Relevant bibliographies by topics / S100A2

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Academic literature on the topic 'S100A2'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "S100A2"

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Zeng, Meng-Lu, Xian-Jin Zhu, Jin Liu, Peng-Chong Shi, Yan-Li Kang, Zhen Lin, and Ying-Ping Cao. "An Integrated Bioinformatic Analysis of the S100 Gene Family for the Prognosis of Colorectal Cancer." BioMed Research International 2020 (November 26, 2020): 1–15. http://dx.doi.org/10.1155/2020/4746929.

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Background. S100 family genes exclusively encode at least 20 calcium-binding proteins, which possess a wide spectrum of intracellular and extracellular functions in vertebrates. Multiple lines of evidences suggest that dysregulated S100 proteins are associated with human malignancies including colorectal cancer (CRC). However, the diverse expression patterns and prognostic roles of distinct S100 genes in CRC have not been fully elucidated. Methods. In the current study, we analyzed the mRNA expression levels of S100 family genes and proteins and their associations with the survival of CRC patients using the Oncomine analysis and GEPIA databases. Expressions and mutations of S100 family genes were analyzed using the cBioPortal, and protein-protein interaction (PPI) networks of S100 proteins and their mutation-related coexpressed genes were analyzed using STRING and Cytoscape. Results. We observed that the mRNA expression levels of S100A2, S100A3, S100A9, S100A11, and S100P were higher and the level of S100B was lower in CRC tissues than those in normal colon mucosa. A high S100A10 levels was associated with advanced-stage CRC. Results from GEPIA database showed that highly expressed S100A1 was correlated with worse overall survival (OS) and disease-free survival (DFS) and that overexpressions of S100A2 and S100A11 were associated with poor DFS of CRC, indicating that S100A1, S100A2, and S100A11 are potential prognostic markers. Unexpectedly, most of S100 family genes showed no significant prognostic values in CRC. Conclusions. Our findings, though still need to be ascertained, offer novel insights into the prognostic implications of the S100 family in CRC and will inspire more clinical trials to explore potential S100-targeted inhibitors for the treatment of CRC.
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Broome, Ann-Marie, David Ryan, and Richard L. Eckert. "S100 Protein Subcellular Localization During Epidermal Differentiation and Psoriasis." Journal of Histochemistry & Cytochemistry 51, no. 5 (May 2003): 675–85. http://dx.doi.org/10.1177/002215540305100513.

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S100 proteins are calcium-activated signaling proteins that interact with target proteins to modulate biological processes. Our present studies compare the level of expression, and cellular localization of S100A7, S100A8, S100A9, S100A10, and S100A11 in normal and psoriatic epidermis. S100A7 and S100A11 are present in the basal and spinous layers in normal epidermis. These proteins appear in the nucleus and cytoplasm in basal cells but are associated with the plasma membrane in spinous cells. S100A10 is present in basal and spinous cells, in the cytoplasm, and is associated with the plasma membrane. S100A8 and S100A9 are absent or are expressed at minimal levels in normal epidermis. In involved psoriatic tissue, S100A10 and S100A11 levels remain unchanged, whereas, S100A7, S100A8, and S100A9 are markedly overexpressed. The pattern of expression and subcellular localization of S100A7 is similar in normal and psoriatic tissue. S100A8 and S100A9 are strongly expressed in the basal and spinous layers in psoriasis-involved tissue. In addition, we demonstrate that S100A7, S100A10, and S100A11 are incorporated into detergent and reducing agent-resistant multimers, suggesting that they are in vivo trans-glutaminase substrates. S100A8 and S100A9 did not form these larger complexes. These results indicate that S100 proteins localize to the plasma membrane in differentiated keratinocytes, suggesting a role in regulating calcium-dependent, membrane-associated events. These studies also indicate, as reported previously, that S100A7, S100A8, and S100A9 expression is markedly altered in psoriasis, suggesting a role for these proteins in disease pathogenesis.
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Mitrović Ajtić, Olivera, Tijana Subotički, Miloš Diklić, Dragoslava Đikić, Milica Vukotić, Teodora Dragojević, Emilija Živković, Darko Antić, and Vladan Čokić. "Regulation of S100As Expression by Inflammatory Cytokines in Chronic Lymphocytic Leukemia." International Journal of Molecular Sciences 23, no. 13 (June 22, 2022): 6952. http://dx.doi.org/10.3390/ijms23136952.

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The calcium-binding proteins S100A4, S100A8, and S100A9 are upregulated in chronic lymphocytic leukemia (CLL), while the S100A9 promotes NF-κB activity during disease progression. The S100-protein family has been involved in several malignancies as mediators of inflammation and proliferation. The hypothesis of our study is that S100A proteins are mediators in signaling pathways associated with inflammation-induced proliferation, such as NF-κB, PI3K/AKT, and JAK/STAT. The mononuclear cells (MNCs) of CLL were treated with proinflammatory IL-6, anti-inflammatory IL-10 cytokines, inhibitors of JAK1/2, NF-κB, and PI3K signaling pathways, to evaluate S100A4, S100A8, S100A9, and S100A12 expression as well as NF-κB activation by qRT-PCR, immunocytochemistry, and immunoblotting. The quantity of S100A4, S100A8, and S100A9 positive cells (p < 0.05) and their protein expression (p < 0.01) were significantly decreased in MNCs of CLL patients compared to healthy controls. The S100A levels were generally increased in CD19+ cells compared to MNCs of CLL. The S100A4 gene expression was significantly stimulated (p < 0.05) by the inhibition of the PI3K/AKT signaling pathway in MNCs. IL-6 stimulated S100A4 and S100A8 protein expression, prevented by the NF-κB and JAK1/2 inhibitors. In contrast, IL-10 reduced S100A8, S100A9, and S100A12 protein expressions in MNCs of CLL. Moreover, IL-10 inhibited activation of NF-κB signaling (4-fold, p < 0.05). In conclusion, inflammation stimulated the S100A protein expression mediated via the proliferation-related signaling and balanced by the cytokines in CLL.
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Böni, R., G. Burg, E. C. Ilg, B. W. Schäfer, A. Doguoglu, R. Dummer, and C. W. Heizmann. "STAINING PATTERN OF THE Ca2+-BINDING PROTEINS S100A1, S100A2, S100A3, S100A4 AND S100A6 IN HUMAN SKIN AND MELANOCYTIC LESIONS." American Journal of Dermatopathology 19, no. 5 (October 1997): 494. http://dx.doi.org/10.1097/00000372-199710000-00022.

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Peterova, Eva, Jan Bures, Paula Moravkova, and Darina Kohoutova. "Tissue mRNA for S100A4, S100A6, S100A8, S100A9, S100A11 and S100P Proteins in Colorectal Neoplasia: A Pilot Study." Molecules 26, no. 2 (January 14, 2021): 402. http://dx.doi.org/10.3390/molecules26020402.

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S100 proteins are involved in the pathogenesis of sporadic colorectal carcinoma through different mechanisms. The aim of our study was to assess tissue mRNA encoding S100 proteins in patients with non-advanced and advanced colorectal adenoma. Mucosal biopsies were taken from the caecum, transverse colon and rectum during diagnostic and/or therapeutic colonoscopy. Another biopsy was obtained from adenomatous tissue in the advanced adenoma group. The tissue mRNA for each S100 protein (S100A4, S100A6, S100A8, S100A9, S100A11 and S100P) was investigated. Eighteen biopsies were obtained from the healthy mucosa in controls and the non-advanced adenoma group (six individuals in each group) and thirty biopsies in the advanced adenoma group (ten patients). Nine biopsies were obtained from advanced adenoma tissue (9/10 patients). Significant differences in mRNA investigated in the healthy mucosa were identified between (1) controls and the advanced adenoma group for S100A6 (p = 0.012), (2) controls and the non-advanced adenoma group for S100A8 (p = 0.033) and (3) controls and the advanced adenoma group for S100A11 (p = 0.005). In the advanced adenoma group, differences between the healthy mucosa and adenomatous tissue were found in S100A6 (p = 0.002), S100A8 (p = 0.002), S100A9 (p = 0.021) and S100A11 (p = 0.029). Abnormal mRNA expression for different S100 proteins was identified in the pathological adenomatous tissue as well as in the morphologically normal large intestinal mucosa.
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Nguyen, Nam Q., Andrew Ruszkiewicz, David Chang, Jenna Bambrick, and Andrew Victor Biankin. "Biomarker assessment from EUS-guided biopsy to predict outcomes and treatment in pancreatic cancer." Journal of Clinical Oncology 32, no. 3_suppl (January 20, 2014): 182. http://dx.doi.org/10.1200/jco.2014.32.3_suppl.182.

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182 Background: Current methods of pre-operative predicting outcome of pancreatic cancer and related pancreatectomy are limited. While several prognostic biomarkers, including S100A2 and S100A4, are associated with poor outcomes, these currently can only be assessed in operatively resected specimens. The amount of tissue from EUS guided fine needle aspirations is often insufficient for biomarker assessment. Procore needles aim to acquire larger volumes of tissue that may be suitable. We aim to (i) evaluate the feasibility of S100A2 and S100A4 assessment in EUS guided biopsy specimens using the Procore needle, and (ii) evaluate the relationship of these biomarkers with outcome. Methods: Clinico-pathological data from 79 patients (70 ± 2yrs; 44M:35F) with pancreatic ductal adenocarcinoma (PDAC) were prospectively acquired. All subjects had EUS guided biopsy with a 22G Procore needle and cell-block preparation was performed. Sections of cell-block material were assessed for S100A2 and S100A4 protein expression using immunohistochemistry. Results: Pre-operative biomarker assessments from EUS acquired specimens were possible in 90% (72/79) of patients, 14 of which then had pancreatectomy. Thirty-five (49%) of patients expressed S100A2 and S100A4, which were co-expressed in 97% of cases. Patients with S100A2/A4 tumours on EUS had a significantly shorter median survival (10.0 vs. 17.5 months, p=0.03). Among patients with S100A2/A4 expressing tumors, pancreatectomy (n=8) didn't lead to a survival benefit compared with those managed non-surgically (n=27) (12.5 vs. 10.0 months, p=0.70). Of patients who had pancreatectomy, those with S100A2/A4 expressing tumors (n=8) had shorter survival than those with S100A2/A4-negative tumors (n=6) (12.5 vs. 20.5 months; p = 0.04). Conclusions: Biomarker assessment from EUS guided biopsy specimens is feasible and successful in 90% of cases. The presence of S100A2 and S100A4 expression predicts both survival and response to pancreatectomy in patients with pancreatic cancer. These findings demonstrate a “proof-of-concept”, that pre-operative EUS guided biopsy could inform clinical decision-making, particularly with regard to selection for operative resection of PDAC.
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Gupta, Sanjay, Tajamul Hussain, Gregory T. MacLennan, Pingfu Fu, Jigar Patel, and Hasan Mukhtar. "Differential Expression of S100A2 and S100A4 During Progression of Human Prostate Adenocarcinoma." Journal of Clinical Oncology 21, no. 1 (January 1, 2003): 106–12. http://dx.doi.org/10.1200/jco.2003.03.024.

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Purpose: To establish the clinical significance of calcium binding proteins S100A2 and S100A4 during progression of human prostate adenocarcinoma. Patients and Methods: Expression pattern of S100A2 and S100A4 was determined in normal human prostate epithelial cells (NHPE); virally transformed prostate epithelial cells (PZ-HPV-7); several human prostate carcinoma cells (22Rv1, DU145, LNCaP, and PC3); tissue samples obtained during transuretheral prostatic resection from patients with benign prostate hyperplasia (BPH), prostatitis, and adenocarcinoma; and paraffin-embedded sections from pair-matched benign and cancer specimens of different tumor grade. Results: High constitutive protein expression of S100A2 was observed in NHPE and PZ-HPV-7 cells, whereas its complete absence was observed in 22Rv1, DU145, LNCaP, and PC3 cells. Tissue samples of BPH and prostatitis exhibited higher mRNA and protein levels of S100A2 than low-grade cancer (Gleason score ≤ 6), whereas a complete loss was observed in high-grade cancer specimens (Gleason score > 6). Immunohistochemical analysis further confirmed high levels of S100A2 in benign tissues and a progressive loss with increasing tumor grade. The protein level of S100A4 was significantly higher in all carcinoma cells compared with NHPE and PZ-HPV-7 cells. The mRNA and protein level of S100A4 was significantly higher in high-grade cancer specimens compared with BPH, prostatitis, and low-grade cancer. The high levels of S100A4 observed in cancer tissue correlated with increasing tumor grade. Conclusion: Loss of S100A2 and increased expression of S100A4 may be an important event during progression of prostate cancer in humans.
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Yamamoto, Maho, Rina Kondo, Haruka Hozumi, Seita Doi, Miwako Denda, Masaki Magari, Naoki Kanayama, Naoya Hatano, Ryo Morishita, and Hiroshi Tokumitsu. "Identification and Biochemical Characterization of High Mobility Group Protein 20A as a Novel Ca2+/S100A6 Target." Biomolecules 11, no. 4 (March 30, 2021): 510. http://dx.doi.org/10.3390/biom11040510.

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During screening of protein-protein interactions, using human protein arrays carrying 19,676 recombinant glutathione s-transferase (GST)-fused human proteins, we identified the high-mobility protein group 20A (HMG20A) as a novel S100A6 binding partner. We confirmed the Ca2+-dependent interaction of HMG20A with S100A6 by the protein array method, biotinylated S100A6 overlay, and GST-pulldown assay in vitro and in transfected COS-7 cells. Co-immunoprecipitation of S100A6 with HMG20A from HeLa cells in a Ca2+-dependent manner revealed the physiological relevance of the S100A6/HMG20A interaction. In addition, HMG20A has the ability to interact with S100A1, S100A2, and S100B in a Ca2+-dependent manner, but not with S100A4, A11, A12, and calmodulin. S100A6 binding experiments using various HMG20A mutants revealed that Ca2+/S100A6 interacts with the C-terminal region (residues 311–342) of HMG20A with stoichiometric binding (HMG20A:S100A6 dimer = 1:1). This was confirmed by the fact that a GST-HMG20A mutant lacking the S100A6 binding region (residues 311–347, HMG20A-ΔC) failed to interact with endogenous S100A6 in transfected COS-7 cells, unlike wild-type HMG20A. Taken together, these results identify, for the first time, HMG20A as a target of Ca2+/S100 proteins, and may suggest a novel linkage between Ca2+/S100 protein signaling and HMG20A function, including in the regulation of neural differentiation.
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McLachlan, Julia L., Alastair J. Sloan, Anthony J. Smith, Gabriel Landini, and Paul R. Cooper. "S100 and Cytokine Expression in Caries." Infection and Immunity 72, no. 7 (July 2004): 4102–8. http://dx.doi.org/10.1128/iai.72.7.4102-4108.2004.

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ABSTRACT The molecular immune response of the pulpal tissue during chronic carious infection is poorly characterized. Our objective was to examine the expression of potential molecular mediators of pulpal inflammation, correlate their levels with disease severity, and determine the cellular localization of key molecules. Results indicated that there was significantly increased transcriptional activity in carious compared to healthy pulp, and the increase correlated positively with disease severity. Semiquantitative reverse transcriptase PCR analysis in 10 carious and 10 healthy pulpal tissue samples of the S100 family members S100A8, S100A9, S100A10, S100A12, and S100A13; the cytokines tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), IL-8, IL-6, and epithelial cell-derived neutrophil attractant 78 (ENA-78); and the structural protein collagen-1α indicated that all genes tested, with the exception of S100A10, were more abundantly expressed in carious teeth. In addition, we found that the closer the carious lesion front was to the pulpal chamber the higher the expression was for all genes except S100A10. Multiple-regression analysis identified a significant positive correlation between the expression levels of S100A8 and IL-1β, ENA-78, and IL-6 and between collagen-1α and S100A8, TNF-α, IL-1β, IL-8, IL-6, and ENA-78. Immunohistochemical studies in carious pulpal tissue indicated that S100A8 and the S100A8/S100A9 complex were predominantly expressed by infiltrating neutrophils. Gene expression analyses in immune system cells supported these findings and indicated that bacterial activation of neutrophils caused upregulation of S100A8, S100A9, and S100A13. This study highlights the complex nature of the molecular immune response that occurs during carious infection.
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Zhu, Li, Futoshi Kohda, Takeshi Nakahara, Takahito Chiba, Gaku Tsuji, Junichi Hachisuka, Takamichi Ito, et al. "Aberrant expression of S100A6 and matrix metalloproteinase 9, but not S100A2, S100A4, and S100A7, is associated with epidermal carcinogenesis." Journal of Dermatological Science 72, no. 3 (December 2013): 311–19. http://dx.doi.org/10.1016/j.jdermsci.2013.07.005.

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Dissertations / Theses on the topic "S100A2"

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Betz, Christine [Verfasser], and Oliver [Akademischer Betreuer] Einsle. "Structural characterization of the metal-binding ligands S100A8/S100A9 and S100B of the receptor for advanced glycation end products = Strukturelle Charakterisierung der metallbindenden Liganden S100A8/S100A9 und S100B des Rezeptors für Advanced Glycation End Products." Freiburg : Universität, 2013. http://d-nb.info/1115813455/34.

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Leukert, Nadja. "Molekulare Charakterisierung verschiedener Komplexformen der Calcium-bindenden Proteine S100A8 und S100A9." [S.l. : s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=967777062.

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van, Hummel Annika Elise. "The Roles of S100A8 and S100A9 in Cartilage: Degradation and Formation." Thesis, The University of Sydney, 2014. http://hdl.handle.net/2123/11521.

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Osteoarthritis (OA) is a debilitating joint disease that increases in prevalence with age, with latest figures show that around 2.4 million Australians suffer from OA. There are currently no disease-modifying drugs available and due to poor management options, the number of joint replacement surgeries is increasing by nearly 10% per annum in Australia. S100A8 and S100A9 calcium-binding proteins are expressed by immune cells, and are involved in inflammatory situations, including inflammatory diseases such as rheumatoid arthritis, where there is an increase in circulating and local (synovial fluid) levels of S100A8 and S100A9. They are present in the body preferentially as a heterodimer (S100A8/S100A9) or less commonly as homodimers. Recently, S100A8 and S100A9 were found in bone and cartilage cells; however their roles in these tissues are still unknown. The aim of this research therefore was to determine the role(s) of S100A8 and S100A9 in cartilage degeneration and OA. The results presented in this thesis have provided insight into the role(s) of S100A8 and S100A9 in cartilage and in OA. S100A8 and S100A9 act as primers of cartilage degradation, through TLR4 and MAPK signalling pathways, but require a second messenger in order to achieve full biochemical breakdown. S100A8 is abundant in chondrocytes of human OA joints, but does not appear to be involved in non-inflammatory mouse models. S100A8, and to a lesser degree S100A9, are also abundant at joint margins and in osteophytes from human OA patients, and may play a role in chondrogenesis. The results presented in this thesis have determined some of the mechanisms of action of S100A8 and S100A9 in cartilage, however, the exact role of S100A8 and S100A9 in OA remain unclear, and further work will need to be performed to fully determine the significance of S100A8 and S100A9 in OA.
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Raquil, Marie-Astrid. "Études des rôles pro-inflammatoires et prolifératifs des protéines S100A8 et S100A9." Thesis, Université Laval, 2008. http://www.theses.ulaval.ca/2008/25415/25415.pdf.

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Sikora, Kristin [Verfasser]. "RAGE-abhängige S100A8- und S100A9-Expression in humanen THP-1 Zellen / Kristin Sikora." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1023749920/34.

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Dubois, Christelle. "Confirmation de biomarqueurs pour le pronostic du sepsis et développement de tests rapides High plasma level of S100A8/S100A9 and S100A12 at admission indicates a higher risk of death in septic shock patients Top-down and bottom-up proteomics of circulating S100A8/S100A9 complexes in plasma of septic shock patients." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS521.

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Le sepsis est la 3eme cause de mortalité dans les pays occidentaux, avec un taux de mortalité entre 20 et 50% selon la sévérité. La « prédiction » du devenir clinique du patient est essentielle pour établir le traitement le plus adéquat. Quelques protéines marqueurs de l'inflammation ou d'une infection (CRP, procalcitonine) sont citées pour le suivi des patients en clinique mais manquent de spécificité pour le sepsis. D'autre part, les études « omiques » ont permis de générer des listes de biomarqueurs potentiels du pronostic vital du sepsis. En revanche, aucun n'a encore été validé et/ou confirmé en fonction de la gravité du sepsis et du devenir du patient. Il faut pour cela accéder non seulement à des cohortes de patients parfaitement caractérisées et également disposer de méthodes quantitatives robustes et validées. La spectrométrie de masse apporte une capacité de spécificité et de multiplexage à haut niveau qui permettait de confirmer l'intérêt d'une ou plusieurs de ces protéines dans le cas du pronostic du sepsis. Les dosages immunologiques apportent quant à eux en plus de la sensibilité et de la spécificité, une mise en œuvre en routine clinique simple et rapide. Dans un premier temps, une liste de biomarqueurs identifiés avec des cohortes de patients a été établie d’après la littérature. Puis, des méthodes de quantification de ces biomarqueurs ont été développées. Nous nous sommes intéressés d’une part à quantifier les calgranulines dans le plasma en développant des ELISA et des méthodes de spectrométrie de masse par des approches bottom-up et top-down. D’autre part, deux méthodes de quantification multiplexes ont été développées par spectrométrie de masse avec et sans étape d’immunopurification en fonction des concentrations des protéines présentes dans le plasma afin de vérifier la pertinence de la liste de biomarqueurs potentiels. Toutes ces méthodes ont été appliquées à une cohorte de 49 patients atteints de choc septique
Sepsis is the 3rd leading cause of death in Western countries, with a mortality rate between 20 and 50% depending on the severity. The 'prediction' of the patient's clinical outcome is essential to establish the most appropriate treatment. Some inflammation or infection markers protein (CRP, procalcitonin) are cited for clinical follow-up of patients but lack specificity for sepsis. On the other hand, "omics" studies have generated lists of potential biomarkers of sepsis prognosis. However, none have yet been validated and/or confirmed based on the severity of the sepsis and the patient's fate. This requires access not only to fully characterized patient cohorts but also to robust and validated quantitative methods. Mass spectrometry provides a high level of specificity and high multiplex capacity and that would allow to confirm the interest of one or more of these proteins for sepsis prognosis. Immunological assays provide, in addition to sensitivity and specificity, a simple and rapid routine clinical implementation. First, a list of biomarkers identified with patient cohorts was established from the literature. Then, methods to quantify these candidate biomarkers were developed. On the one hand, we have been interested in quantifying calgranulins in plasma by developing ELISAs and mass spectrometry methods using bottom-up and top-down approaches. On the other hand, two multiplex quantification methods by mass spectrometry with and without immunopurification step according to protein concentrations have been developed to verify the relevance of the list of potential biomarkers. All these methods were applied to a cohort of 49 patients with septic shock
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Zwicker, Stephanie. "Psoriasin (S100A7) and koebnerisin (S100A15) in the model of inflammation." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-185702.

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Ludwig, Stefan [Verfasser]. "Die S100-Proteine S100A8 und S100A9 sowie der Heterodimerkomplex S100A8/A9 im Serum und Plasma als Marker des Prostatakarzinoms : Untersuchungen zu präanalytischen Einflussfaktoren und zur diagnostischen Differenzierung zwischen benigner Prostatahyperplasie und Prostatakarzinom / Stefan Ludwig." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2008. http://d-nb.info/1023022486/34.

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Belot, Nathalie. "Caractérisation du rôle des protéines S100A4 et S100A6 dans la migration de cellules gliales tumorales." Doctoral thesis, Universite Libre de Bruxelles, 2004. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211198.

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Laouedj, Malika. "Effets des protéines S100A8 et S100A9 dans la différenciation cellulaire dans la leucémie myéloïde aiguë." Doctoral thesis, Université Laval, 2017. http://hdl.handle.net/20.500.11794/27761.

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Tableau d’honneur de la Faculté des études supérieures et postdoctorales, 2016-2017
Les leucémies myéloïdes aiguës (LMA) sont des hémopathies rares, mais très agressives. Elles résultent d’un dérèglement du processus d’hématopoïèse qui se caractérise par une prolifération incontrôlée de cellules sanguines immatures engagées dans la lignée myéloïde. En dépit des traitements actuels qui reposent sur l’utilisation d’agents chimiothérapeutiques ciblant les cellules en prolifération, le pronostic des patients souffrants de LMA est très sombre. En effet, seuls 30% des patients souffrants de LMA survivent au-delà de 5 ans suivant la prise en charge thérapeutique. L’identification des acteurs participant au développement et au maintien des LMA est donc cruciale pour l’élaboration d’une stratégie thérapeutique efficace et ciblée. S100A8 et S100A9 sont des protéines fixatrices de calcium exprimées par les neutrophiles et les monocytes. Ce sont des alarmines jouant des rôles clés dans l’inflammation et dans des pathologies causées par une inflammation excessive. Les protéines S100A8 et S100A9 exercent également de multiples fonctions dans divers tumeurs solides. Elles favorisent la formation de niche pré-métastasique et inhibe la réponse immunitaire antitumorale. Une analyse du génome par séquençage a mis en évidence que S100A8 et S100A9 sont fortement exprimées chez les patients atteints de LMA. De plus, l’expression de la protéine S100A8 chez les patients souffrants de LMA serait corrélée avec un faible taux de survie. Principalement étudiées dans les tumeurs solides, les fonctions des protéines S100A8 et S100A9 dans les néoplasies hématologiques telles que les leucémies sont très peu documentées. Dans ces travaux de thèse, nous nous sommes donc intéressés aux rôles exercés par les protéines S100A8 et S100A9 dans les leucémies myéloïdes aiguës. À l’aide d’un modèle murin de LMA induit par la surexpression des facteurs HOXA9 et MEIS1 dans des cellules souches/progénitrices hématopoïétiques, nous avons démontré l’existence d’une fraction de cellules exprimant les protéines S100A8 et S100A9. Celle-ci est également retrouvée chez les patients atteints de leucémies aiguës myélomonocytaires et monocytaires (M4-M5 d’après la classification FAB). Les études menées in vivo et in vitro révèlent que la protéine S100A9 induit la différenciation des cellules leucémiques, tandis que la protéine S100A8, préviens l’effet de S100A9 permettant de maintenir ainsi le phénotype immature des cellules LMA. Le traitement par la protéine recombinante S100A9 permet d’accroitre la maturation des cellules LMA, diminue leur prolifération et prolonge la survie des souris LMA. De la même façon le traitement par les anticorps anti-S100A8 provoque un effet similaire au traitement par la protéine S100A9. Nos résultats suggèrent que de forts ratios de S100A9 sur S100A8 sont requis pour induire la différenciation des cellules LMA. Le mécanisme intracellulaire par lequel S100A9 induit la différenciation des cellules leucémiques a également été étudié dans le cadre de cette thèse. Nous avons identifié que S100A9 via la liaison au récepteur TLR (Toll-like receptor) active les voies de signalisations Mitogen Activated Protein Kinase p38, Jun N-terminal Kinase et extracellular signal-regulated kinases 1 et 2 et provoque la différenciation des cellules leucémiques. Les essais menés sur des cellules primaires de patients malades ont permis de confirmer la capacité de S100A9 et de S100A8 à réguler la différenciation des cellules leucémiques. En somme, les données présentées dans cette thèse contribuent à une meilleure compréhension des rôles des protéines S100A8 et S100A9 dans la différenciation des cellules myéloïdes. Par ailleurs, nos données permettent également d’entrevoir les bénéfices thérapeutiques liés au blocage de S100A8 ou à l’augmentation de S100A9 dans les LMA.
Acute myeloid leukemias (AMLs) are rare but still aggressive hematological diseases. They are the result of a perturbed hematopoietic process characterized by an uncontrolled proliferation of hematopoietic cells committed to the myeloid lineage. Despite current therapy based on chemotherapeutic agents, aimed at killing proliferating cells, prognosis of AML patients is dismal and only 30 % of patients survived beyond 5 years. Identification of actors involved in the initiation and sustaining LMA is crucial to the development of efficient and targeted therapy strategy. S100A8 and S100A9 are calcium-binding proteins predominantly expressed by neutrophils and monocytes, and play key roles in both normal and pathological inflammation. Recently, both proteins were found to promote tumor progression through the establishment of pre-metastatic niches and to inhibit antitumor immune responses. Although S100A8 and S100A9 have been studied in solid cancers, their functions in hematological malignancies remain poorly understood. However, S100A8 and S100A9 are highly expressed in acute myeloid leukemia (AML), and S100A8 expression has been linked to a poor prognosis in AML. Although the roles of these proteins were studies in solid tumor, little is known in their functions in hematological malignancies. We studied in this thesis the role of S100A8 and S100A9 in acute myeloid leukemia. Using AML mouse model of AML surexpressing HOXA9 and MEIS1 in hematopoietic stem and progenitor cells, we identified a small subpopulation of cells expressing S100A8 and S100A9. This subpopulation was consistently found in AML samples from patients with myelomonocytic and monocytic leukemias (M4 and M5 according FAB classification). In vitro and in vivo analyses revealed that S100A9 induces AML cell differentiation, whereas S100A8 prevents differentiation induced by S100A9 activity and maintains AML immature phenotype. Treatment with recombinant S100A9 proteins increased AML cell maturation, induced growth arrest, and prolonged survival in an AML mouse model. Interestingly, anti-S100A8 antibody treatment had effects similar to S100A9 therapy in vivo, suggesting that high ratios of S100A9 over S100A8 are required to induce differentiation. In this thesis, the mechanism of S100A9 leading to differentiation of leukemic cells was also study. Our in vitro studies on the mechanisms/pathways involved in leukemic cell differentiation revealed that binding of S100A9 to toll-like receptor 4 (TLR4) promotes activation of p38 mitogen-activated protein kinase, extracellular signal-regulated kinases 1 and 2, and Jun N-terminal kinase signaling pathways, leading to myelomonocytic and monocytic AML cell differentiation. Overall, our findings indicate that S100A8 and S100A9 are regulators of myeloid differentiation in leukemia and have therapeutic potential in myelomonocytic and monocytic AMLs.
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Books on the topic "S100A2"

1

Tirkos, Sam. Investigation of S100A8 and S100A9 as potential genetic modifiers of the pulmonary phenotype in cystic fibrosis mice. Ottawa: National Library of Canada, 2003.

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Dubois, Josephine. Untersuchung von linearen und zirkulären Transkripten des TRAM1- und S100A6-Genlokus im Kontext des Harnblasenkarzinoms. Wiesbaden: Springer Fachmedien Wiesbaden, 2022. http://dx.doi.org/10.1007/978-3-658-40358-4.

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White, Alexander S. Photographer's guide to the canon powershot s100. [Place of publication not identified]: White Knight Press, 2011.

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Brant, Stephen. Distribution of renal S100 proteins in psysiological and pathological models. London: University of East London, 2000.

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McKendry, Amanda Jayne. Comparison of HMB45 monoclonal antibody and S100 poprtein in the immunohistochemical diagnosis of melanoma. [S.l: The Author], 1993.

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Ruiz, Rafael. S100b: Serum Detection, Functions and Clinical Significance. Nova Science Publishers, Incorporated, 2015.

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Dubois, Josephine. Untersuchung Von Linearen und Zirkulären Transkripten des TRAM1- und S100A6-Genlokus Im Kontext des Harnblasenkarzinoms. Springer Fachmedien Wiesbaden GmbH, 2023.

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Cuna. S100 Money & Negotiable Instruments. Kendall Hunt Pub Co, 1994.

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S102 A science foundation course. Milton Keynes: Open University, 1988.

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World Cup 1994 (LADYBD/S100). Ladybird Books Ltd, 1994.

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Book chapters on the topic "S100A2"

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Donato, Rosario, Guglielmo Sorci, and Ileana Giambanco. "S100A6." In Encyclopedia of Signaling Molecules, 4805–13. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101531.

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Donato, Rosario, Guglielmo Sorci, and Ileana Giambanco. "S100A6." In Encyclopedia of Signaling Molecules, 1–10. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101531-1.

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Gressner, A. M., and O. A. Gressner. "S100A12-Protein." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_2726-1.

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Gressner, A. M., and O. A. Gressner. "S100A12-Protein." In Springer Reference Medizin, 2097. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_2726.

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Prudovsky, Igor, Thallapuranam Krishnaswamy Suresh Kumar, and Rosario Donato. "S100a13." In Encyclopedia of Signaling Molecules, 4801–4. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101530.

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Prudovsky, Igor, Thallapuranam Krishnaswamy Suresh Kumar, and Rosario Donato. "S100a13." In Encyclopedia of Signaling Molecules, 1–4. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101530-1.

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Sreejit, Gopalkrishna, Sunil Kiran Nooti, Baskaran Athmanathan, and Prabhakara Reddy Nagareddy. "S100A8/A9 in Myocardial Infarction." In Methods in Molecular Biology, 739–54. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9030-6_46.

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House, Reniqua P., Sarah C. Garrett, and Anne R. Bresnick. "Moving Aggressively: S100A4 and Tumor Invasion." In Signaling Pathways and Molecular Mediators in Metastasis, 91–113. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2558-4_4.

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Ambartsumian, Noona, Jörg Klingelhöfer, and Mariam Grigorian. "The Multifaceted S100A4 Protein in Cancer and Inflammation." In Methods in Molecular Biology, 339–65. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9030-6_22.

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Most, Patrick, Philip Raake, Christophe Weber, Hugo A. Katus, and Sven T. Pleger. "S100A1 Gene Therapy in Small and Large Animals." In Methods in Molecular Biology, 407–20. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-230-8_25.

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Conference papers on the topic "S100A2"

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Gunaldi, M., Y. Okuturlar, A. Üstüngüler, C. Akarsu, and A. Kural. "Abstract P4-04-23: Clinical importance of S100A9 and S100A2 in breast cancer." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p4-04-23.

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Wu, Li-Wha. "Abstract 3085: Epithelial S100A2 reduced upper aerodigestive track carcinogenesis by immunomodulation." 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.am2018-3085.

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Hung, Jung-Jyh. "Abstract PO061: Prognostic significance of S100A2 expression in patients with resected lung adenocarcinoma." 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-po061.

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Crowe, L. A. N., M. Akbar, K. Patommel, S. M. Kitson, E. Garcia Melchor, D. S. Gilchrist, G. A. Murrell, I. B. McInnes, and N. L. Millar. "AB0068 Alarmins s100a8 and s100a9 modulate the inflammatory microenvironment in early tendinopathy." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.7019.

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Wellmerling, J., D. J. Tschumperlin, and Q. Tan. "Single Cell Analysis of Gene Variation Across Multiple Datasets Identifies Erratic S100A2 Expression as a Feature of the IPF Distal Lung Epithelium." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a2184.

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Lee, Eunmi, Maria Ouzounova, Raziye Piranlioglu, Abdeljabar El Andaloussi, Sena Arbag, Gang Zhou, and Hasan Korkaya. "Abstract 2956: Chemical library screen identifies compounds that target S100A8/S100A9 complex and MDSC accumulation." 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.am2017-2956.

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Ghavami, Saeid, Thomas Vogl, Johannes Roth, Helmut Unruh, and Andrew J. Halayko. "S100A8 And S100A9 Homo-, And Hetero-Dimers Affect Extracellular Matrix In Human Smooth Muscle With Different Down Stream Signalling." 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.a6682.

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Gemicioglu, Bilun, Ozgur Yasar, and Tulay Akcay. "Significance of serum YKL-40, S100A8, S100A9, calprotectin, periostin and LRG1 levels in patients with newly diagnosed, controlled and uncontrolled asthma." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2023.

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Katono, Ken, Yuichi Sato, Shinichiro Ryuge, Ryo Nagashio, Masanori Yokoba, Masato Katagiri, Kazu Shiomi, Yukitoshi Satoh, and Noriyuki Masuda. "Co-expression of S100A14 and S100A16 is a predictive marker for platinum-based adjuvant chemotherapy in resected lung adenocarcinomas." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa3339.

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Karouzakis, Emmanuel, Agnieszka Pajak, Niels Riksen, Leo Joosten, Mihai Netea, Esther Lutgens, Eric Stroes, et al. "OP0221 OLIGOMERIC S100A4 INDUCES MONOCYTE INNATE IMMUNE MEMORY." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.5675.

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Reports on the topic "S100A2"

1

Emberley, Ethan D., and Peter Watson. The Role of S100A7/RANBPM Interaction in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada396984.

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Emberley, Ethan, and Peter Watson. The Role of S100A7/RANBPM Interaction in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada412819.

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Emberley, Ethan D., and Peter Watson. The Role of S100A7/RANBPM Interaction in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada418754.

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West, Nathan. Exploring and Exploiting the Protein S100A7 as a New Target for Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, January 2010. http://dx.doi.org/10.21236/ada520729.

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Kim, Edward J., and David Helfman. Characterization of Molecular Factors Critical to the S100A4 (A Metastasis-Associated Protein) - Dependent Increase in Motility of Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada424207.

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State Savings Bank of Tasmania - Hobart (Chief Office) - Depositors Ledgers - Hobart - Accounts - S1 - S1000 -1908-1912. Reserve Bank of Australia, March 2021. http://dx.doi.org/10.47688/rba_archives_2006/20525.

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OVERHANG EFFECT ON WEB CRIPPLING CAPACITY OF COLDFORMED AUSTENITIC STAINLESS STEEL SHS MEMBERS: AN EXPERIMENTAL STUDY. The Hong Kong Institute of Steel Construction, August 2022. http://dx.doi.org/10.18057/icass2020.p.343.

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This paper studies the overhang effects on ultimate bearing capacities of cold-formed austenitic stainless steel square hollow section (SHS) members undergoing web crippling between EndTwo-Flange (ETF) and Interior-Two-Flange (ITF) loading conditions. A total of 16 web crippling tests were conducted with specimens covering various overhang lengths. Tensile coupon tests were performed to obtain the material properties of the test specimens. The web crippling capacities obtained from the tests were compared with the nominal capacities predicted by the SEI/ASCE 8-22 Specification for the design of cold-formed stainless steel structural members. It is shown that the SEI/ASCE 8-22 Specification leads to overly conservative web crippling capacity predictions for the tubular specimens with overhangs. The applicability of the overhang effect enhancement factor codified in the AISI S100- 16 Specification to the studied stainless steel specimens was evaluated. It is revealed that the accuracy and consistency of the web crippling capacity predictions can be enhanced by employing the enhancement factor codified in the AISI S100-16 Specification, yet such a treatment still leads to rather scatter predictions and can lead to unconservative capacity estimations. An extended investigation is currently underway to propose improved design rules for cold-formed stainless steel tubular members with overhangs under ETF loading condition.
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Government Savings Bank of New South Wales - Balmain - Depositors Ledgers - Friendly Society (Loose Leaf System) Cheque Accounts S1-S100 (incl. Continuation) - 1930-1933. Reserve Bank of Australia, March 2021. http://dx.doi.org/10.47688/rba_archives_2006/22603.

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A SURROGATE MODEL TO ESTIMATE THE AXIAL COMPRESSIVE CAPACITY OF COLD-FORMED STEEL OPEN BUILT-UP SECTIONS. The Hong Kong Institute of Steel Construction, August 2022. http://dx.doi.org/10.18057/icass2020.p.316.

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This paper proposed a surrogate model to simplify the process of estimating the axial compressive capacity of cold-formed steel (CFS) open built-up sections composed of lipped channels with different section sizes, thickness, length, and connector spacing. The surrogate model was developed based on the current design methods, i.e., the Effective Width Method (EWM) and Direct Strength Method (DSM), which are codified in the North American Specification AISI S100-16. This new model features two surface regression equations with a boundary inequality criteria, anchored on two important parameters, i.e., modified slenderness ratio, (KL/r)m and minimum thickness-to-width ratio (t/w)min of the built-up sections. The model was validated with 1089 sets of the experimental results data collected from previous research tested on the axial capacity of CFS open built-up sections with the different design configurations. The proposed surrogate model is aimed to simplify the design process among practising engineers for a quick preliminary calculation of the axial compressive capacity of these new CFS open built-up sections.
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