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Статті в журналах з теми "Gremlin 1"

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Claesson-Welsh, Lena. "Gremlin: vexing VEGF receptor agonist." Blood 116, no. 18 (November 4, 2010): 3386–87. http://dx.doi.org/10.1182/blood-2010-09-299412.

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Abstract Gremlins are mischievous creatures in English folklore, believed to be the cause of otherwise unexplainable breakdowns (the word gremlins is derived from the Old English “gremian” or “gremman,” “to vex”). Gremlin (or Gremlin-1) is also the designation of a secreted protein that is known to regulate bone formation during development. In this issue of Blood, Mitola et al report the novel role of Gremlin as a VEGFR2 agonist1 and the function of the Gremlin protein seems vexing indeed.
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Beck, Sandra, Thomas Simmet, Iris Müller, Florian Lang, and Meinrad Gawaz. "Gremlin-1 C-Terminus Regulates Function of Macrophage Migration Inhibitory Factor (MIF)." Cellular Physiology and Biochemistry 38, no. 2 (2016): 801–8. http://dx.doi.org/10.1159/000443035.

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Background/Aims: The counterbalance of macrophage migration inhibitory factor (MIF) and Gremlin-1 is a useful tool to predict the acuity of coronary artery disease (CAD) and plaque stability. Gremlin1 is an endogenous antagonist of MIF and therefore influences plaque vulnerability. This study was designed to elucidate the mechanistic basis determining the biophysical binding of Gremlin-1 to MIF. Methods: An in silico model suggested that several charged C-terminal amino acids are crucial in mediating Gremlin-1/MIF-binding. We produced several single amino acid exchange mutants of Gremlin-1 by site-directed mutagenesis. These Gremlin-1 mutants were tested for their ability to reduce MIF effects on monocytes. Results: We observed that the critical element of the Gremlin-1 molecule for regulating MIF-induced chemotactic activity lies at the C-terminal region. A single amino acid exchange of an arginine to an alanine residue is sufficient to abolish the antagonistic effect of Gremlin-1 on MIF. Therefore, the Gremlin-1 mutant R172A failed to reduce MIF-induced monocyte differentiation into macrophages. Conclusion: Gremlin-1 C-terminus is essential for antagonizing MIF effects. Our results could offer a novel strategy utilizing Gremlin-1 to target pro-inflammatory effects of MIF in various diseases.
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Chatterjee, Madhumita, Alexander Behrendt, Martina Schmid, Sandra Beck, Martina Schneider, Andreas Mack, Iris Müller, Tobias Geisler, and Meinrad Gawaz. "Platelets as a novel source of Gremlin-1: Implications for thromboinflammation." Thrombosis and Haemostasis 117, no. 02 (2017): 311–24. http://dx.doi.org/10.1160/th16-08-0665.

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SummaryPlatelets mediating haemostasis-thrombosis are central players in coronary artery disease (CAD). We characterised platelets as a novel source of Gremlin-1. Platelets express Gremlin-1 like inflammatory and endothelial cells. Gremlin-1 co-localised with P-selectin containing randomly distributed α–granules under resting state, which were peripheralised following platelet activation or adhesion over fibrinogen-coated surface. Gremlin-1 release upon activation with ADP, CRP, and TRAP was detected as enhanced surface expression; also in activated platelet supernatant as detected by Western Blot following CRP activation and by ELISA upon activation with ADP, CRP, PAR-1, and PAR4 agonist. Recombinant (rh)Gremlin-1 synergistically enhanced CRP-triggered intracellular calcium mobilisation, ADP-TRAP induced platelet activation, aggregation, and thrombin-activation triggered apoptosis; also thrombus formation ex vivo. Intracellular localisation of macrophage migration inhibitory factor (MIF) and Gremlin-1 a high-affinity binding partner and functional antagonist of MIF were found in intracoronary thrombus sections from acute coronary syndrome (ACS) patients and showed moderate overlap in α-granules of platelets. Intra-platelet Gremlin-1 levels were significantly decreased in ACS patients as compared to stable CAD (n=235). rhGremlin-1 also counteracted the anti-apoptotic and anti-thrombotic effects of rhMIF on platelets. Platelet-derived-Gremlin-1 prompted monocyte migration, facilitated adhesion under static and dynamic arterial flow conditions to collagen-adherent activated platelets; supported monocyte survival against BH-3-mimetic–induced apoptosis and macrophage differentiation in monocyte-platelet co-culture system, which were counteracted upon Gremlin-1 neutralisation. Thus platelet derived Gremlin-1 might contribute to the elevated circulating levels of Gremlin-1 in ACS and serve as a thrombo-inflammatory mediator in cardiovascular pathophysiologies.
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Rowan, Simon C., Lucie Piouceau, Joanna Cornwell, Lili Li, and Paul McLoughlin. "Gremlin 1 blocks vascular endothelial growth factor signaling in the pulmonary microvascular endothelium." Pulmonary Circulation 10, no. 1 (October 4, 2018): 204589401880720. http://dx.doi.org/10.1177/2045894018807205.

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The bone morphogenetic protein (BMP) antagonist gremlin 1 plays a central role in the pathogenesis of hypoxic pulmonary hypertension (HPH). Recently, non-canonical functions of gremlin 1 have been identified, including specific binding to the vascular endothelial growth factor receptor-2 (VEGFR2). We tested the hypothesis that gremlin 1 modulates VEGFR2 signaling in the pulmonary microvascular endothelium. We examined the effect of gremlin 1 haploinsufficiency on the expression of VEGF responsive genes and proteins in the hypoxic (10% O2) murine lung in vivo. Using human microvascular endothelial cells in vitro we examined the effect of gremlin 1 on VEGF signaling. Gremlin 1 haploinsufficiency (Grem1+/–) attenuated the hypoxia-induced increase in gremlin 1 observed in the wild-type mouse lung. Reduced gremlin 1 expression in hypoxic Grem1+/– mice restored VEGFR2 expression and endothelial nitric oxide synthase (eNOS) expression and activity to normoxic values. Recombinant monomeric gremlin 1 inhibited VEGFA-induced VEGFR2 activation, downstream signaling, and VEGF-induced increases in Bcl-2, cell number, and the anti-apoptotic effect of VEGFA in vitro. These results show that the monomeric form of gremlin 1 acts as an antagonist of VEGFR2 activation in the pulmonary microvascular endothelium. Given the previous demonstration that inhibition of VEGFR2 causes marked worsening of HPH, our results suggest that increased gremlin 1 in the hypoxic lung, in addition to blocking BMP receptor type-2 (BMPR2) signaling, contributes importantly to the development of PH by a non-canonical VEGFR2 blocking activity.
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Mitola, Stefania, Cosetta Ravelli, Michela Corsini, Alessandra Gianoncelli, Federico Galvagni, Kurt Ballmer-Hofer, Marco Presta, and Elisabetta Grillo. "Production and Biochemical Characterization of Dimeric Recombinant Gremlin-1." International Journal of Molecular Sciences 23, no. 3 (January 21, 2022): 1151. http://dx.doi.org/10.3390/ijms23031151.

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Gremlin-1 is a secreted cystine-knot protein that acts as an antagonist of bone morphogenetic proteins (BMPs), and as a ligand of heparin and the vascular endothelial growth factor receptor 2 (VEGFR2), thus regulating several physiological and pathological processes, including embryonic development, tissue fibrosis and cancer. Gremlin-1 exerts all these biological activities only in its homodimeric form. Here, we propose a multi-step approach for the expression and purification of homodimeric, fully active, histidine-tagged recombinant gremlin-1, using mammalian HEK293T cells. Ion metal affinity chromatography (IMAC) of crude supernatant followed by heparin-affinity chromatography enables obtaining a highly pure recombinant dimeric gremlin-1 protein, exhibiting both BMP antagonist and potent VEGFR2 agonist activities.
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Elemam, Noha Mousaad, Abdullah Imadeddin Malek, Esraa Elaraby Mahmoud, Waseem El-Huneidi, and Iman M. Talaat. "Insights into the Role of Gremlin-1, a Bone Morphogenic Protein Antagonist, in Cancer Initiation and Progression." Biomedicines 10, no. 2 (January 28, 2022): 301. http://dx.doi.org/10.3390/biomedicines10020301.

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The bone morphogenic protein (BMP) antagonist Gremlin-1 is a biologically significant regulator known for its crucial role in tissue differentiation and embryonic development. Nevertheless, it has been reported that Gremlin-1 can exhibit its function through BMP dependent and independent pathways. Gremlin-1 has also been reported to be involved in organ fibrosis, which has been correlated to the development of other diseases, such as renal inflammation and diabetic nephropathy. Based on growing evidence, Gremlin-1 has recently been implicated in the initiation and progression of different types of cancers. Further, it contributes to the stemness state of cancer cells. Herein, we explore the recent findings on the role of Gremlin-1 in various cancer types, including breast, cervical, colorectal, and gastric cancers, as well as glioblastomas. Additionally, we highlighted the impact of Gremlin-1 on cellular processes and signaling pathways involved in carcinogenesis. Therefore, it was suggested that Gremlin-1 might be a promising prognostic biomarker and therapeutic target in cancers.
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Zhu, Zhenbiao, Xiaowei Xing, Shisi Huang, and Yuanyuan Tu. "NAT10 Promotes Osteogenic Differentiation of Mesenchymal Stem Cells by Mediating N4-Acetylcytidine Modification of Gremlin 1." Stem Cells International 2021 (April 12, 2021): 1–10. http://dx.doi.org/10.1155/2021/8833527.

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Objective. To investigate the function of NAT10 in mesenchymal stem cell (MSC) osteogenic differentiation and study the mechanism by which NAT10 affects MSC osteogenesis by mediating Gremlin 1 N4-acetylcytidine (ac4C) modification. Methods. Osteogenic differentiation of MSCs was induced, and the osteogenic ability was evaluated with alizarin red S (ARS) and alkaline phosphatase (ALP) assays. The NAT10 expression level during MSC osteogenesis was measured by western blot (WB). MSCs were transfected with lentiviruses to inhibit (Sh-NAT10) or overexpress NAT10 (Over-NAT10), and the osteogenic differentiation ability was assessed by ARS, ALP, and osteogenic gene marker assays. β-Catenin, Akt, and Smad signaling pathway component activation levels were assessed, and the expression levels of key Smad signaling pathway molecules were determined by PCR and WB. The Gremlin 1 mRNA ac4C levels were analyzed using RIP-PCR, and the Gremlin 1 mRNA degradation rate was determined. Sh-Gremlin 1 was transfected to further investigate the role of NAT10 and Gremlin 1 in MSC osteogenesis. Results. During MSC osteogenesis, NAT10 expression, ARS staining, and the ALP level gradually increased. Decreasing NAT10 expression inhibited, and increasing NAT10 expression promoted MSC osteogenic differentiation. NAT10 affected the BMP/Smad rather than the Akt and β-Catenin signaling pathway activation by regulating Gremlin 1 expression. The Gremlin 1 mRNA ac4C level was positively regulated by NAT10, which accelerated Gremlin 1 degradation. Sh-Gremlin 1 abolished the promotive effect of NAT10 on MSC osteogenic differentiation. Conclusion. NAT10 positively regulated MSC osteogenic differentiation through accelerating the Gremlin 1 mRNA degradation by increasing its ac4C level. These results may provide new mechanistic insight into MSC osteogenesis and bone metabolism in vivo.
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Aoshima, Yoichiro, Yasunori Enomoto, Shigeki Muto, Shiori Meguro, Hideya Kawasaki, Isao Kosugi, Tomoyuki Fujisawa, et al. "Gremlin-1 for the Differential Diagnosis of Idiopathic Pulmonary Fibrosis Versus Other Interstitial Lung Diseases: A Clinical and Pathophysiological Analysis." Lung 199, no. 3 (March 26, 2021): 289–98. http://dx.doi.org/10.1007/s00408-021-00440-y.

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Abstract Purpose The differential diagnosis of interstitial lung diseases (ILDs), particularly idiopathic pulmonary fibrosis (IPF) versus other non-IPF ILDs, is important for selecting the appropriate treatment. This retrospective study aimed to explore the utility of gremlin-1 for the differential diagnosis. Methods Serum gremlin-1 concentrations were measured using an ELISA in 50 patients with IPF, 42 patients with non-IPF ILD, and 30 healthy controls. The baseline clinical data, including pulmonary functions, prognosis, and three serum biomarkers (Krebs von den Lungen-6 [KL6], surfactant protein-D [SP-D], and lactate dehydrogenase [LDH]), were obtained through a medical record review for analyzing their associations with serum gremlin-1 concentrations. To evaluate the origin of gremlin-1, we performed immunostaining on lung sections. Results Serum gremlin-1 concentrations were significantly higher in patients with IPF (mean concentration, 14.4 ng/mL), followed by those with non-IPF ILD (8.8 ng/mL) and healthy controls (1.6 ng/mL). The area under the curve for IPF versus non-IPF ILDs was 0.759 (95% confidence interval, 0.661–0.857), which was superior to that of KL6/SP-D/LDH. The sensitivity and specificity for gremlin-1 (cutoff, 10.4 ng/mL) was 72 and 69%, respectively. By contrast, serum gremlin-1 concentrations were not associated with the pulmonary functions nor the prognosis in all patients with ILDs. In immunostaining, the gremlin-1 was broadly upregulated in IPF lungs, particularly at myofibroblasts, bronchiolar/alveolar epithelium, and CD163-positive M2-like macrophages. Conclusions Gremlin-1 may be a useful biomarker to improve the diagnostic accuracy for IPF compared to non-IPF ILDs, suggesting a role of this molecule in the pathogenesis of IPF.
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Park, Sin-Aye. "Role of Gremlin-1 in Cancer." Biomedical Science Letters 24, no. 4 (December 31, 2018): 285–91. http://dx.doi.org/10.15616/bsl.2018.24.4.285.

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Lavoz, Carolina, Jonay Poveda, Laura Marquez-Exposito, Sandra Rayego-Mateos, Raul R. Rodrigues-Diez, Alberto Ortiz, Jesús Egido, Sergio Mezzano, and Marta Ruiz-Ortega. "Gremlin activates the Notch pathway linked to renal inflammation." Clinical Science 132, no. 11 (June 5, 2018): 1097–115. http://dx.doi.org/10.1042/cs20171553.

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Preclinical studies suggest that Gremlin participates in renal damage and could be a potential therapeutic target for human chronic kidney diseases. Inflammation is a common characteristic of progressive renal disease, and therefore novel anti-inflammatory therapeutic targets should be investigated. The Notch signaling pathway is involved in kidney development and is activated in human chronic kidney disease, but whether Gremlin regulates the Notch pathway has not been investigated. In cultured tubular cells, Gremlin up-regulated gene expression of several Notch pathway components, increased the production of the canonical ligand Jagged-1, and caused the nuclear translocation of active Notch-1 (N1ICD). In vivo administration of Gremlin into murine kidneys elicited Jagged-1 production, increased N1ICD nuclear levels, and up-regulated the gene expression of the Notch effectors hes-1 and hey-1. All these data clearly demonstrate that Gremlin activates the Notch pathway in the kidney. Notch inhibition using the γ-secretase inhibitor DAPT impaired renal inflammatory cell infiltration and proinflammatory cytokines overexpression in Gremlin-injected mice and in experimental models of renal injury. Moreover, Notch inhibition blocked Gremlin-induced activation of the canonical and noncanonical nuclear factor-κB (NF-κB) pathway, identifying an important mechanism involved in the anti-inflammatory actions of Notch inhibition. In conclusion, Gremlin activates the Notch pathway in the kidney and this is linked to NF-κB-mediated inflammation, supporting the hypothesis that Notch inhibition could be a potential anti-inflammatory strategy for renal diseases.
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Дисертації з теми "Gremlin 1"

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Scheitza, Sandra [Verfasser], and Meinrad [Akademischer Betreuer] Gawaz. "Die Rolle von Gremlin-1 für die kardiale Entwicklung im Zebrafischembryo / Sandra Scheitza ; Betreuer: Meinrad Gawaz." Tübingen : Universitätsbibliothek Tübingen, 2013. http://d-nb.info/116060648X/34.

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Church, Rachel Henrietta. "Elucidating the mechanisms of Gremlin 1-mediated bone morphogenetic protein antagonism and acute kidney injury in vivo." Thesis, Queen's University Belfast, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.695301.

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Diabetic nephropathy (ON) is a major microvascular complication associated with diabetes. DN is characterised by a progressive loss in renal function and associated renal fibrosis. Currently, no cure exists for DN and therapeutic strategies seek to slow the decline in renal function, through glycaemic and blood pressure control. Acute kidney injury (AKI) is a condition that can arise due to a range of pre-renal, renal and post- renal causes. AKI is associated with decreased glomerular filtration rate (GFR), resulting in accumulation of nitrogenous waste products and other complications. The precise molecular mechanisms of renal damage in these diseases is still not fully understood and needs to be further elucidated. Bone morphogenetic proteins (BMPs) have been shown to be anti-fibrotic in models of renal fibrosis. Gremlin1 (Grem1), a BMP antagonist is upregulated in conditions such as ON. It is hypothesised that Grem1 binding to BMPs is crucial to its pathogenic role in renal fibrosis. The specific interactions of Grem1 and BMPs in disease have not been fully determined. The overarching aim of this thesis was to better define the role of Grem1 binding to BMPs in vitro, in order to contribute to our understanding of these interactions in the context of kidney disease. Using a range of in vitro methods, we determined that Grem1 relative binding affinity is BMP-2>-4>-7, and that the post-translational modifications of glycosylation and phosphorylation of Grem1 may not be essential for BMP antagonism. We also found that Grem2 differentially inhibits BMP-2, -4 and -7 signalling in vitro. We determined that isolation of Grem1-BMP complexes are difficult using standard in vitro methods, and that direct mass spectrometry (MS) approaches may be advantageous. We have determined that mice with tubular specific deletion of Grem1 (Grem1 TEC -1-) display somewhat attenuated renal damage in a folic acid (FA) induced model of AKI. These findings provide a mechanistic insight into the possible molecular interactions between Grem1 and BMPs, and may have implications in the context of renal fibrosis. Given the high binding observed between Grem1 and BMP-2, this complex formation may be favoured in the 'diseased' kidney. Furthermore, Grem1 inhibition of BMP-7 may not occur via direct interaction. Manipulation of the Grem1-BMP axis has been explored as a potential therapeutic strategy by many research groups, and this is further supported by our findings that Grem1 TEC -1- mice display attenuated renal injury in a model of AKI. Further work will be required to further define these interactions in models in renal fibrosis.
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Schneider, Martina Constanze [Verfasser], and Meinrad [Akademischer Betreuer] Gawaz. "Die Rolle von Gremlin-1 und seiner Bindungspartner im kardiovaskulären System / Martina Constanze Schneider ; Akademischer Betreuer: Meinrad Gawaz." Tübingen : Universitätsbibliothek Tübingen, 2015. http://d-nb.info/1168057973/34.

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Schmid, Martina [Verfasser], and Tobias [Akademischer Betreuer] Geisler. "Der Einfluss von Gremlin-1 in der koronaren Herzkrankheit und seine funktionelle Bedeutung / Martina Schmid ; Betreuer: Tobias Geisler." Tübingen : Universitätsbibliothek Tübingen, 2018. http://d-nb.info/1168148677/34.

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Schneider, Martina [Verfasser], and Meinrad [Akademischer Betreuer] Gawaz. "Die Rolle von Gremlin-1 und seiner Bindungspartner im kardiovaskulären System / Martina Constanze Schneider ; Akademischer Betreuer: Meinrad Gawaz." Tübingen : Universitätsbibliothek Tübingen, 2015. http://d-nb.info/1168057973/34.

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Tavlaki, Elli [Verfasser], and Tobias [Akademischer Betreuer] Geisler. "Diagnostic and prognostic implications of myocardial Gremlin-1 expression in patients with structural myocardial disease / Elli Tavlaki ; Betreuer: Tobias Geisler." Tübingen : Universitätsbibliothek Tübingen, 2016. http://d-nb.info/119769501X/34.

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Karathanos, Athanasios [Verfasser], and Tobias [Akademischer Betreuer] Geisler. "Macrophage migration inhibitory factor and gremlin-1 in patients with coronary artery disease and diabetes : patterns of expression and interaction / Athanasios Karathanos ; Betreuer: Tobias Geisler." Tübingen : Universitätsbibliothek Tübingen, 2018. http://d-nb.info/1196701288/34.

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Clark, Kimberley Claire. "The Role of Gremlin1 in Multiple Myeloma." Thesis, 2020. http://hdl.handle.net/2440/127291.

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Multiple myeloma (MM) is a fatal haematological malignancy characterised by the clonal proliferation of malignant plasma cells (PC) within the bone marrow (BM). In most instances, MM PCs are reliant on factors made by cells of the BM stroma for their survival and growth. To date, the nature and cellular composition of the BM tumour microenvironment and the critical factors which drive tumour progression remain imprecisely defined. The studies presented here show that Gremlin1 (Grem1), a highly conserved protein, which is abundantly secreted by a subset of BM mesenchymal stromal cells, plays a critical role in MM disease development. We describe, for the first time, a novel positive feedback loop between MM PCs and BM stroma, and that inhibiting this vicious cycle with a neutralising antibody directed against Grem1 dramatically reduced tumour burden in a preclinical mouse model of MM. Analysis of human BM stromal samples by quantitative PCR showed that GREM1 expression was significantly higher in MM patient-derived BM stromal cells compared to stromal cells from healthy, age-matched individuals (p<0.01 t-test). Additionally, a positive correlation between MM tumour burden and stromal-cell associated Grem1 expression was observed in 5TGM1 MM PC tumour-bearing mice (p<0.05, R=0.64, Pearson Correlation). Furthermore, BM-stromal cells cultured with 5TGM1 MM PCs expressed significantly higher levels of Grem1, compared to stromal cells alone (p<0.01, t-test), suggesting that MM PCs promote increased Grem1 expression in stromal cells. MM PC induction of stromal-Grem1 serves to drive a positive feedback loop, as proliferation of the murine MM cell line, 5TGM1, was found to be significantly increased when co-cultured with Grem1-overexpressing stromal cells (p<0.01, t-test). To further examine the role of Grem1 in MM tumour establishment and growth in vivo, we utilised the 5TGM1/KaLwRij mouse model of MM. Following 5TGM1 tumour cell inoculation, mice were randomly assigned to either a neutralising Grem1 antibody (anti-Grem1 antibody, UCB-Pharma) or IgG control treatment arm. Our studies showed that compared to Ig control-treated mice, anti-Grem1-treated mice showed a 54% decrease in tumour burden. This effect was even more pronounced when mice received treatment with a Grem1 neutralising antibody prior to 5TGM1 tumour cell inoculation, resulting in an 80% reduction in tumour burden. Moreover, MM tumour burden was reduced in a Vk*MYC/Grem1-genetic knockout mouse model, although this did not reach statistical significance. Collectively, the data presented in this thesis suggests that Grem1 is a key stromal-derived PC mitogen that promotes MM disease initiation and progression, and that antibody-mediated targeting of Grem1 significantly reduces disease burden. With few effective therapies directed against the critical relationship between MM PCs and the BM, the findings presented here, represent a novel treatment strategy to limit MM disease burden.
Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2020
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Книги з теми "Gremlin 1"

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Gremlin Trouble Volume 1. Elizabeth Bryan, 1998.

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Robinson, Erin. Golden Gremlin : A Sinister Shade Mystery: Volume 1. Independently Published, 2019.

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3

Cómo domar a tu gremlin: Un método sorprendentemente simple para dejar de sabotearte a ti mismo. Sirio, 2021.

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4

Hobmaier, Franziska. Die Einrichtung völkervertraglicher Gremien. Mohr Siebeck, 2021. http://dx.doi.org/10.1628/978-3-16-160967-1.

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Council for Education, Recruitment and Training for the Hotel, Catering and Tourism Industry., ed. Greman for the hotel, catering and tourism industry: Level 1. Dublin: CERT, 1992.

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Armitage, Dannielle. Eat Sleep Gremio Repeat - Gremio Art Planner and Organizer: Gremio, A5 Size Weekly Planner, Goals Journal and Agenda to Improve Time Management, Productivity and Live Happier. Undated - Start Anytime, Lasts 1 Year,Tax. Independently Published, 2021.

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Vallejo Zambrano, Cristhian Rubén, Ricardo Aspren Jiménez Jiménez, Clelia Celeste Ricaurte Jijón, Néstor Jamil Palma Moreno, María Belén Del Valle Pilay, Marcela Elizabeth Gómez Chumo, Simón Alfonso Ávila Meza, Libeth Larrea Ricaurte, Luis Felipe Zambrano Cedeño, and Yansen Hernán Acosta Macías. Compendio didáctico de neurocirugía básica. Mawil Publicaciones de Ecuador, 2021, 2022. http://dx.doi.org/10.26820/978-9942-602-08-4.

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En el contexto histórico actual el conocimiento busca la profundidad de los cambios surgidos de la realidad, es así como el sistema nervioso se define como el conjunto de estructuras que dirige y regula el funcionamiento correcto del organismo. Por consiguiente, se afirma que, dentro de la escala de evolución de las especies, es el sistema más evolucionado de la naturaleza y extraordinariamente complejo. Desde estas consideraciones la Neurocirugía es la ciencia médica que estudia las enfermedades que afectan al sistema nervioso que requieren o pueden requerir un tratamiento quirúrgico en algún momento de su evolución. El sistema nervioso es el conjunto de estructuras que dirige y regula el funcionamiento correcto del organismo. Desde esta perspectiva, conceptualmente la Neurocirugía es “aquella disciplina de la Medicina y especialidad de la Cirugía que se ocupa del estudio y tratamiento (esto es, prevención, diagnóstico, evaluación, terapéutica, cuidado intensivo y rehabilitación), de las enfermedades quirúrgicas o potencialmente quirúrgicas del Sistema Nervioso Central, Periférico y Autónomo, incluyendo sus cubiertas, vascularización y anejos como la hipófisis, así como del manejo operatorio y no operatorio del dolor, cualquiera que sea la edad del paciente” (1). En este marco relacional, atendiendo a su argumento presentado a continuación se hace alusión a este compendio de los avances de la medicina a nivel Neurológico de gran relevancia y aporte para los futuros médicos y especialistas del gremio médico.
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Частини книг з теми "Gremlin 1"

1

Appleman, Dan. "Gremlins in Your Machine." In Always Use Protection, 3–5. Berkeley, CA: Apress, 2004. http://dx.doi.org/10.1007/978-1-4302-0904-1_1.

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Rabuzin, Kornelije. "Query Languages for Graph Databases." In Encyclopedia of Information Science and Technology, Fourth Edition, 2031–42. IGI Global, 2018. http://dx.doi.org/10.4018/978-1-5225-2255-3.ch176.

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In the past few years many NoSQL databases have emerged, including graph databases. NoSQL databases have certain advantages and they can be used in certain domains as an alternative to relational databases. In order to use graph databases, one needs to be familiar with specific languages like Cypher Query Language (CQL) or Gremlin. However, some statements in CQL can be considered too complex for end users as it is shown later on. Because of that the main idea of this paper is to explore two other languages for graph databases. One of them is new and it is used to pose queries visually. Since CQL does not support recursion, views, etc., the other language is used to show how to use recursion and views on a graph database.
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Rabuzin, Kornelije. "Query Languages for Graph Databases." In Advances in Computer and Electrical Engineering, 645–59. IGI Global, 2019. http://dx.doi.org/10.4018/978-1-5225-7598-6.ch047.

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In the past few years, many NoSQL databases have emerged, including graph databases. NoSQL databases have certain advantages and they can be used in certain domains as an alternative to relational databases. In order to use graph databases, one needs to be familiar with specific languages like Cypher Query Language (CQL) or Gremlin. However, some statements in CQL can be considered too complex for end users as it is shown later on. Because of that, the main idea of this chapter is to explore two other languages for graph databases. One of them is new and it is used to pose queries visually. Since CQL does not support recursion, views, etc., the other language is used to show how to use recursion and views on a graph database.
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Brennan, Jason, and Phillip Magness. "Neither Gremlins nor Poltergeists." In Cracks in the Ivory Tower, 1–21. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780190846282.003.0001.

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This chapter first discusses the serious moral flaws in higher education. Universities’ problems are deep and fundamental: Most academic marketing is semi-fraudulent, grading is largely nonsense, students do not study or learn much, students cheat frequently, professors and administrators waste students’ money and time to line their own pockets, professors pump out unemployable graduate students for self-serving reasons, and so on. This book argues that academia’s problems are ingrained. Bad behaviors result from regular people reacting to bad incentives baked into academia. Chapter 1 also lists seven basic economic ideas and principles that people—including people who write about higher education—routinely ignore.
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Schmitt, Laura. "1. Kapitel: Rechts- und Vermögensfähigkeit der betriebsverfassungsrechtlichen Gremien." In Die Haftung betriebsverfassungsrechtlicher Gremien und ihrer Mitglieder, 94–302. Nomos Verlagsgesellschaft mbH & Co. KG, 2017. http://dx.doi.org/10.5771/9783845284040-94.

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Schmitt, Laura. "Titelei/Inhaltsverzeichnis." In Die Haftung betriebsverfassungsrechtlicher Gremien und ihrer Mitglieder, 1–86. Nomos Verlagsgesellschaft mbH & Co. KG, 2017. http://dx.doi.org/10.5771/9783845284040-1.

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FREER, D. "Technical Issues: Killing the Gremlins before They Kill Your Pictures." In Microstock Photography, 77–101. Elsevier, 2007. http://dx.doi.org/10.1016/b978-0-240-80896-3.50009-1.

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Тези доповідей конференцій з теми "Gremlin 1"

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Mthunzi, L., S. C. Rowan, L. Piouceau, S. Devlin, U. Knaus, and P. McLoughlin. "Gremlin-1 Modulates Macrophage Polarization." 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.a5279.

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Duffy, L., and S. O’Reilly. "P059 Dissecting the role of gremlin 1 in systemic sclerosis." In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.51.

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Yin, Miao, Mira Tissari, Emmi I. Joensuu, Jenni Tamminen, Irene Ylivinkka, Mikko Rönty, Kaisa Lehti, Marko Hyytiäinen, Marjukka Myllärniemi, and Katri Koli. "Abstract 1894: Gremlin-1 is an important regulator of invasiveness in malignant mesothelioma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1894.

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Worthley, Daniel L., Yiling Si, Samuel Asfaha, Benedikt Westphalen, Yagnesh Tailor, Michael Churchill, Jean-Philippe Pradere, Robert Schwabe, Siddhartha Mukherjee, and Timothy Wang. "Abstract 2299: Gremlin 1 labels a mesenchymal progenitor in the gastrointestinal tract, bone and tumor microenvironment." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2299.

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Schiavi, Elisa, Silvia Cantoni, Giorgia Volpi, Massimiliano Cont, Fiorella Pastore, Stefano Cavalli, Fabio Dardi, Gino Villetti, and Fabrizio Facchinetti. "Macitentan modulates pulmonary mRNA levels of gremlin 1 in a rat model of pulmonary arterial hypertension." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa1418.

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Worthley, Daniel L., Michael Quante, Samuel Asfaha, Christoph Benedikt Westphalen, Jean-Philippe Pradere, Juliane Troeger, Robert Schwabe, and Timothy C. Wang. "Abstract 2969: Gremlin 1 labels a mesenchymal progenitor cell in the gastrointestinal tract, bone marrow and cancer microenvironment." 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.am2012-2969.

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Park, Sin-Aye, Bae-Jung Choi, Wonki Kim та Young-Joon Surh. "Abstract 4001: Gremlin-1 augments the estrogen-related receptor α signaling: Implications for progression of breast cancer in synergistic manner". У Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4001.

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