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Gotowe bibliografie tematyczne / Paracrine signalling

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Gotowa bibliografia na temat „Paracrine signalling”

Autor: Grafiati

Data publikacji: 3 czerwca 2025

Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Paracrine signalling"

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Michael Lavigne, G., Hayley Russell, Barbara Sherry, and Ruian Ke. "Autocrine and paracrine interferon signalling as ‘ring vaccination’ and ‘contact tracing’ strategies to suppress virus infection in a host." Proceedings of the Royal Society B: Biological Sciences 288, no. 1945 (2021): 20203002. http://dx.doi.org/10.1098/rspb.2020.3002.

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The innate immune response, particularly the interferon response, represents a first line of defence against viral infections. The interferon molecules produced from infected cells act through autocrine and paracrine signalling to turn host cells into an antiviral state. Although the molecular mechanisms of IFN signalling have been well characterized, how the interferon response collectively contribute to the regulation of host cells to stop or suppress viral infection during early infection remain unclear. Here, we use mathematical models to delineate the roles of the autocrine and the paracr

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Faccenda, Danilo, and Michelangelo Campanella. "Mitochondria Regulate Inflammatory Paracrine Signalling in Neurodegeneration." Journal of Neuroimmune Pharmacology 15, no. 4 (2020): 565–66. http://dx.doi.org/10.1007/s11481-020-09952-5.

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Lin, Yongshun, and Fen Wang. "FGF signalling in prostate development, tissue homoeostasis and tumorigenesis." Bioscience Reports 30, no. 5 (2010): 285–91. http://dx.doi.org/10.1042/bsr20100020.

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The FGFs (fibroblast growth factors) regulate a broad spectrum of biological activities by activating transmembrane FGFR (FGF receptor) tyrosine kinases and their coupled intracellular signalling pathways. In the prostate, the mesenchymal–epithelial interactions mediated by androgen signalling and paracrine factors are essential for gland organogenesis, homoeostasis and tumorigenesis. FGFs mediate these mesenchymal–epithelial interactions in the prostate by paracrinal crosstalk through a diverse set of ligands and receptors. Gain- and loss-of-function studies in mouse models have demonstrated

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Yauch, Robert L., Stephen E. Gould, Suzie J. Scales, et al. "A paracrine requirement for hedgehog signalling in cancer." Nature 455, no. 7211 (2008): 406–10. http://dx.doi.org/10.1038/nature07275.

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Momiji, Hiroshi, Kirsty L. Hassall, Karen Featherstone, et al. "Disentangling juxtacrine from paracrine signalling in dynamic tissue." PLOS Computational Biology 15, no. 6 (2019): e1007030. http://dx.doi.org/10.1371/journal.pcbi.1007030.

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Schumacher, Neele, Stefan Rose-John, and Dirk Schmidt-Arras. "ADAM-Mediated Signalling Pathways in Gastrointestinal Cancer Formation." International Journal of Molecular Sciences 21, no. 14 (2020): 5133. http://dx.doi.org/10.3390/ijms21145133.

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Tumour growth is not solely driven by tumour cell-intrinsic mechanisms, but also depends on paracrine signals provided by the tumour micro-environment. These signals comprise cytokines and growth factors that are synthesized as trans-membrane proteins and need to be liberated by limited proteolysis also termed ectodomain shedding. Members of the family of A disintegrin and metalloproteases (ADAM) are major mediators of ectodomain shedding and therefore initiators of paracrine signal transduction. In this review, we summarize the current knowledge on how ADAM proteases on tumour cells but also

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Gonzalez-Meljem, Jose Mario, and Juan Pedro Martinez-Barbera. "Adamantinomatous craniopharyngioma as a model to understand paracrine and senescence-induced tumourigenesis." Cellular and Molecular Life Sciences 78, no. 10 (2021): 4521–44. http://dx.doi.org/10.1007/s00018-021-03798-7.

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AbstractCellular senescence is a process that can prevent tumour development in a cell autonomous manner by imposing a stable cell cycle arrest after oncogene activation. Paradoxically, senescence can also promote tumour growth cell non-autonomously by creating a permissive tumour microenvironment that fuels tumour initiation, progression to malignancy and metastasis. In a pituitary tumour known as adamantinomatous craniopharyngioma (ACP), cells that carry oncogenic β-catenin mutations and overactivate the WNT signalling pathway form cell clusters that become senescent and activate a senescenc

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Zoni, Eugenio, Gabri van der Pluijm, Peter C. Gray та Marianna Kruithof-de Julio. "Epithelial Plasticity in Cancer: Unmasking a MicroRNA Network for TGF-β-, Notch-, and Wnt-Mediated EMT". Journal of Oncology 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/198967.

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Epithelial-to-mesenchymal transition (EMT) is a reversible process by which cancer cells can switch from a sessile epithelial phenotype to an invasive mesenchymal state. EMT enables tumor cells to become invasive, intravasate, survive in the circulation, extravasate, and colonize distant sites. Paracrine heterotypic stroma-derived signals as well as paracrine homotypic or autocrine signals can mediate oncogenic EMT and contribute to the acquisition of stem/progenitor cell properties, expansion of cancer stem cells, development of therapy resistance, and often lethal metastatic disease. EMT is

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Moreira, Lucia M., Abhijit Takawale, Mohit Hulsurkar, et al. "Paracrine signalling by cardiac calcitonin controls atrial fibrogenesis and arrhythmia." Nature 587, no. 7834 (2020): 460–65. http://dx.doi.org/10.1038/s41586-020-2890-8.

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Hooper, Joan E. "Distinct pathways for autocrine and paracrine Wingless signalling inDrosophila embryos." Nature 372, no. 6505 (1994): 461–64. http://dx.doi.org/10.1038/372461a0.

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Rozprawy doktorskie na temat "Paracrine signalling"

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Tamiya, Shigeo. "Autocrine and paracrine signalling mechanisms in lens cells." Thesis, University of East Anglia, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365025.

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Keightley, Margaret Claire. "Autocrine and paracrine regulation of endothelial cell function by F-Prostanoid receptor signalling." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4809.

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Endometrial adenocarcinoma, originating from the glandular epithelial cells of the uterine endometrial lining, is one of the most prevalent cancers amongst women in the Western world. The prostaglandin F2α (PGF2α) receptor (FP) is upregulated in endometrial adenocarcinoma. A previous microarray analysis of endometrial adenocarcinoma cells (Ishikawa) identified numerous targets of PGF2α-FP signalling including angiogenic factors, VEGF-A, FGF-2, CXCL1 and CXCL8 and antiangiogenic factors ADAMTS1. The regulation of VEGF-A, FGF-2, CXCL1 and CXCL8 was confirmed by previous studies using an in vitro

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Estévez, Cebrero María de los Ángeles. "Influence of paracrine signalling within the tumour microenvironment on progression in breast cancer models." Thesis, University of Nottingham, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.727116.

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Introduction: Cancer cells are affected by paracrine signalling from surrounding stromal cells. Here we investigate the role of kinases in this signalling using a model breast cancer (BC) co-culture system to identify novel paracrine signalling mechanisms supporting the growth and survival of tumour cells and potentially modulating epithelial to mesenchymal transition (EMT). Methods: The influence of paracrine signalling of the MSCs in the growth of luminal and basal-like breast cancer cells after the knock-down of human kinases, selected through a screen of a siRNA library, was investigated u

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Curley, Michael Kings. "Dissecting the paracrine interactions contributing to normal testicular function and during the ageing process." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/28972.

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The mammalian testis is divided into two distinct compartments which carry out its principal functions. Spermatogenesis occurs within the seminiferous tubules and androgen biosynthesis primarily occurs in the interstitial space. Both these processes are entirely dependent upon the two major testicular somatic cell populations - the Sertoli and Leydig cells respectively. In human males, testicular spermatogenic and endocrine function declines during the ageing process. Of particular significance is the reported age-related decrease in Leydig cell androgen production as androgens have been sugge

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Alsoufi, Zainab. "Qualitative study of NFκB models in macrophages". Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/qualitative-study-of-nfib-models-in-macrophages(5815a336-e2b9-45f1-be37-339c2cd258dc).html.

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Macrophages are the largest cells in the immune system and they regulate inflammatory signalling and inform cell fate decisions. Many signals, including those mediated by Tumor Necrosis Factor alpha (TNFα) converge on a few key intracellular signalling pathways, including the Nuclear Factor kappa B (NFκB) network. The NFκB signalling pathway plays a vital role in the regulation of many different cellular responses, including the production of TNFα itself, which is required to sustain and propagate immune responses to, for example, infection or tissue damage. In this thesis we report on studies

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McCosker, Helen Clare. "Prognostic significance of IGF and ECM induced signalling proteins in breast cancer patients." Thesis, Queensland University of Technology, 2012. https://eprints.qut.edu.au/53580/1/Helen_McCosker_Thesis.pdf.

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Breast cancer is a leading contributor to the burden of disease in Australia. Fortunately, the recent introduction of diverse therapeutic strategies have improved the survival outcome for many women. Despite this, the clinical management of breast cancer remains problematic as not all approaches are sufficiently sophisticated to take into account the heterogeneity of this disease and are unable to predict disease progression, in particular, metastasis. As such, women with good prognostic outcomes are exposed to the side effects of therapies without added benefit. Furthermore, women with aggres

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Coelho, Tiago Rodrigo da Costa. "Unveiling paracrine dissemination and toxicity of neuronal TrkB-ICD via secretome signalling in Alzheimer’s disease." Master's thesis, 2021. http://hdl.handle.net/10362/123379.

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The brain-derived neurotrophic factor (BDNF) is a neurotrophin that binds to the TrkB full-length receptor (TrkB-FL), triggering cascades responsible for neuroprotection. This BDNF/TrkB-FL system is known to be impaired in Alzheimer’s disease (AD)due to an amyloid-β-mediated TrkB-FL cleavage, leading tothe formation of two fragments,a membrane-bound truncated receptor (TrkB-T’) and an intracellular domain fragment (TrkB-ICD). TrkB-ICD hastyrosine kinase activity, promotescognitive impairments,and modifiesgene expression.Notwithstanding, its intracellul

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"Effects of ultrasound field distance of low-intensity pulsed ultrasound (LIPUS) on rat fracture healing and osteocyte-osteoblast paracrine signalling." 2012. http://library.cuhk.edu.hk/record=b5549463.

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临床及动物实验的文献报告表明, 低能量脉冲超声波 (LIPUS) 能促进骨折愈合。可是, 不同研究小组针对LIPUS的功效所提供的数据结果往往并不一致。为了找出导致数据结果不一致的原因, 以及提升LIPUS的生物功效, 科研人员正致力于测定超声波在骨折治疗中的最佳信号参数。在临床运用上, LIPUS对骨折的治疗一般是以经皮方式应用的。故此, 不同层次深度的骨折会暴露在不同的超声波场区里。超声波场有两个不同的区域, 就是近场区 (接近超声波换能器的区域) 及远场区 (远离超声波换能器的区域)。在我们早期的临床研究中, 我们曾使用超声波的近场区治疗胫骨的复杂性骨折。我们发现, 当超声波换能器置于胫骨骨折处的前方, 骨痂集中生成于胫骨骨折处的背面。这研究结果显示, 近场区以外的超声波场或许更具促进骨痂形成的功效。再者, 针对LIPUS声场仿真分析的结果显示, 近场区内的声压分布是不稳定的, 而远场区内的声压则远比近场区的均及稳定。由于声压的稳定性会大大影响超声波于组织内的能量透射, 我们相信在超声波场中, 骨折的深度会影响LIPUS的生物效应。<br>本研究采用大鼠闭合性股骨骨折模型及细胞培养实验, 探究不同的超声波场区对骨折愈合的影响。本研究作出了以下三个科研假设: (1) LIPUS 的远场区在促进骨折愈合的应用上有着更高的生物效应; (2) LIPUS 的远场区能透

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Książki na temat "Paracrine signalling"

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Menasché, Philippe. Stem Cell Therapy Post-AMI. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0010.

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• Experimental studies suggest that bone marrow-derived stem cells can improve function of infarcted myocardium• This benefit seems to involve paracrine signalling and limitation of left ventricular remodelling rather than true regeneration of cardiomyocytes from donor cells• These experimental findings have been translated in the clinical setting into significant, although moderate, improvements in cardiac function and LV remodelling but the extent to which these benefits impact on event-free long term survival remains to be determined• Optimisation of this therapeutic strategy will require a

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Części książek na temat "Paracrine signalling"

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Fedoroff, Sergey, Chunhai Hao, Ijaz Ahmed, and Larry J. Guilbert. "Paracrine and Autocrine Signalling in Regulation of Microglia Survival." In Biology and Pathology of Astrocyte-Neuron Interactions. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4757-9486-1_22.

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Perachiotti, Anna, and Philippa D. Darbre. "Differential Effects of Growth Factors Acting by Autocrine and Paracrine Pathways in Breast Cancer Cells." In Intercellular Signalling in the Mammary Gland. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_18.

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Forsyth, Isabel A., James A. Taylor, Maggy Villa, and R. Stewart Gilmour. "Evidence of Growth Factor Production by Sheep Myoepithelial and Alveolar Epithelial Cells: Potential for Autocrine/Paracrine Interactions." In Intercellular Signalling in the Mammary Gland. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_15.

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Kelly, Regis b. "An introduction to the nerve tertninal." In Neurotransmitter Release. Oxford University PressOxford, 1999. http://dx.doi.org/10.1093/oso/9780199637676.003.0001.

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Abstract Synaptic transmission between nerve cells can usefully be viewed as a specialized example of cell-to-cell communication. A cell in a metazoan organism communicates most simply by releasing a signal which diffuses until it is detected by receptors on a neighbouring cell, a process called paracrine communication. If the signalling cell is very far away from the target cell simple diffusion will not work. In such cases the signalling cells can release the signal into the bloodstream, which carries it by the blood flow into the vicinity of the target cell. This is called endocrine communi

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Tahara, E., W. Yasui, and H. Yokozaki. "Abnormal growth factor networks in neoplasia." In Cell Proliferation in Cancer. Oxford University PressOxford, 1995. http://dx.doi.org/10.1093/oso/9780198547914.003.0006.

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Abstract Human tumours often exhibit aberrant expression or genetic alterations of growth factors and their receptors (Table 6.1), that may confer growth autonomy or interfere with programmed cell death by autocrine, paracrine, and juxtacrine mechanisms. A number of growth factors, receptors, and protein kinases involved in growth factor-induced signalling are encoded by proto-oncogenes (1, 2). Tumour progression and invasion are thought to require the accumulation of multiple growth factor anomalies (3).

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Szlosarek, Peter W., and Frances R. Balkwill. "Cytokines and cancer." In Introduction to the Cellular and Molecular Biology of Cancer. Oxford University PressOxford, 2005. http://dx.doi.org/10.1093/oso/9780198568537.003.0014.

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Abstract Complex multicellular organisms maintain cellular homeostasis at the local tissue level via a diverse array of secreted low-molecular weight mediators collectively called cytokines. These include tumour necrosis factor-a (TNF-a), interleukins (ILs), interferons (IFNs), colony-stimulating factors, chemokines, angiogenic factors, and growth factors. Unlike classical endocrine hormones, these proteins act in an autocrine, paracrine, and/or juxtacrine fashion on a variety of cells, ranging from stem cells to those that are fully differentiated. Cytokines act within an informational networ

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Bozdag, Gurkan, Baris Ata, and Engin Türkgeldi. "Menstrual Cycle and Ovulation." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0152.

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Understanding the physiology of follicular development is important in order to extrapolate the preclinical data to the clinical side. In this context, there has been an increasing effort to figure out the autocrine/paracrine signalling and microenvironment that will determine the fate of a follicle. The processes of atresia or further development to later stages reaching to a dominant follicle appear to be regulated by highly complicated system that consists oocyte and granulosa cell derived factors, peptides, cytokines, and sex steroids. Additionally, recent research on the menstrual cycle t

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Jabbour, Henry N., Kurt J. Sales, and Hilary Od Critchley. "Endocrine and paracrine signalling in the human endometrium: potential role for for the prostanoid family in implantation." In Implantation and Early Development. Cambridge University Press, 2005. http://dx.doi.org/10.1017/cbo9781107784680.003.

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Naylor, M. S., and F. R. Balkwill. "The role of cytokines in tumour progression." In Cell Proliferation in Cancer. Oxford University PressOxford, 1995. http://dx.doi.org/10.1093/oso/9780198547914.003.0005.

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Abstract Cytokines make up the fourth major class of soluble intercellular signalling mole cules alongside hormones, neurotransmitters, and prostaglandins/leukotrienes. They possess a number of common features despite the variety of molecular structures and properties. Cytokines are all polypeptides of low molecular weight (generally less than 80 kDa) that bind to high affinity cell surface receptors and cause changes in macromoleculer synthesis in target cells. Cytokines may act in a paracrine, autocrine (including intracellular autocrine loops), and juxtacrine manner (i.e., cytokines express

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Funder, John W. "Hormones and receptors: fundamental considerations." In Oxford Textbook of Endocrinology and Diabetes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.1022.

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The original endocrine physiologists viewed hormones as responses to homoeostatic challenge, any signal a call to arms; the word is thus derived from the classical Greek ωρμαειν‎—‘to arouse’. In the twenty-first century a hormone is a molecule—small or large, protein or lipid—secreted in a regulated fashion from one organ and acting on another. The definition is firmly based on the anatomy of the seventeenth century, the histology of the nineteenth, and the physiology of the twentieth. It has been shaped by convention and clinical specialization: gut hormones are the marches between endocrinol

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Streszczenia konferencji na temat "Paracrine signalling"

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Ghayad, Sandra E., Ghina Rammal, Farah Ghamloush, Hussein Basma, and Raya Saab. "Abstract 2452: Exosomes as mediators of paracrine signalling that promote invasive behavior in rhabdomyosarcoma." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2452.

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Maia, Ana, Zuguang Gu, André Koch, et al. "Abstract PS16-36: Paracrine signalling with stromal fibroblasts drives recovery of cancer cells after chemotherapy treatment." In Abstracts: 2020 San Antonio Breast Cancer Virtual Symposium; December 8-11, 2020; San Antonio, Texas. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.sabcs20-ps16-36.

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West, Adrian R., Yemeng Chen, Darren J. Cole, Elizabeth Cowley, and Geoffry N. Maksym. "Inhibition Of Airway Smooth Muscle Contractile Phenotype By Airway Epithelial Cells May Require Bi-directional Paracrine Signalling." 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.a2301.

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