGF was not completely abolished by increasing the amount of TGFb However, the inhibition by TGFb was greatly enhanced if the cells were pretreated for 1-3 hours with TGFb before addition of bFGF, and the inhibition was almost total, if the' preincubationtime with TGFb was 6 hours.Sequential chanqes of serum-containing medium prior to addition ofbFGF also blocked the PA stimulatory effect of bFGF. This inhibitory activity of serum was reduced by incubation of the serum with anti-TGFb-IgG. After pro-longed incubation of cultures treated simultaneously with bFGF' and TGFb, the inhibitory effect of the added bFGF dominated as assayed by PAlevels. TGFbdid not alter the receptor binding of labeled bFGF, nor did a 6 hour pretreatment with TGFb reducethe amount of bound bFGF. The major difference between effects by bFGF and TGFb was thatwhile bFGF effectively enhanced PA-activi-ty expressed by the cells, TGF decreased the amounts of both cell-associated and secreted PA activity by decreasing enzyme production and proenzyme activation. Both bFGF and TGFb increased the secretion of the endothelial type 1 plasminogen activatorinhibitor (PAI 1). The highest concentration of TGFb is found in platelets, and it is known to be released during clot formation. The suppression of PA production by theendothelium by the release of TGFb shouldresult in a decrease in the fibrinolytic activity and promote clot maintenance. In addition, the rapid stimulation of high levels of PAI 1 secretion from the surrounding capillarycells by platelet released TGFb may further suppress fibrinolysis'. The reversabil it.y of theTGFb effect and domination of bFGF stimulation may be important in relation to the subsequentonset of clot lysis or angiogenesis leadino to thrombus reorganization and wound healing.

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Dempsey, NG, P. Miller, and M. Lippman. "Abstract P2-06-03: Leukemia inhibitory factor receptor as a tumor suppressor: A study on migration and invasion of breast cancer cells upon LIFR stimulation." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p2-06-03.

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Kang, Hyung-Gyoo, and Timothy J. Triche. "Abstract 4336: Macrophage migration inhibitory factor (MIF) plays roles in proliferation, survival and migration of Ewing tumor cells by activation of a CD74-CD44 receptor complex." 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.am2012-4336.

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