Literatura científica selecionada sobre o tema "Secretory phenotype"
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Artigos de revistas sobre o assunto "Secretory phenotype"
Sukla, Krishna, Pooja Kunte, Rajashree Kamat, Deepa Raut, Dattatray Bhat, Akshay Dedaniya, Giriraj Chandak, Anand Chaphekar e Chittaranjan Yajnik. "FUT Genotypes, Secretor Status, H.pylori Antibody Levels and Vitamin-B12 Concentrations in Indians". Current Developments in Nutrition 5, Supplement_2 (junho de 2021): 951. http://dx.doi.org/10.1093/cdn/nzab050_018.
Texto completo da fonteStrzyz, Paulina. "Controlling the senescence-associated secretory phenotype". Nature Reviews Molecular Cell Biology 17, n.º 12 (21 de novembro de 2016): 740. http://dx.doi.org/10.1038/nrm.2016.157.
Texto completo da fonteTamò, Luca, Kleanthis Fytianos, Fabienne Caldana, Cedric Simillion, Anis Feki, Izabela Nita, Manfred Heller, Thomas Geiser e Amiq Gazdhar. "Interactome Analysis of iPSC Secretome and Its Effect on Macrophages In Vitro". International Journal of Molecular Sciences 22, n.º 2 (19 de janeiro de 2021): 958. http://dx.doi.org/10.3390/ijms22020958.
Texto completo da fonteSokol, Ethan, Sophia Maund, Jeffrey Ross e Timothy Wilson. "Abstract P3-09-10: NTRK1/2/3 fusions are observed in both secretory and non-secretory breast cancers". Cancer Research 82, n.º 4_Supplement (15 de fevereiro de 2022): P3–09–10—P3–09–10. http://dx.doi.org/10.1158/1538-7445.sabcs21-p3-09-10.
Texto completo da fonteBusarcevic, Ivan, Svetlana Vojvodic e Una Vojvodic. "Association between secretor status and Lewis phenotype with seronegative spondyloarthritis as indicator of autoimmunity". Genetika 52, n.º 1 (2020): 127–36. http://dx.doi.org/10.2298/gensr2001127b.
Texto completo da fonteSalmina, Alla B., Yana V. Gorina, Alexander I. Erofeev, Pavel M. Balaban, Ilya B. Bezprozvanny e Olga L. Vlasova. "Optogenetic and chemogenetic modulation of astroglial secretory phenotype". Reviews in the Neurosciences 32, n.º 5 (8 de fevereiro de 2021): 459–79. http://dx.doi.org/10.1515/revneuro-2020-0119.
Texto completo da fonteTominaga-Yamanaka, Kumiko, Kotb Abdelmohsen, Jennifer L. Martindale, Xiaoling Yang, Dennis D. Taub e Myriam Gorospe. "NF90 coordinately represses the senescence-associated secretory phenotype". Aging 4, n.º 10 (31 de outubro de 2012): 695–708. http://dx.doi.org/10.18632/aging.100497.
Texto completo da fonteCampisi, J. "Protumorigenic Effects of the Senescence-Associated Secretory Phenotype". AACR Education book 2008, n.º 1 (12 de abril de 2008): 505–9. http://dx.doi.org/10.1158/aacr.edb-08-8139.
Texto completo da fonteWang, Rong, Bharath Sunchu e Viviana I. Perez. "Rapamycin and the inhibition of the secretory phenotype". Experimental Gerontology 94 (agosto de 2017): 89–92. http://dx.doi.org/10.1016/j.exger.2017.01.026.
Texto completo da fonteWildes, Tanya M., Jacob Paasch, Mark A. Fiala, Ling Chen, Ravi Vij, Keith E. Stockerl-Goldstein, Sheila Stewart, Graham A. Colditz e Michael Tomasson. "The Senescence-Associated Secretory Phenotype In Multiple Myeloma". Blood 122, n.º 21 (15 de novembro de 2013): 5357. http://dx.doi.org/10.1182/blood.v122.21.5357.5357.
Texto completo da fonteTeses / dissertações sobre o assunto "Secretory phenotype"
Roeske, Cassandra. "Role of the Heterotrimeric Go Protein Alpha-subunit on the Cardiac Secretory Phenotype". Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24191.
Texto completo da fonteBenyamini, Payam. "The mammalian ribosome receptor, p180, mediates RER membrane biogenesis and establishment of a secretory phenotype". Diss., Restricted to subscribing institutions, 2007. http://proquest.umi.com/pqdweb?did=1324373401&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.
Texto completo da fonteKabir, T. D. "Micromanaging fibroblast senescence : the role of small non-coding RNAs in senescence associated secretory phenotype (SASP)". Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/9141/.
Texto completo da fonteGonzalez, Meljem J. M. "The role of cytokine signalling, cellular senescence and its secretory phenotype in normal pituitary development and tumourigenesis". Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1546237/.
Texto completo da fonteBuhl, Juliane [Verfasser], e Peter [Akademischer Betreuer] Angel. "The senescence-associated secretory phenotype regulates the growth behavior of pediatric pilocytic astrocytoma / Juliane Buhl ; Betreuer: Peter Angel". Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1191760510/34.
Texto completo da fonteHari, Priya. "Identification and study of a role for toll-like receptors in oncogene-induced senescence". Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31443.
Texto completo da fontePungsrinont, Thanakorn [Verfasser], Aria [Gutachter] Baniahmad, Jörg [Gutachter] Müller e Marcus V. [Gutachter] Cronauer. "Analysis of senescence-associated secretory phenotype induced by different androgen receptor ligands in human prostate cancer cells / Thanakorn Pungsrinont ; Gutachter: Aria Baniahmad, Jörg Müller, Marcus V. Cronauer". Jena : Friedrich-Schiller-Universität Jena, 2021. http://d-nb.info/1238141684/34.
Texto completo da fontePerry, Elizabeth Holly. "Association of ABO, Lewis and Secretor phenotypes and genotypes with Neisseria gonorrhoeae thesis submitted in (partial) fulfilment of the Master of Applied Science, Auckland University of Technology, November 2003". Full thesis. Abstract, 2003. http://puka2.aut.ac.nz/ait/theses/PerryE.pdf.
Texto completo da fonteVannier, Daphné. "Découverte d'une sénescence associée à un phénotype sécrétoire déclenchée par les défauts mécaniques de la cellule endothéliale lors de la perte de CCM2 dans un modèle de cavernome cérébral". Thesis, Université Grenoble Alpes, 2020. https://thares.univ-grenoble-alpes.fr/2020GRALV012.pdf.
Texto completo da fonteCCM (Cerebral Cavernous Malformations) lesions are formed by stacks of tortuous, dilated and hemorrhagic capillaries located in the brain. These brain capillaries are devoid of mural cells and are formed of a monolayer of weakly joined endothelial cells (EC). The loss of function mutation in one of the 3 ccm genes (ccm1, ccm2 and ccm3) is sufficient to induce the formation of CCM lesions in humans.In the different ccm mutant models, the ECs present defective tensional homeostasis characterized by a lack of coordination between the cell-matrix and cell-cell forces. This results in the formation of contractile actomyosin fibers anchored on numerous focal adhesions containing B1 integrin and in the loss of VE-cadherin-dependent intercellular junctions. The association of CCM1-3 proteins forms a molecular scaffold that controls downstream of RhoA the activity of ROCK1 and ROCK2 on the organization of the acto-myosin cytoskeleton. The CCM complex recruits ROCK2 at the VE-cadherin dependent junctions to promote a network of cortical actin stabilizing these intercellular junctions while at the same time, it inhibits the activity of ROCK1 to reduce the formation of ventral stress fibers and thus limit the adhesion of the EC to the extracellular matrix. It is known that the microenvironment in the lesion is reshaped in particular by immune cells that infiltrate it to trigger a chronic inflammatory response and promote the expansion of the lesion. It is also known that mutant ECs secrete metalloproteases and cytokines, that they overproduce ROS and that they undergo an endothelio-mesenchymal transition (endoMT). Finally, CCM lesions are mosaics of mutant and wild-type ECs recruited into the lesion over time. However, whether a link exists between all these phenomena conducive to the progression of the CCM lesion is not known and remains to be elucidated.My work during this PhD allowed me to propose a model that unifies all these cellular behaviors. Indeed, I have highlighted a premature aging of endothelial cells depleted in CCM2. I have shown that this senescence is associated with a secretory behavior SASP (Senescence Associated with a Secretory Phenotype) which gives the EC the ability to actively reshape its environment, in particular by degrading it locally, to invade it and attract by chemo-attraction wild EC and immune cells. The second major contribution of my work has been to show that this SASP is due to the dysregulation of the mechanics of the EC. Indeed, I have shown that the increase in intracellular contractility, associated with the loss of balance between the activities of ROCK1 and ROCK2, is responsible for this SASP. Inhibiting myosin II or depleting ROCK1 or ROCK2 restores the expression of half of the genes dysregulated by the loss of CCM2, blocks the appearance of senescence markers as well as the invasive and chemo-attractive capacities of CCM2-depleted ECs. These results open the way to the identification of new therapeutic targets responsible for the appearance and expansion of CCM lesions
Halkoum, Rym. "Rôle du glyoxal dans la sénescence cellulaire : implications dans le vieillissement de la peau". Electronic Thesis or Diss., Sorbonne université, 2021. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2021SORUS016.pdf.
Texto completo da fonteSenescence is a well-characterized cellular state associated with specific markers such as permanent cell proliferation arrest, and the secretion of messenger molecules by cells expressing the Senescence-Associated Secretory Phenotype (SASP). The SASP can display autocrine and paracrine effects which contribute to the senescent phenotype reinforcement and propagation. The SASP composition depends on many factors such as the cell type or the nature of the stress that induces senescence. Since the skin constitutes a barrier with the external environment, it is particularly subjected to different types of stresses, and consequently prone to premature cellular aging. Glyoxal, a dicarbonyl compound produced during glucose metabolism and lipid peroxidation, is a precursor of Advanced Glycation End-products (AGEs), whose presence marks normal and pathological aging. My thesis work showed that glyoxal treatment provokes oxidative stress by increasing reactive oxygen species and AGEs levels and induce senescence in human keratinocytes. Furthermore, glyoxal-induced senescence bears a unique molecular progression profile: an “early-stage” when AKT-FOXO3a-p27KIP1 pathway mediates cell-cycle arrest, and a “late-stage” senescence maintained by the p16INK4/pRb pathway. Moreover, we characterized the resulting secretory phenotype during early senescence by mass spectrometry in order to find new targets for senomorphic ingredients. Our study provides evidence that glyoxal can affect keratinocyte functions and act as a driver of human skin aging
Capítulos de livros sobre o assunto "Secretory phenotype"
Rodier, Francis. "Detection of the Senescence-Associated Secretory Phenotype (SASP)". In Methods in Molecular Biology, 165–73. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-239-1_10.
Texto completo da fonteMalaquin, Nicolas, Véronique Tu e Francis Rodier. "Assessing Functional Roles of the Senescence-Associated Secretory Phenotype (SASP)". In Methods in Molecular Biology, 45–55. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8931-7_6.
Texto completo da fonteVelarde, Michael C., Marco Demaria e Judith Campisi. "Senescent Cells and Their Secretory Phenotype as Targets for Cancer Therapy". In Cancer and Aging, 17–27. Basel: S. KARGER AG, 2013. http://dx.doi.org/10.1159/000343572.
Texto completo da fonteHari, Priya, e Juan Carlos Acosta. "Detecting the Senescence-Associated Secretory Phenotype (SASP) by High Content Microscopy Analysis". In Methods in Molecular Biology, 99–109. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6670-7_9.
Texto completo da fonteFrasca, Daniela. "The Senescence-Associated Secretory Phenotype: Induction, Regulation, Function and Therapeutic Interventions to Counteract the Negative Effects". In Cellular and Molecular Aspects of Ageing, 123–38. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-55022-5_9.
Texto completo da fonteGerst, J. E. "SNC1 and SNC2". In Secretory Pathway, 172. Oxford University PressOxford, 1994. http://dx.doi.org/10.1093/oso/9780198599425.003.0107.
Texto completo da fonteBankaitis, V. "SEC14". In Secretory Pathway, 156–57. Oxford University PressOxford, 1994. http://dx.doi.org/10.1093/oso/9780198599425.003.0095.
Texto completo da fonteMarcusson, D., B. Horazdovsky, e S. D. Emr. "VPS10". In Secretory Pathway, 234. Oxford University PressOxford, 1994. http://dx.doi.org/10.1093/oso/9780198599425.003.0137.
Texto completo da fonteSegev, N. "YPT1". In Secretory Pathway, 121–23. Oxford University PressOxford, 1994. http://dx.doi.org/10.1093/oso/9780198599425.003.0074.
Texto completo da fonteés, F. K. ép. "SEC53". In Secretory Pathway, 52. Oxford University PressOxford, 1994. http://dx.doi.org/10.1093/oso/9780198599425.003.0033.
Texto completo da fonteTrabalhos de conferências sobre o assunto "Secretory phenotype"
Schlegel, Julian, Sophie Domhan, Jürgen Debus e Amir Abdollahi. "Abstract B63: Differences between replicative senescence- versus radiation- associated secretory phenotype". In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-b63.
Texto completo da fonteSinger, C. A., M. A. Ba e J. Evasovic. "miR-106b∼25 Promotes a Secretory Airway Smooth Muscle Phenotype in Asthma". In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4412.
Texto completo da fonteSchaum, Nicholas, Christopher Wiley, Fatouma Almirah, Jose A. Lopez-Dominguez, Gary Scott, Christopher Benz, Judith Campisi e Albert R. Davalos. "Abstract 4864: Small-molecule MDM2 antagonists attenuate the senescence-associated secretory phenotype". In 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.am2018-4864.
Texto completo da fonteSantos, B., L. Gaspar, C. Carvalhas-Almeida, A. T. Barros-Viegas, S. Carmo-Silva, C. Santos, S. Carvalho et al. "Unraveling the impact of obstructive sleep apnea on senescent associate secretory phenotype". In Sleep and Breathing 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/23120541.sleepandbreathing-2021.82.
Texto completo da fontePatel, Rupesh S., Rodrigo Romero, Anthony C. Liang, Emma V. Watson, Megan Burger, Peter M. K. Westcott, Kim L. Mercer et al. "Abstract IA17: The role of the senescence-associated secretory phenotype in cancer". In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-ia17.
Texto completo da fonteHohloch, J., F. Selt, T. Hielscher, F. Sahm, D. Capper, D. Usta, J. Ecker et al. "Oncogene-induced senescence and the senescence-associated secretory phenotype in pilocytic astrocytoma". In 30. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch-onkologische Forschung. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1602221.
Texto completo da fonteZhang, Jing, Lian Wu, Chunxue Bai, Mervyn J. Merrilees e Peter N. Black. "Pulmonary Fibroblasts From Patients With COPD Have A Senescence-associated Secretory Phenotype". 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.a4924.
Texto completo da fonteWoldhuis, R. R., I. H. Heijink, M. Van Den Berge, W. Timens, B. Oliver, M. De Vries e C. Brandsma. "COPD-derived fibroblasts secrete higher levels of senescence associated secretory phenotype (SASP) proteins". In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.28.
Texto completo da fonteHassibi, Shyreen, Jonathan Baker, Louise Donnelly e Peter Barnes. "The RNA binding protein HuR regulates the senescence-associated secretory phenotype under conditions of oxidative stress". In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2374.
Texto completo da fonteKenny, Sarah, Ziling Huang, Kiwhan Kim, Allyson Capili, Susan Carpenter, Diane Ward e Suzanne Cloonan. "Mitochondrial iron regulates AEC2 dysfunction, senescence and senescent associated secretory phenotype in response to bleomycin challenge." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.222.
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