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Gotowe bibliografie tematyczne / Membrane-Bound TGF-Β

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Gotowa bibliografia na temat „Membrane-Bound TGF-Β”

Autor: Grafiati

Data publikacji: 30 listopada 2024

Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Membrane-Bound TGF-Β"

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Elderbroom, Jennifer L., Jennifer J. Huang, Catherine E. Gatza та ін. "Ectodomain shedding of TβRIII is required for TβRIII-mediated suppression of TGF-β signaling and breast cancer migration and invasion". Molecular Biology of the Cell 25, № 16 (2014): 2320–32. http://dx.doi.org/10.1091/mbc.e13-09-0524.

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The type III transforming growth factor β (TGF-β) receptor (TβRIII), also known as betaglycan, is the most abundantly expressed TGF-β receptor. TβRIII suppresses breast cancer progression by inhibiting migration, invasion, metastasis, and angiogenesis. TβRIII binds TGF-β ligands, with membrane-bound TβRIII presenting ligand to enhance TGF-β signaling. However, TβRIII can also undergo ectodomain shedding, releasing soluble TβRIII, which binds and sequesters ligand to inhibit downstream signaling. To investigate the relative contributions of soluble and membrane-bound TβRIII on TGF-β signaling a

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Kim, Pyeung-Hyeun, Young-Saeng Jang, Ha-Eon Song, et al. "Mechanism underlying the induction of Foxp3+ regulatory T cells by lactoferrin." Journal of Immunology 200, no. 1_Supplement (2018): 47.16. http://dx.doi.org/10.4049/jimmunol.200.supp.47.16.

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Abstract Lactoferrin (LF) is multifunctional in the immune response. We have previously demonstrated that LF acts like TGF-β in IgA B cell differentiation. Therein, we explored whether LF affects peripheral regulatory T cell (Treg) differentiation. Indeed, LF induced Foxp3+ Treg differentiation by itself and in combination with TGF-β1 synergized to express Foxp3. It was conceivable that LF may increase Foxp3 expression through secretion of active TGF-β or facilitating latent TGF-β to active form. There was little active TGF-β in the supernatant from LF-stimulated T cells. Surprisingly, however

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Yan, Xiaohua, та Ye-Guang Chen. "Smad7: not only a regulator, but also a cross-talk mediator of TGF-β signalling". Biochemical Journal 434, № 1 (2011): 1–10. http://dx.doi.org/10.1042/bj20101827.

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TGF-β (transforming growth factor-β) is a pleiotropic cytokine regulating diverse cellular processes. It signals through membrane-bound receptors, downstream Smad proteins and/or other signalling mediators. Smad7 has been well established to be a key negative regulator of TGF-β signalling. It antagonizes TGF-β signalling through multiple mechanisms in the cytoplasm and in the nucleus. Smad7 can be transcriptionally induced by TGF-β and other growth factors and serves as an important cross-talk mediator of the TGF-β signalling pathway with other signalling pathways. Accordingly, it plays pivota

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Kim, Sun Kyung, Morkos A. Henen, and Andrew P. Hinck. "Structural biology of betaglycan and endoglin, membrane-bound co-receptors of the TGF-beta family." Experimental Biology and Medicine 244, no. 17 (2019): 1547–58. http://dx.doi.org/10.1177/1535370219881160.

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Betaglycan and endoglin, membrane-bound co-receptors of the TGF-β family, are required to mediate the signaling of a select subset of TGF-β family ligands, TGF-β2 and InhA, and BMP-9 and BMP-10, respectively. Previous biochemical and biophysical methods suggested alternative modes of ligand binding might be responsible for these co-receptors to selectively recognize and potentiate the functions of their ligands, yet the molecular details were lacking. Recent progress determining structures of betaglycan and endoglin, both alone and as bound to their cognate ligands, is presented herein. The st

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Sisto, Margherita, Domenico Ribatti, and Sabrina Lisi. "SMADS-Mediate Molecular Mechanisms in Sjögren’s Syndrome." International Journal of Molecular Sciences 22, no. 6 (2021): 3203. http://dx.doi.org/10.3390/ijms22063203.

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There is considerable interest in delineating the molecular mechanisms of action of transforming growth factor-β (TGF-β), considered as central player in a plethora of human conditions, including cancer, fibrosis and autoimmune disease. TGF-β elicits its biological effects through membrane bound serine/threonine kinase receptors which transmit their signals via downstream signalling molecules, SMADs, which regulate the transcription of target genes in collaboration with various co-activators and co-repressors. Until now, therapeutic strategy for primary Sjögren’s syndrome (pSS) has been focuse

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Weber, Florian, Oliver Treeck, Patricia Mester, and Christa Buechler. "Expression and Function of BMP and Activin Membrane-Bound Inhibitor (BAMBI) in Chronic Liver Diseases and Hepatocellular Carcinoma." International Journal of Molecular Sciences 24, no. 4 (2023): 3473. http://dx.doi.org/10.3390/ijms24043473.

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BAMBI (bone morphogenetic protein and activin membrane-bound inhibitor) is a transmembrane pseudoreceptor structurally related to transforming growth factor (TGF)-β type 1 receptors (TGF-β1Rs). BAMBI lacks a kinase domain and functions as a TGF-β1R antagonist. Essential processes such as cell differentiation and proliferation are regulated by TGF-β1R signaling. TGF-β is the best-studied ligand of TGF-βRs and has an eminent role in inflammation and fibrogenesis. Liver fibrosis is the end stage of almost all chronic liver diseases, such as non-alcoholic fatty liver disease, and at the moment, th

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Dhandapani, Krishnan M., F. Marlene Wade, Virendra B. Mahesh та Darrell W. Brann. "Astrocyte-Derived Transforming Growth Factor-β Mediates the Neuroprotective Effects of 17β-Estradiol: Involvement of Nonclassical Genomic Signaling Pathways". Endocrinology 146, № 6 (2005): 2749–59. http://dx.doi.org/10.1210/en.2005-0014.

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Abstract 17β-Estradiol (E2) and selective estrogen receptor modulators (SERMs), such as tamoxifen, mediate numerous effects in the brain, including neurosecretion, neuroprotection, and the induction of synaptic plasticity. Astrocytes, the most abundant cell type in the brain, influence many of these same functions and thus may represent a mediator of estrogen action. The present study examined the regulatory effect and underlying cell signaling mechanisms of E2-induced release of neurotropic growth factors from primary rat cortical astrocyte cultures. The results revealed that E2 (0.5, 1, and

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Gallardo-Vara, Ruiz-Llorente, Casado-Vela, et al. "Endoglin Protein Interactome Profiling Identifies TRIM21 and Galectin-3 as New Binding Partners." Cells 8, no. 9 (2019): 1082. http://dx.doi.org/10.3390/cells8091082.

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Endoglin is a 180-kDa glycoprotein receptor primarily expressed by the vascular endothelium and involved in cardiovascular disease and cancer. Heterozygous mutations in the endoglin gene (ENG) cause hereditary hemorrhagic telangiectasia type 1, a vascular disease that presents with nasal and gastrointestinal bleeding, skin and mucosa telangiectases, and arteriovenous malformations in internal organs. A circulating form of endoglin (alias soluble endoglin, sEng), proteolytically released from the membrane-bound protein, has been observed in several inflammation-related pathological conditions a

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Zhu, Qingwei, Yong Hwan Kim, Douglas Wang, S. Paul Oh, and Kunxin Luo. "SnoN facilitates ALK1–Smad1/5 signaling during embryonic angiogenesis." Journal of Cell Biology 202, no. 6 (2013): 937–50. http://dx.doi.org/10.1083/jcb.201208113.

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In endothelial cells, two type I receptors of the transforming growth factor β (TGF-β) family, ALK1 and ALK5, coordinate to regulate embryonic angiogenesis in response to BMP9/10 and TGF-β. Whereas TGF-β binds to and activates ALK5, leading to Smad2/3 phosphorylation and inhibition of endothelial cell proliferation and migration, BMP9/10 and TGF-β also bind to ALK1, resulting in the activation of Smad1/5. SnoN is a negative regulator of ALK5 signaling through the binding and repression of Smad2/3. Here we uncover a positive role of SnoN in enhancing Smad1/5 activation in endothelial cells to p

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Yang, Young, та Sujeong Park. "Abstract LB010: LY6K depletion modulates TGF-β and EGF signaling". Cancer Research 83, № 8_Supplement (2023): LB010. http://dx.doi.org/10.1158/1538-7445.am2023-lb010.

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Abstract Lymphocyte antigen 6 complex locus K (LY6K), a glycosylphosphatidylinositol-anchored protein, plays a dynamic role in cancer metastasis. In the current study, we deciphered the effects of LY6K on transforming growth factor-β (TGF-β) and epidermal growth factor (EGF) signaling through clathrin- and caveolin-1 (CAV-1)-mediated endocytosis. LY6K expression level is elevated in higher grade cervical cancer patients correlating with poor overall survival, progression-free survival, and disease-free survival. LY6K-depletion in HeLa and SiHa cancer cells suppressed EGF-induced proliferation

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Rozprawy doktorskie na temat "Membrane-Bound TGF-Β"

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Wnent, Dorothee Anna [Verfasser], Daniel [Akademischer Betreuer] Drömann та Guido [Akademischer Betreuer] Stichtenoth. "Pulmonales Geweberemodeling und Reparaturmechanismen im TGF-β Pseudorezeptor BMP and activin membrane bound inhibitor Knockout Modell nach ex vivo Infektion mit Nontypeable Haemophilus influenzae / Dorothee Anna Wnent ; Akademische Betreuer: Daniel Drömann, Guido Stichtenoth". Lübeck : Zentrale Hochschulbibliothek Lübeck, 2021. http://d-nb.info/1232284416/34.

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Boyer, Thomas. "Impact des cellules myéloïdes immunosuppressives dans l’induction de cellules souches cancéreuses." Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0221.

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Le micro-environnement tumoral est fortement influencé par les cellules myéloïdes, dont les macrophages, les neutrophiles et les monocytes sont des représentants majeurs. Les recherches des dernières décennies ont montré que presque toutes les tumeurs sont infiltrées par des cellules myéloïdes, rendant impossible l'existence de tumeurs "froides" en ce qui concerne ces cellules. De plus, les résultats de nombreuses études cliniques se focalisant sur le compartiment immunitaire myéloïde montrent clairement que ces cellules sont presque universellement associées avec un pronostique clinique négat

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