Bibliografías temáticas / Alarmine HMGB1

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Literatura académica sobre el tema "Alarmine HMGB1"

Autor: Grafiati
Publicado: 21 de diciembre de 2024
Última modificación: 31 de julio de 2025

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Artículos de revistas sobre el tema "Alarmine HMGB1"

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De Martinis, Massimo, Lia Ginaldi, Maria Maddalena Sirufo, et al. "Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review." Medicina 56, no. 3 (2020): 138. http://dx.doi.org/10.3390/medicina56030138.

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Alarmins are endogenous mediators released by cells following insults or cell death to alert the host’s innate immune system of a situation of danger or harm. Many of these, such as high-mobility group box-1 and 2 (HMGB1, HMGB2) and S100 (calgranulin proteins), act through RAGE (receptor for advanced glycation end products), whereas the IL-1 and IL-33 cytokines bind the IL-1 receptors type I and II, and the cellular receptor ST2, respectively. The alarmin family and their signal pathways share many similarities of cellular and tissue localization, functions, and involvement in various physiolo
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Lu, Huijiao, Mengyi Zhu, Lin Qu, Hongwei Shao, Rongxin Zhang, and Yan Li. "Oncogenic Role of HMGB1 as an Alarming in Robust Prediction of Immunotherapy Response in Colorectal Cancer." Cancers 14, no. 19 (2022): 4875. http://dx.doi.org/10.3390/cancers14194875.

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Objective: To assess the correlation between HMGB1 expression and the patient prognosis in a multicancer context. Methods: The potential oncogenic role of HMGB1 was explored in forty tumors through the TCGA, GEO, and Oncomine datasets. We analyzed the clinical prognostic value and antitumor immunotherapy of HMGB1 in a multicancer context using GEO (GSE111636). Results: High expression of HMGB1 is present in multicancer cases, and its low expression is closely associated with the prognostic survival of patients, in terms of both overall and disease-free survival in ACC and LUAD. Further investi
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Palumbo, Antonino, Fabiola Atzeni, Giuseppe Murdaca, and Sebastiano Gangemi. "The Role of Alarmins in Osteoarthritis Pathogenesis: HMGB1, S100B and IL-33." International Journal of Molecular Sciences 24, no. 15 (2023): 12143. http://dx.doi.org/10.3390/ijms241512143.

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Osteoarthritis (OA) is a multifactorial disease in which genetics, aging, obesity, and trauma are well-known risk factors. It is the most prevalent joint disease and the largest disability problem worldwide. Recent findings have described the role of damage-associated molecular patterns (DAMPs) in the course of the disease. In particular, alarmins such as HMGB1, IL-33, and S100B, appear implicated in enhancing articular inflammation and favouring a catabolic switch in OA chondrocytes. The aims of this review are to clarify the molecular signalling of these three molecules in OA pathogenesis, t
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Casciaro, Marco, Eleonora Di Salvo, and Sebastiano Gangemi. "HMGB-1 in Psoriasis." Biomolecules 12, no. 1 (2021): 60. http://dx.doi.org/10.3390/biom12010060.

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Psoriasis is a multifactorial pathology linked to systemic inflammation. Enhanced keratinocytes proliferation and a minor maturation state of the cells are typical features. Perivascular T cells, dendritic cells, macrophages, and neutrophilic granulocytes are part of the scenario completed by apoptosis dysregulation. Several proinflammatory mediators, alarmins and growth factors are increased too, both in the skin and the patients’ blood. HMGB1 is important as an alarmin in several inflammatory conditions. Released after cellular damage, HMGB1 acts as a danger signal. Several studies have cons
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Yang, De, Yuri V. Postnikov, Yana Li, et al. "High-mobility group nucleosome-binding protein 1 acts as an alarmin and is critical for lipopolysaccharide-induced immune responses." Journal of Experimental Medicine 209, no. 1 (2011): 157–71. http://dx.doi.org/10.1084/jem.20101354.

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Alarmins are endogenous mediators capable of promoting the recruitment and activation of antigen-presenting cells (APCs), including dendritic cells (DCs), that can potentially alert host defense against danger signals. However, the relevance of alarmins to the induction of adaptive immune responses remains to be demonstrated. In this study, we report the identification of HMGN1 (high-mobility group nucleosome-binding protein 1) as a novel alarmin and demonstrate that it contributes to the induction of antigen-specific immune responses. HMGN1 induced DC maturation via TLR4 (Toll-like receptor 4
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Jiang, Lili, Yijia Shao, Yao Tian, Changsheng Ouyang, and Xiaohua Wang. "Nuclear Alarmin Cytokines in Inflammation." Journal of Immunology Research 2020 (December 4, 2020): 1–8. http://dx.doi.org/10.1155/2020/7206451.

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Pathogen-associated molecular patterns (PAMPs) are some nonspecific and highly conserved molecular structures of exogenous specific microbial pathogens, whose products can be recognized by pattern recognition receptor (PRR) on innate immune cells and induce an inflammatory response. Under physiological stress, activated or damaged cells might release some endogenous proteins that can also bind to PRR and cause a harmful aseptic inflammatory response. These endogenous proteins were named damage-associated molecular patterns (DAMPs) or alarmins. Indeed, alarmins can also play a beneficial role i
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Briquet, Sylvie, Nadou Lawson-Hogban, Bertrand Boisson, et al. "Disruption of Parasitehmgb2Gene Attenuates Plasmodium berghei ANKA Pathogenicity." Infection and Immunity 83, no. 7 (2015): 2771–84. http://dx.doi.org/10.1128/iai.03129-14.

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Eukaryotic high-mobility-group-box (HMGB) proteins are nuclear factors involved in chromatin remodeling and transcription regulation. When released into the extracellular milieu, HMGB1 acts as a proinflammatory cytokine that plays a central role in the pathogenesis of several immune-mediated inflammatory diseases. We found that thePlasmodiumgenome encodes two genuine HMGB factors,PlasmodiumHMGB1 and HMGB2, that encompass, like their human counterparts, a proinflammatory domain. Given that these proteins are released from parasitized red blood cells, we then hypothesized thatPlasmodiumHMGB migh
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Bidwell, Joseph P., Jieping Yang, and Alexander G. Robling. "Is HMGB1 an osteocyte alarmin?" Journal of Cellular Biochemistry 103, no. 6 (2008): 1671–80. http://dx.doi.org/10.1002/jcb.21572.

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Yang, De, Yuri Postnikov, Yana Li, et al. "High mobility group nucleosome-binding protein 1 acts as an alarmin critical for the induction of immune response (113.7)." Journal of Immunology 186, no. 1_Supplement (2011): 113.7. http://dx.doi.org/10.4049/jimmunol.186.supp.113.7.

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Abstract Alarmins, defined as endogenous mediator(s) capable of promoting the recruitment and activation of antigen-presenting cells (APCs) including dendritic cells (DCs), can potentially promote immunity, however, their essential contribution to the induction immune responses remain to be demonstrated. Here we report the identification of HMGN1 as a novel alarmin that is critical to the induction of antigen-specific immune response. HMGN1 induced DC maturation and recruitment of APCs and activated NF-κB and multiple MAPKs, in a MyD88-dependent manner. HMGN1 promoted antigen-specific immune r
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10

Mezentsev, A. V., E. V. Denisova, V. V. Sobolev, and I. M. Korsunskaya. "The role of alarmins in the pathogenesis of psoriasis." Meditsinskiy sovet = Medical Council, no. 14 (September 28, 2023): 62–70. http://dx.doi.org/10.21518/ms2023-276.

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Alarmins are a group of immune activating proteins/peptides that initiate an inflammatory process by interacting with immune cells. The alarmins are biosynthesized as a result of cell injury, often due to proteolysis of native proteins. Most often, the alarmins are released into the extracellular matrix as a result of infection, burn or trauma. Several studies have been conducted recently to determine the role of alarmins in the pathogenesis of autoimmune diseases. This work was aimed to assess the clinical potential of alarmins and characterize their role in the pathogenesis of psoriasis. The
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Tesis sobre el tema "Alarmine HMGB1"

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Lorvellec, Marie. "Dialogue entre le complément C1 et l'alarmine HMGB1 dans l'inflammation." Electronic Thesis or Diss., Université Grenoble Alpes, 2024. http://www.theses.fr/2024GRALV033.

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La protéase C1s est un élément central dans l’initiation de la voie classique du système du complément. Elle était auparavant considérée comme ciblant exclusivement les protéines C2 et C4 dans cette cascade protéolytique. Des découvertes récentes ont cependant mis en lumière la présence de C1s libre constitutivement active dans certaines pathologies, suggérant un rôle plus large de cette protéase au-delà de l'activation du complément. Parmi les cibles non-canoniques identifiées de C1s figure la protéine HMGB1, initialement décrite comme une protéine nucléaire impliquéedans la condensation de l
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Sigaut, Stéphanie. "Activation microgliale : mécanismes et conséquences à long terme." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC198/document.

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La neuro-inflammation induite par l'inflammation systémique ou générée en réponse à une lésion cérébrale aiguë a des conséquences cliniques néfastes : elle est mise en cause dans l'aggravation des lésions cérébrales aiguës chez l'homme, aussi bien chez l'adulte que chez l'enfant. La microglie est l'effecteur cérébral principal de cette réponse inflammatoire, et peut présenter selon les situations un profil neurotoxique ou, au contraire, anti-inflammatoire et régulateur. La compréhension des mécanismes d'activation microgliale et de leurs conséquences est capitale pour une meilleure prise en ch
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3

Bremer, Lisa. "Hyaluronan (HA) fragments as initiators or enhancers of inflammation in arthritis." Thesis, KTH, Skolan för bioteknologi (BIO), 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-215225.

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Malamis, Dimitrios. "Systemic levels of inflammatory mediators in periodontitis." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1436961245.

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"Molecular Mechanisms Regulating the Activation of Eosinophils Induced by S. aureus–associated NOD2/TLR2 Ligands, Alarmin HMGB1 and Antimicrobial Peptide LL-37 in Allergic Inflammation." 2016. http://repository.lib.cuhk.edu.hk/en/item/cuhk-1292458.

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Actas de conferencias sobre el tema "Alarmine HMGB1"

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Fölsch, K., A. Volmari, CF Manthey, AW Lohse, S. Huber, and P. Hübener. "Intestinale Entzündung und Karzinogenese werden durch das Alarmin HMGB1 reguliert." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695395.

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Davalos, Albert R., Misako Kawahara, Gautam K. Malhotra, et al. "Abstract A3: p53-dependent release of alarmin HMGB1 is a central mediator of senescent phenotypes." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-a3.

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Davalos, Albert R., Misako Kawahara, Gautam Malhotra, Christian Beausejour, Francis Rodier, and Judith Campisi. "Abstract LB-483: p53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes." 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-lb-483.

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Rozycki, Henry J., Adam Brock, Melissa Yopp, Christopher Corday, Shauna Webb-Parker, and Tsuyoshi Tanabe. "Increased CXCL2 Production From Mouse Type II Alveolar Epithelial Cells In Response To The Alarmin HMGB1." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4269.

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