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Academic literature on the topic 'SERPINH1'

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Published: 7 July 2024
Last updated: 7 July 2024

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Journal articles on the topic "SERPINH1":

1

Al-Khatib, Sohaib M., Ayah N. Al-Bzour, Mohammad N. Al-Majali, Laila M. Sa’d, Joud A. Alramadneh, Nour R. Othman, Abdel-Hameed Al-Mistarehi, and Safwan Alomari. "Exploring Genetic Determinants: A Comprehensive Analysis of Serpin B Family SNPs and Prognosis in Glioblastoma Multiforme Patients." Cancers 16, no. 6 (March 10, 2024): 1112. http://dx.doi.org/10.3390/cancers16061112.

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Serpins are serine proteinase inhibitors, with several serpins being overexpressed in cancer cells. Thus, we aim to analyze the single-nucleotide polymorphism (SNP) of Serpinb11 and its association with GBM survival. A cohort of 63 GBM patients recruited from King Abdullah University Hospital in Jordan underwent polymorphism analysis and overall survival (OS) assessments. The Cancer Genome Atlas (GBM) cohort was useful for validation. We constructed a risk score using the principal component analysis for the following Serpin genes: Serpinb3, Serpinb5, Serpinb6, Serpinb11, and Serpinb12, and patients were grouped into high- vs. low-risk groups based on the median cutoff. Univariable Cox models were used to study the survival outcomes. We identified a significant association between rs4940595 and survival. In the TCGA cohort, Serpinb3 alterations showed worse OS. Univariable Cox showed worse PFS outcomes with higher SERPINB5 and SERPINB6 expression. A Serpin B 5-gene risk score showed a trend towards worse PFS in the high-risk group. Upregulated DEGs showed GO enrichment in cytokine regulation and production, positive regulation of leukocyte activation, and the MAPK cascade. The high-risk group showed a significantly higher infiltration of M2 macrophages and activated mast cells. Our findings showed a significant role of the Serpin B family in GBM survival in the Jordanian population.
2

Jin, Xiao-Sheng, Lu-Xi Chen, Ting-Ting Ji, and Rong-Zhou Li. "SERPINH1 promoted the proliferation and metastasis of colorectal cancer by activating PI3K/Akt/mTOR signaling pathway." World Journal of Gastrointestinal Oncology 16, no. 5 (May 15, 2024): 1890–907. http://dx.doi.org/10.4251/wjgo.v16.i5.1890.

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BACKGROUND Serpin peptidase inhibitor clade H member 1 (SERPINH1) was initially recognized as an oncogene implicated in various human malignancies. Nevertheless, the clinical relevance and functional implications of SERPINH1 in colorectal cancer (CRC) remain largely elusive. AIM To investigate the effects of SERPINH1 on CRC cells and its specific mechanism. METHODS Quantitative real-time polymerase chain reaction, western blotting analysis, The Cancer Genome Atlas data mining and immunohistochemistry were employed to examine SERPINH1 expression in CRC cell lines and tissues. A series of in-vitro assays were performed to demonstrate the function of SERPINH1 and its possible mechanisms in CRC. RESULTS SERPINH1 demonstrated elevated expression levels in both CRC cells and tissues, manifested at both mRNA and protein tiers. Elevated SERPINH1 levels correlated closely with advanced T stage, lymph node involvement, and distant metastasis, exhibiting a significant association with poorer overall survival among CRC patients. Subsequent investigations unveiled that SERPINH1 overexpression notably bolstered CRC cell proliferation, invasion, and migration in vitro , while conversely, SERPINH1 knockdown elicited the opposite effects. Gene set enrichment analysis underscored a correlation between SERPINH1 upregulation and genes associated with cell cycle regulation. Our findings underscored the capacity of heightened SERPINH1 levels to expedite G1/S phase cell cycle progression via phosphatidylinositol 3-kinase/AKT/mechanistic target of rapamycin pathway activation, thereby facilitating CRC cell invasion and migration. CONCLUSION These findings imply a crucial involvement of SERPINH1 in the advancement and escalation of CRC, potentially positioning it as a novel candidate for prognostic assessment and therapeutic intervention in CRC management.
3

Haj, Amelia K., Sean J. Jurgens, Xin Wang, Justine Ryu, Seung Hoan Choi, Steven P. Grover, Simone Sanna-Cherchi, Alec A. Schmaier, Patrick Ellinor, and Pavan K. Bendapudi. "Rare Germline Loss-of-Function Variants in HSP47 ( SERPINH1) Are Associated with an Intermediate Osteogenesis Imperfecta Phenotype Characterized By Atopic Inflammation and Increased Risk of Thrombosis." Blood 142, Supplement 1 (November 28, 2023): 3934. http://dx.doi.org/10.1182/blood-2023-189896.

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Background: There has been considerable interest in the collagen-specific chaperone HSP47 ( SERPINH1) as a potential drug target for the treatment of cirrhosis, fibrotic disease, and more recently, thrombosis (Thienel et al., Science 380, 178-187, 2023). While homozygous or compound heterozygous loss of function in SERPINH1 is known to cause a rare form of osteogenesis imperfecta (OI) in humans, little is known about the clinical effects of moderately decreased HSP47 activity. In order to assess the potential safety and efficacy of an antithrombotic strategy based on HSP47 blockade, we evaluated the clinical impacts of heterozygous loss-of-function variants in SERPINH1 in a dataset of over 400,000 individuals. Aims: Determine the clinical effects of SERPINH1 loss of function in a large-scale whole exome sequencing dataset. Methods: The UK Biobank (UKBB) contains paired whole exome sequencing and clinical data on 415,921 subjects in addition to plasma proteomics data for a subset of participants (N= 48,892). We identified all rare (MAF<0.1%)variants in SERPINH1 that were predicted in silico to alter protein activity (functional impact score ≥0.7). Using Firth's logistic regression, we controlled for age, sex, ancestry, and other risk factors and assessed the association between the presence of qualifying SERPINH1 variants and four thrombotic disorders: venous thromboembolism (VTE), non-cardioembolic ischemic stroke (NCEIS), myocardial infarction (MI), and peripheral arterial disease (PAD). Replication was performed in a composite dataset from the NIH All of Us program and the Mass General Brigham (MGB) Biobank (N=150,017). We also evaluated differences in the plasma levels of 1,472 proteins (Olink Explore 1536 proteomics panel) between carriers and non-carriers of qualifying SERPINH1 variants. Results: Rare qualifying variants in SERPINH1 were identified in 382 UKBB participants (100% heterozygous). On average, SERPINH1 variant carriers were of significantly shorter stature (P=3.97 x 10-5) and lower weight (P=0.006) than individuals without such variants, and this effect was more pronounced in subjects with higher functional impact scores ( Figure 1). By contrast, bone mineral density did not differ significantly as measured by calcaneal quantitative ultrasound and femur shaft dual x-ray absorptiometry. The presence of SERPINH1 variants was associated with significantly increased risk of VTE (OR=1.87, 95% CI: 1.21-2.76, P=0.006), MI (OR=1.98, 95% CI: 1.27-2.96, P=0.003), PAD (OR=2.37, 95% CI: 1.29-3.98, P=0.007), and NCEIS (OR=2.67, 95% CI: 1.24-4.98, P=0.015). Restricting the analysis to high-confidence loss-of-function variants (i.e., nonsense, frameshift, and essential splice site mutations) markedly boosted effect size estimates for MI, PAD, and NCEIS. The VTE and MI disease associations replicated in the composite dataset (VTE OR=3.29, 95% CI: 1.46-7.39, P=0.004; MI OR=2.31, 95% CI: 1.05-5.08, P=0.038). Additionally, the association with NCEIS demonstrated a strong trend towards significance in the replication dataset (OR=2.08, 95% CI: 0.90-4.83, P=0.088). Plasma proteome analysis showed a significant increase in several proteins related to asthma, atopic inflammation, and/or eosinophil activation among individuals with qualifying SERPINH1 variants, including RNASE3, DPP10, TSPAN1, CCL20, and IL10RA ( Figure 2). In order to further investigate these differences in circulating protein profile, we assessed the risk of obstructive asthma in a meta-analysis of the UKBB, All of Us, and MGB datasets (total N=565,455) and found that SERPINH1 variant carriers were significantly more likely to have disease (OR=1.32, 95% CI: 1.03-1.69, P=0.026). Conclusions: Loss of function in SERPINH1 is associated with a significantly increased risk of both venous and arterial thrombosis, raising concerns that long-term therapeutic inhibition of HSP47 may not be a safe or effective antithrombotic strategy. Our data indicate that SERPINH1 variant carriers experience higher levels of eosinophil-driven inflammation, which has consistently been linked to cardiovascular disease. Further, heterozygous SERPINH1 variant carriers appear to have an intermediate OI phenotype characterized by shorter stature but without significant differences in bone mineral density compared to non-carriers.
4

Mueller, S. K., A. L. Nocera, S. T. Dillon, T. A. Libermann, O. Wendler, and B. S. Bleier. "Tissue and Exosomal Serine Protease Inhibitors Are Significantly Overexpressed in Chronic Rhinosinusitis With Nasal Polyps." American Journal of Rhinology & Allergy 33, no. 4 (February 27, 2019): 359–68. http://dx.doi.org/10.1177/1945892419831108.

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Background The fibrinolysis pathway has been previously implicated in the etiopathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP). Objective The purpose of this study was (1) to explore protein derangements of selected protease inhibitors of the serpin superfamily in CRSwNP and (2) to correlate the protease inhibitor derangements of the fibrinolysis pathway in tissue with exosomal samples to evaluate the potential of an exosomal noninvasive “liquid biopsy” for CRSwNP. Methods Institutional review board approved study in which matched tissue and mucus exosomal proteins (SerpinB2, SerpinF2, SerpinG1, and SerpinE1) were compared between control and CRSwNP patients using Western Blot analysis (n = 6/group) and immunohistochemistry (IHC). Transcriptome analysis (n = 10/group) on the same proteins was performed using whole transcriptome sequencing. Semiquantitative analysis of the Western Blots was performed using the Whitney–Mann U test. Results The transcriptomic data set showed multiple differentially expressed genes including SerpinB2 (fold changes [FC] 7.38), SerpinE1 (FC 1.42), SerpinF2 (FC 2.03), and SerpinG1 (FC 0.72). Western Blot and IHC analysis showed an overexpression of the Serpin protease inhibitors in tissue (SerpinB2, P < .01; SerpinE1, P < .01; SerpinF2, P < .01; and SerpinG1, P < .01) indicating a downregulation of the fibrinolysis cascade. The mucus exosomal serpin proteins exhibited similar findings. Conclusion Our analysis supported that protease inhibitors of the fibrinolysis pathway, especially SerpinB2, SerpinF2, and SerpinG1, are highly deranged in patients with CRSwNP. These findings suggest a downregulation of the fibrinolysis pathway via proteolytic cascade imbalance leading to excessive polyp fibrin deposition. Our data further supported our hypothesis that exosomal proteomic analyses may be used as noninvasive “liquid biopsy” for CRSwNP and a novel method to study chronic sinonasal inflammation.
5

Zhang, Yin, Chun-Yuan Li, Wei Ge, and Yi Xiao. "Exploration of the Key Proteins in the Normal-Adenoma-Carcinoma Sequence of Colorectal Cancer Evolution Using In-Depth Quantitative Proteomics." Journal of Oncology 2021 (June 11, 2021): 1–19. http://dx.doi.org/10.1155/2021/5570058.

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Purpose. In most cases, the carcinogenesis of colorectal cancer (CRC) follows the normal-adenoma-carcinoma (N-A-C) sequence. In this study, we aimed to identify the key proteins in the N-A-C sequence. Methods. Differentially expressed proteins (DEPs) in normal, adenoma, and carcinoma tissues were identified using the Tandem Mass Tag- (TMT-) based quantitative proteomics approach. The landscape of proteomic variation in the N-A-C sequence was explored using gene set enrichment analysis (GSEA) and Proteomaps. Key proteins in the N-A-C sequence were identified, verified, and validated based on our proteomic data, external proteomic data, and external transcriptomic data in the ProteomeXchange, CPTAC, GEO, and TCGA databases. The prognostic value of the key proteins in our database was evaluated by univariate and multivariate Cox regression analysis. The effects of the key proteins on adenoma organoids and colorectal cancer cells were explored in functional studies. Results. Based on our proteomic profiles, we identified 1,294 DEPs between the carcinoma (CG) and normal (NG) groups, 919 DEPs between the adenoma group (AG) and NG, and 1,030 DEPs between the CG and AG. Ribosome- and spliceosome-related pathways were mainly enriched in the N-A process. Extracellular matrix- and epithelial-mesenchymal transition- (EMT-) related pathways were mainly enriched in the A-C process. RRP12 and SERPINH1 were identified, verified, and validated as candidate key proteins in the N-A and A-C processes, respectively. Furthermore, RRP12 and SERPINH1 knockdown impeded the viability and proliferation of adenoma organoids. SERPINH1 was validated as a risk factor for disease-free survival (DFS) based on the TCGA and our database, whereas RRP12 did not show prognostic value. SERPINH1 knockdown was accompanied by EMT-related protein variation, increased apoptosis, and reduced proliferation, invasion, and migration of CRC cells in vitro. Conclusions. RRP12 and SERPINH1 may play an important role in the N-A and A-C processes, respectively. Furthermore, SERPINH1 showed favorable prognostic value for DFS in CRC patients. We speculate that SERPINH1 might promote not only the A-C process but also the development of CRC.
6

Bertram, Stefanie, Juliet Padden, Julia Kälsch, Maike Ahrens, Leona Pott, Ali Canbay, Frank Weber, et al. "Novel immunohistochemical markers differentiate intrahepatic cholangiocarcinoma from benign bile duct lesions." Journal of Clinical Pathology 69, no. 7 (January 4, 2016): 619–26. http://dx.doi.org/10.1136/jclinpath-2015-203418.

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AimsThe distinction between intrahepatic cholangiocarcinoma (ICC) and benign bile duct lesions can be challenging. Using our previously identified potential biomarkers for ICC, we examined whether these are useful for the differential diagnosis of ICC, bile duct adenoma and reactive bile duct proliferations in an immunohistochemical approach and identified a diagnostic marker panel including known biomarkers.MethodsSubjects included samples from 77 patients with ICC, 33 patients with bile duct adenoma and 47 patients with ductular reactions in liver cirrhosis. Our previously identified biomarkers (stress-induced phosphoprotein 1 (STIP1), SerpinH1, 14-3-3Sigma) were tested immunohistochemically following comparison with candidates from the literature (cluster of differentiation 56, heat shock protein (HSP)27, HSP70, B-cell-lymphoma2, p53, ki67).ResultsThe expression of SerpinH1 and 14-3-3Sigma was significantly higher in ICC than in bile duct adenomas and ductular reactions (p<0.05), whereas STIP1 expression was significantly higher (p<0.05) in ICC than in ductular reactions, but the difference to the bile duct adenoma group was not significant. A panel of the biomarker SerpinH1, 14-3-3Sigma and ki67 (≥2 marker positive) showed a high diagnostic accuracy (sensitivity 87.8%, specificity 95.9%, accuracy 91.8%) in the differential diagnosis of ICC versus non-malignant bile duct lesions.ConclusionsThis suggests that 14-3-3Sigma and SerpinH1 may be useful in the differential diagnosis of malignant, benign and reactive bile duct lesions in addition to ki67 where a cut-off of >5% might be used for the distinction of malignant and non-malignant lesions.
7

Zhang, Yin, Chun-Yuan Li, Meng Pan, Jing-Ying Li, Wei Ge, Lai Xu, and Yi Xiao. "Exploration of the Key Proteins of High-Grade Intraepithelial Neoplasia to Adenocarcinoma Sequence Using In-Depth Quantitative Proteomics Analysis." Journal of Oncology 2021 (November 29, 2021): 1–13. http://dx.doi.org/10.1155/2021/5538756.

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Purpose. In this study, we aimed to provide a comprehensive description of typical features and identify key proteins associated with the high-grade intraepithelial neoplasia- (HIN-) adenocarcinoma (AC) sequence. Methods. We conducted tandem mass tag-based quantitative proteomic profiling of normal mucosa, HIN, and AC tissues. Protein clusters representative of the HIN-AC sequence were identified using heatmaps based on Pearson’s correlation analysis. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Reactome analyses were performed using the Database for Annotation, Visualization, and Integrated Discovery (DAVID) database, ClueGO plugin in Cytoscape, and the Metascape database. The prognostic value of the key proteins and their effects on the tumor microenvironment and consensus molecular subtype were explored based on The Cancer Genome Atlas. Results. We identified 536 proteins categorized into three clusters. Among the biological processes and pathways of the highly expressed proteins in the HIN-AC sequence, proteins were predominantly enriched in response to gut microbiota, cell proliferation, leukocyte migration, and extracellular matrix (ECM) organization events. SERPINH1 and P3H1 were identified as the key proteins that promote the HIN-AC sequence. In the correlation analysis of infiltrating immune cells, both SERPINH1 and P3H1 expression correlated negatively with tumor purity, while correlating positively with abundance of CD8+ T cells, B cells, macrophage/monocytes, dendritic cells, cancer-associated fibroblasts, endothelial cells, neutrophils, and natural killer cells. Furthermore, both SERPINH1 and P3H1 expression positively correlated with common immune checkpoints and mesenchymal molecular subtype. High P3H1 expression was associated with poor disease-free survival and overall survival. Conclusions. ECM-related biological processes and pathways are typical features of the HIN-AC sequence. SERPINH1 and P3H1 might be the key proteins in this sequence and be related to ECM remodeling and immune suppression status in CRC.
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van Leeuwen, L. Leonie, Mitchel J. R. Ruigrok, Henri G. D. Leuvenink, and Peter Olinga. "Slice of Life: Porcine Kidney Slices for Testing Antifibrotic Drugs in a Transplant Setting." Transplantology 4, no. 2 (April 14, 2023): 59–70. http://dx.doi.org/10.3390/transplantology4020007.

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Circulatory death donor (DCD) kidneys are increasingly used to enlarge the donor pool. These kidneys undergo ischemia-reperfusion injury, frequently leading to renal fibrosis. Transforming growth factor beta 1 (TGF-β1) and matrix metalloproteases have been identified as central mediators of fibrosis and inhibition of these targets could attenuate fibrosis. We studied whether galunisertib, doxycycline, taurine, and febuxostat alleviated fibrosis in precision-cut kidney slices (PCKS). PCKS were prepared from porcine kidneys that were exposed to 30 min of warm ischemia followed by 3 h of oxygenated hypothermic machine perfusion. We subsequently incubated PCKS for 48 h at 37 °C with the described compounds. To further elucidate the antifibrotic effects of galunisertib, we cultured PCKS with TGF-β1. We first screened the effects of the compounds without TGF-β1. Most significant effects were observed for galunisertib which lowered the expression of ACTA2, TGFB1, FN2, and SERPINE1. We then investigated the effects of galunisertib in fibrotic PCKS incubated with TGF-β1. TGF-β1 significantly increased expression of TGFB1, FN1, SERPINE1, and SERPINH1. Galunisertib, however, attenuated the expression of all fibrosis-related genes. Galunisertib appears to be a promising antifibrotic compound requiring further research in a preclinical model and may ultimately be administered during machine perfusion as an antifibrotic treatment in a transplant setting.
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Brzhozovskiy, Alexander G., Alexey S. Kononikhin, Lyudmila Ch Pastushkova, Daria N. Kashirina, Maria I. Indeykina, Igor A. Popov, Marc-Antoine Custaud, Irina M. Larina, and Evgeny N. Nikolaev. "The Effects of Spaceflight Factors on the Human Plasma Proteome, Including Both Real Space Missions and Ground-Based Experiments." International Journal of Molecular Sciences 20, no. 13 (June 29, 2019): 3194. http://dx.doi.org/10.3390/ijms20133194.

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The aim of the study was to compare proteomic data on the effects of spaceflight factors on the human body, including both real space missions and ground-based experiments. LC–MS/MS-based proteomic analysis of blood plasma samples obtained from 13 cosmonauts before and after long-duration (169–199 days) missions on the International Space Station (ISS) and for five healthy men included in 21-day-long head-down bed rest (HDBR) and dry immersion experiments were performed. The semi-quantitative label-free analysis revealed significantly changed proteins: 19 proteins were significantly different on the first (+1) day after landing with respect to background levels; 44 proteins significantly changed during HDBR and 31 changed in the dry immersion experiment. Comparative analysis revealed nine common proteins (A1BG, A2M, SERPINA1, SERPINA3, SERPING1, SERPINC1, HP, CFB, TF), which changed their levels after landing, as well as in both ground-based experiments. Common processes, such as platelet degranulation, hemostasis, post-translational protein phosphorylation and processes of protein metabolism, indicate common pathogenesis in ground experiments and during spaceflight. Dissimilarity in the lists of significantly changed proteins could be explained by the differences in the dynamics of effective development in the ground-based experiments. Data are available via ProteomeXchange using the identifier PXD013305.
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Al-Khatib, Sohaib, Mohammad Nitham Almajali, Ayah Al-Bzour, Joud Al-Ramadneh, Laila Sa'd, and Noor Othman. "Abstract 5594: Exploring genetic determinants: A comprehensive analysis of SERPINB family variants and prognosis in Jordanian glioblastoma multiforme patients." Cancer Research 84, no. 6_Supplement (March 22, 2024): 5594. http://dx.doi.org/10.1158/1538-7445.am2024-5594.

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Abstract Background: Glioblastoma multiforme (GBM) is a major concern with high fatality rate. In Jordan, the incidence of GBM has notably increased, emphasizing the urgency for population-specific research. Serpins are serine proteinase inhibitors, with several Serpins being overexpressed in cancer cells however the exact mechanism by which they affect GBM progression remains unclear. Thus, we aim to analyze the single-nucleotide polymorphism (SNP) of SERPINB11 and its association with GBM survival. Methods: A cohort of 63 GBM patients recruited from King Abdullah University Hospital (KAUH) in Jordan, underwent genomic DNA extraction, polymorphism analysis, and overall survival (OS) assessments. The Serpin B family were validated using The Cancer Genome Atlas (TCGA-GBM) cohort of 160 patients. We constructed a risk-score using the principal component analysis for the following Serpin genes: Serpinb3, Serpinb5, Serpinb6, Serpinb11, and Serpinb12, and patients were grouped into high- vs. low-risk based on median cutoff. Univariable Cox models were used to study the survival outcomes, differential expression analysis between the high- and low-risk groups was carried out to identify the differentially expressed genes (DEGs), gene ontology (GO and tumor microenvironment analyses were carried out. Results: In our primary cohort, we identified a significant association between rs4940595 (SERPINB11) SNP and survival, with the G/T- genotype showing worse prognosis compared to the G/G-T/T genotype in the over dominant model (HR: 2.75, 95% CI: 1.29-5.88, p-value=0.009). In the TCGA validation-cohort, alterations in the SERPINB3gene showed significantly worse OS (Median: 9.53 vs. 14.3, p-value=0.044) compared to the no alteration group. Univariable Cox showed worse PFS outcomes with higher SERPINB5 (HR: 1.67, 95% CI: 1.15-2.43, p-value=0.007) and SERPINB6 expression (HR: 1.44, 95% CI: 1.06-1.96, p-value=0.021). A Serpin B 5-gene risk score was constructed revealing significant association with IDH mutation status and a trend towards worse PFS in the high-risk group. Upregulated DEGs showed GO enrichment in cytokine regulation and production, positive regulation of leukocyte activation and MAPK cascade. While the downregulated DEGs were enriched in forebrain development, and negative regulation of neuron differentiation. The high-risk group showed a significantly higher infiltration of M2 macrophages and activated mast cells. Conclusion: Our findings showed a significant role of the Serpin B family with GBM survival in the Jordanian population. Molecular analyses showed potential mechanisms underlying these associations. Our exploration of SERPINB family and associated SNPs provides valuable insights into the molecular landscape of GBM, paving the way for potential targeted interventions and personalized treatment strategies. Citation Format: Sohaib Al-Khatib, Mohammad Nitham Almajali, Ayah Al-Bzour, Joud Al-Ramadneh, Laila Sa'd, Noor Othman. Exploring genetic determinants: A comprehensive analysis of SERPINB family variants and prognosis in Jordanian glioblastoma multiforme patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 5594.
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Dissertations / Theses on the topic "SERPINH1":

1

Furtado, Clara Fernanda Barbirato. "Investigação de mutações nos genes LEPRE1, CRTAP, PPIB, FKBP10, SERPINH1 e SERPINF1 causadoras da osteogênese imperfeita recessiva." Universidade Federal do Espírito Santo, 2015. http://repositorio.ufes.br/handle/10/4522.

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Made available in DSpace on 2016-08-29T15:34:42Z (GMT). No. of bitstreams: 1 tese_8279_Tese_Clara Fernanda Barbirato.pdf: 794712 bytes, checksum: 13290894bcf3053215336989ea116592 (MD5) Previous issue date: 2015-02-13
A Osteogênese Imperfeita (OI) é uma doença clínica e geneticamente heterogênea caracterizada, predominantemente, por fragilidade e deformidade ósseas e por fraturas recorrentes. A maioria dos casos de OI resulta de mutações autossômicas dominantes nos genes COL1A1 e COL1A2, que codificam as cadeias formadoras do colágeno tipo I, principal proteína dos ossos. Nos últimos anos, um número crescente de casos decorrentes de mutações recessivas vem sendo relatado em genes associados à biossíntese do colágeno tipo I ou à formação e a mineralização óssea, como os genes LEPRE1, CRTAP, PPIB, FKBP10, SERPINH1 e SERPINF1. Mutações nesses genes, em geral, levam ao desenvolvimento de fenótipos graves e letais de OI. Neste trabalho, foram analisados os genes LEPRE1, CRTAP, PPIB, FKBP10, SERPINH1 e SERPINF1 de 25 pacientes com OI utilizando-se as técnicas de SSCP e sequenciamento. Ao todo, 29 variações genéticas foram detectadas, entre mutações e polimorfismos. Das onze variações encontradas no gene LEPRE1, estão a já bem descrita c.1080+1G>T e as mutações potencialmente deletérias c.2024G>A / p.Lys363Glu e c.1501C>T / p.Arg501Trp. No gene FKBP10, foi encontrada a também descrita duplicação c.831dupC, além da c.1546G>A / p.Leu516Phe, predita como causadora da doença. Observou-se que os genes FKBP10 e LEPRE1 contêm as principais mutações encontradas neste trabalho e sugere-se que os mesmos sejam preferencialmente analisados em estudos de triagem e identificação de mutações em OI. Até o momento, não existem relatos de mutações nos genes LEPRE1, CRTAP, PPIB, FKBP10, SERPINH1 e SERPINF1 em pacientes brasileiros e este trabalho fornece novas informações sobre os aspectos genéticos da OI recessiva
Osteogenesis Imperfecta (OI) is a clinically and genetically heterogeneous disease predominantly characterized by bone fragility and deformity and recurrent fractures. Most cases of OI result of autosomal dominant mutations in COL1A1 and COL1A2 genes that encode the chains forming type I collagen, the main protein in bones. In the past few years, an increasing number of cases due to recessive mutations has been reported in genes associated with the biosynthesis of type I collagen or to the formation and bone mineralization, such as LEPRE1, CRTAP, PPIB, FKBP10, SERPINH1 and SERPINF1. Mutations in these genes, in general, lead to the development of severe and lethal OI phenotypes. In this work, LEPRE1, CRTAP, PPIB, FKBP10, SERPINH1 and SERPINF1 of 25 OI patients were analyzed using SSCP and automated sequencing. Altogether, 29 genetic variations were detected, mutations and polymorphisms. Among the eleven variants found in LEPRE1 gene, there are the already well described c.1080 + 1G> T and the potentially deleterious mutations c.2024G> A / p.Lys363Glu and c.1501C> T / p.Arg501Trp . In FKBP10 gene, the previously described duplication c.831dupC, and c.1546G>A / p.Leu516Phe, predicted to be disease causing, were detected. It was observed that FKBP10 and LEPRE1 contain the most important mutations found in the patients studied in this work and it is suggested that LEPRE1 and FKBP10 should be preferably analyzed in studies of screening and identification of mutations in patients with OI. To date, there are no reports of mutations in LEPRE1, CRTAP, PPIB, FKBP10, SERPINH1 and SERPINF1 genes in Brazilian patients and this study provides new information on the genetic aspects of recessive OI.
2

Wegehaupt, Oliver Philipp [Verfasser], and Michael [Akademischer Betreuer] Köttgen. "BAG2, BAT3, DNAJB11, GNB2L1 und SERPINH1 interagieren in einem Netzwerk mit dem Polycystin-1-TRPP2-Signalmodul." Freiburg : Universität, 2016. http://d-nb.info/1122647816/34.

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3

Pierce, Charles. "The role of the gene SERPINH1 as a pharmacogenetic biomarker for choroidal neovascularization (CNV) responses to anti vascular endothelial growth factor (VEGF) treatment in clinical practice." Thesis, University of Southampton, 2015. https://eprints.soton.ac.uk/417281/.

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Age related macular degeneration is the commonest cause of blindness in the western world and current treatment regimens represent a significant output for national health services. The disease process is multifactorial in origin and has a variable progression and response to current methods of treatment. A targeted approach with individualized therapy based on recognized biomarkers to predict disease outcome would be the ideal treatment modality. We plan to investigate the role of genes known to influence the progression of early AMD to the advanced stage (wet AMD) with emphasis on genes involved in complement regulation (SERPING1, CFB, CFI, CFH, C2 and C3). The investigation will also encompass other genotypes involved in AMD pathogenesis. Polymorphic variations in the gene SERPING1, which codes for complement 1 inhibitor (C1Inh), have been previously implicated in AMD pathogenesis. Many clinical trials involving complement antagonists are currently proceeding at various stages of development. We plan to investigate the role of C1Inh in AMD development and explore its potential as a therapeutic agent, utilising Ccl2-/-/Cx3cr1-/- (in the presence of an rd8 mutation in the Crb1 gene) and wild type C57BL/6 mice. In the neurodegenerative condition Alzheimer’s disease, acute or chronic and chronic systemic inflammation have been associated with progression of symptoms. Both chronic and acute inflammation have been implicated in choroidal angiogenesis and subsequent AMD development. We hypothesised that systemic inflammation may alter the response of AMD to the anti-vascular endothelial growth factor (VEGF) agent ranibizumab. Inflammatory markers may therefore offer an objective indicator of future treatment response. These experiments will provide a comprehensive analysis of prognostic indicators for AMD and investigate a potentially new therapeutic agent.
4

Prévot, Pierre-Paul. "Rôles de la protéine Iris dans l'accomplissement du repas sanguin de la tique Ixodes ricinus." Doctoral thesis, Universite Libre de Bruxelles, 2007. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210730.

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Les tiques sont des arthropodes ectoparasites obligatoires qui se nourrissent sur une grande variété de vertébrés sur une large partie du globe. Au cours de leur repas, les tiques sécrètent dans leur salive de nombreux facteurs leur permettant de contourner bon nombre des défenses de l’hôte. Bien que la littérature rapporte beaucoup d’informations au sujet des effets du repas de la tique sur l’hôte, la nature des facteurs actifs exprimés par les glandes salivaires de la tique est peu connue. Au cours d’anciens travaux au sein du laboratoire, le crible de deux banques d’ADN complémentaires - issues de la rétro-transcription des ARN messagers synthétisés par les glandes salivaires de la tique Ixodes ricinus – a permis l’identification de 27 protéines dont l'expression est spécifiquement induite ou régulée positivement pendant le repas sanguin de la tique I. ricinus. Parmi ces protéines, la protéine Seq24, induite au cours du repas sanguin, présente la capacité de moduler les immunités innée et acquise de l’hôte. En conséquence, la protéine Seq24 a été nommée Iris pour « Ixodes ricinus Immunosuppressor ». Au cours de la présente étude, notre but fût de caractériser le rôle d’Iris et de déterminer son importance dans le repas sanguin de la tique I. ricinus.

La protéine Iris appartient à la famille des inhibiteurs de sérine protéases et présente une homologie significative avec l’inhibiteur d’élastase de leucocytes. Une analyse in silico a confirmé qu’Iris présentait la structure des serpines, et notamment le RCL (Reactive Center Loop), boucle responsable de l’activité anti-protéasique. Comme attendu (sur base de l’analyse in silico), Iris inhibe de manière spécifique l’activité de plusieurs sérine protéases, et en particulier l’élastase de leucocyte. Ces tests effectués, nous avons essayé de comprendre quel(s) pouvai(en)t être le(s) rôle(s) d’Iris dans l’accomplissement du repas sanguin de la tique, c’est à dire dans la lutte contre les différents systèmes de défenses de l’hôte.

Tout d’abord, des tests ont démontré la capacité d’Iris à inhiber les mécanismes de l’hémostase. Des tests sur du plasma et du sang complet ont montré qu’Iris allonge le temps de fibrinolyse, la voie intrinsèque de la coagulation et l’adhésion plaquettaire. L’utilisation de mutants a également démontré que si les deux premières activités sont dépendantes du RCL, et donc d’un mode de fonctionnement anti-protéolytique, l’adhésion plaquettaire est indépendante de ce système. Ce résultat met en évidence l’existence d’autres sites actifs, isolés par analyse in silico, nommés Receptor Binding Domain (RBD).

Un travail antérieur du laboratoire avait permis d’indiquer la capacité de la protéine recombinante Iris semi-purifiée à inhiber la production de TNF-a, d’IL-6, et d’IL-8 (cytokines pro-inflammatoires) ainsi que l’IFN-g par des PBMCs (Peripherical Blood Mononuclear Cells) humaines. Ces résultats ont été confirmés avec de la protéine purifiée. Des analyses complémentaires ont démontré qu’un mutant d’Iris - dépourvu d’activité anti-protéasique - conserve l’activité pro-inflammatoire. Là encore, ce mécanisme semble impliquer un ou plusieurs RBD. L’utilisation d’anticorps dirigés contre ces zones a permis de déterminer le domaine d’interaction (aa :105-120) impliqué dans cette fonction. D’autre part, une analyse par FACS a permis de démontrer qu’Iris interagit uniquement avec les cellules d’origine monocytaire.

Enfin, nous avons également analysé l’importance d’Iris au cours du repas sanguin de la tique par une approche vaccinale. Les résultats observés indiquent que 30 % des tiques nourries sur des lapins immunisés par la protéine rIris ne survivent pas au repas.
Doctorat en sciences, Spécialisation biologie moléculaire
info:eu-repo/semantics/nonPublished

5

Ulbricht, David, Jan Pippel, Stephan Schultz, René Meier, Norbert Sträter, and John T. Heiker. "A unique serpin P1′ glutamate and a conserved β-sheet C arginine are key residues for activity, protease recognition and stability of serpinA12 (vaspin)." Portland Press, 2015. https://ul.qucosa.de/id/qucosa%3A33439.

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SerpinA12 (vaspin) is thought to be mainly expressed in adipose tissue and has multiple beneficial effects on metabolic, inflammatory and atherogenic processes related to obesity. KLK7 (kallikrein 7) is the only known protease target of vaspin to date and is inhibited with a moderate inhibition rate. In the crystal structure, the cleavage site (P1-P1′) of the vaspin reactive centre loop is fairly rigid compared with the flexible residues before P2, possibly supported by an ionic interaction of P1′ glutamate (Glu379) with an arginine residue (Arg302) of the β-sheet C. A P1′ glutamate seems highly unusual and unfavourable for the protease KLK7. We characterized vaspin mutants to investigate the roles of these two residues in protease inhibition and recognition by vaspin. Reactive centre loop mutations changing the P1′ residue or altering the reactive centre loop conformation significantly increased inhibition parameters, whereas removal of the positive charge within β-sheet C impeded the serpin–protease interaction. Arg302 is a crucial contact to enable vaspin recognition by KLK7 and it supports moderate inhibition of the serpin despite the presence of the detrimental P1′ Glu379, which clearly represents a major limiting factor for vaspin-inhibitory activity. We also show that the vaspin-inhibition rate for KLK7 can be modestly increased by heparin and demonstrate that vaspin is a heparin-binding serpin. Noteworthily, we observed vaspin as a remarkably thermostable serpin and found that Glu379 and Arg302 influence heat-induced polymerization. These structural and functional results reveal the mechanistic basis of how reactive centre loop sequence and exosite interaction in vaspin enable KLK7 recognition and regulate protease inhibition as well as stability of this adipose tissue-derived serpin.
6

Mkaouar, Héla. "Rôle des serpines, inhibiteurs de protéases à serine, du microbiote digestif humain dans les maladies inflammatoires de l'intestin." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS108.

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Les inhibiteurs des protéases à sérine (Serpins) constituent une classe d'enzymes très peu étudiée chez les bactéries. Dans ce travail de thèse nous nous sommes intéressés à l'étude des serpins provenant du microbiote intestinal et l'investigation de leur potentiel anti-inflammatoire pour le traitement des maladies inflammatoires chroniques de l'intestin (MICI) chez l'homme. Pour cela nous avons identifié les serpins provenant du microbiote intestinal humain et analysé leur diversité ainsi que leur distribution entre les individus malades et sains. Ces données nous ont permis d'isoler les serpins significativement associées aux MICI. La purification de quarte d'entre elles nous a amené à démontrer qu'elles inhibent les protéases humaines impliquées dans les MICI. L'analyse biochimique et cinétique approfondie de ces protéines a montré qu'elles possèdent des propriétés originales notamment leur efficacité d'inhibition élevée. L'étude de l'effet protecteur de trois serpins chez un modèle animal de colite a démontré pour la première fois l'efficacité des serpins in vivo démontrant ainsi leur potentiel thérapeutique
Serine protease inhibitors (Serpins) are a class of proteins that reamin poorly studied in bacteria. In this thesis we are interested in the study of serpins originating from the intestinal microbiota and the investigation of their anti-inflammatory potential for the treatment of inflammatory bowel diseases (IBD) in humans. For this we have identified serpins from the human gut microbiota and analyzed their diversity as well as their distribution between healthy and IBD patients. These data allowed isolating serpins significantly associated with IBD. The purification of four of them led us to demonstrate that they inhibit human proteases involved in IBD. Biochemical and kinetic analysis of these proteins showed that they exhibit original properties, in particular their high inhibition efficiency. The study of the protective effect of three serpins in an animal model of colitis demonstrated for the first time the efficacy of serpins in vivo demonstrating thus their therapeutic potential
7

Götzfried, Jessica Tanja Tamara [Verfasser], and Karl-Peter [Akademischer Betreuer] Hopfner. "Genetic, biochemical and preclinical studies on a tandem cluster of two human serpins: alpha-1-antitrypsin and serpina2 / Jessica Tanja Tamara Götzfried ; Betreuer: Karl-Peter Hopfner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1160876223/34.

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Souza, Lucas Rodrigo de. "Desenvolvimento de bibliotecas baseadas em serpinas para geração de inibidores de calicreínas teciduais humanas." reponame:Repositório Institucional da UFABC, 2017.

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Orientador: Prof. Dr. Luciano Puzer
Tese (doutorado) - Universidade Federal do ABC, Programa de Pós-Graduação em Biossistemas, 2017.
As calicreinas teciduais humanas (KLKs) compreendem uma familia de quinze serino proteases encontradas em uma diversidade de fluidos e tecidos biologicos. Estas enzimas sao identificadas como possuindo papel em diferentes doencas como Alzheimer, cancer, dermatite atopica, esclerose multipla, Parkinson, psoriase e outras. Existe, portanto, uma crescente demanda por inibidores especificos para cada uma das calicreinas e este e o objetivo do nosso grupo de pesquisa na UFABC. Neste trabalho pretendemos gerar inibidores para as calicreinas teciduais humanas 3, 5 e 7, utilizando bibliotecas baseadas em duas serpinas diferentes: uma expressando a forma Pittsburgh do inibidor de proteinase-¿¿1 (IP-¿¿1 M358R), randomizada nos residuos 352-356 (P7-P3); e outra expressando a serpina bacteriana vioserpina, randomizada nos residuos 343-347 (P3-P2f). A abordagem do phage display foi eficaz para gerar as bibliotecas e o protocolo de bioselecao utilizado adequado para enriquecer diversas variantes reativas. Na selecao da biblioteca do IP-¿¿1 M358R, consensos PSEAL e PSRIL foram observados, para KLK5 e KLK7, respectivamente, e varias das sequencias selecionadas exibiram maiores taxas de inibicao para ambas as calicreinas, quando comparadas a molecula molde (IP-¿¿1 M358R). A variante HDVIL e o consenso PSRIL foram identificados como sendo altamente seletivos para a KLK7, com constantes de segunda ordem 14 e 33 vezes maiores que as para KLK5. Pudemos realizar uma selecao efetiva da biblioteca de vioserpina contra a KLK7, cujas variantes enriquecidos demonstraram uma preferencia geral pelo aminoacido Serina ocupando as posicoes P3, P1f, P2f e P1, seguido por uma Tirosina, tambem preferida em P2. A tecnica de phage display foi, portanto, eficiente como base para um estudo de especificidade, e para o desenvolvimento de melhores e mais especificos inibidores para as Calicreinas Teciduais Humanas, e pode ser utilizada para o desenvolvimento de novas bibliotecas, com outras regioes da RCL randomizadas, ou mesmo baseadas em outras serpinas.
The human tissue kallikreins (KLKs) comprise a family of fifteen serine proteases found in a diversity of biological fluids and tissues. These enzymes are identified as having a role in different diseases such as Alzheimer's, cancer, atopic dermatitis, multiple sclerosis, Parkinson's, psoriasis, and others. Thus there is a growing demand for specific inhibitors for each of these kallikreins, and this is the aim of our group at UFABC. In this work we intended to generate inhibitors for the human tissue kallikreins 3, 5 and 7, using libraries based on two different serpins: one expressing the Pittsburgh form of the human serpin á1-proteinase inhibitor (á1-PI M358R), randomized at residues 352-356 (P7-P3); and another one expressing the bacterial vioserpin, randomized at residues 343-347 (P3-P2¿). The phage display approach was effective to generate the libraries and the biopanning protocol used suitable to enrich numerous reactive variants. On the á1-PI M358R selection, loose consensus of PSEAL and PSRIL were observed, for KLK5 and KLK7, respectively, and several of the selected sequences exhibited higher inhibition rates when compared to the template molecule for both kallikreins. The variant HDVIL and consensus PSRIL were found to be highly selective for the KLK7, with second order constants 14- and 33-fold higher than the ones for KLK5. We could only perform an effective selection with the vioserpin library for the KLK7, whose enriched variants demonstrated a general preference for the amino acid Serine occupying the positions P3, P1¿, P2¿ and P1, followed by a Tyrosine, also preferred on the P2. The phage display approach was therefore effective as basis for a specificity study, and for the development of improved, more specific inhibitors for the Human Tissue Kallikreins, and can be used to develop new libraries, with other randomized RCL regions, or even based on other serpins.
9

Evans, Dyfed Ll. "The heparin activateable serpins." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385390.

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Aymonnier, Karen. "La protease Nexine-1, une cible prometteuse dans le traitement de l'hémophilie et son rôle dans les polynucléaires neutrophiles." Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCC049.

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L’hémophilie A est une maladie hémorragique rare caractérisée par un déficit du facteur de la coagulation VIII (FVIII). De nouvelles stratégies thérapeutiques ne reposant pas sur l’injection de FVIII se développent. Nous proposons une approche innovante qui consiste à cibler un anticoagulant naturel présent dans les plaquettes, la Protéase Nexine-1 (PN-1). La PN-1 est un inhibiteur puissant de la thrombine, enzyme clé de la coagulation. Bloquer la PN-1 favoriserait ainsi la génération de thrombine et donc la coagulation chez les patients hémophiles. Nous avons montré que bloquer la PN-1 améliore effectivement la génération de thrombine dans les plasmas de patients hémophiles. Nos données obtenues in vivo ont également montré une restauration de la coagulation et des temps de saignement chez des souris hémophiles déficientes en PN-1. L’ensemble de nos résultats indique que la PN-1 constitue une nouvelle cible thérapeutique intéressante pour le traitement de l’hémophilie.Le rôle potentiel de la PN-1 dans la régulation des mécanismes inflammatoires n’est pas connu. Au niveau des cellules inflammatoires, sa présence n’a été démontrée que dans les monocytes-macrophages et son expression n’a encore jamais été étudiée dans les polynucléaires neutrophiles. Nous avons ainsi mis en évidence pour la première fois la présence de PN-1 dans les neutrophiles et avons montré que le déficit en PN-1 limite le recrutement des neutrophiles in vivo. Ces travaux ont permis d’identifier la PN-1 comme un nouveau régulateur des mécanismes de recrutement des neutrophiles
Hemophilia is a disease caused by the lack of Factor VIII (FVIII), leading to insufficient thrombin production, and therefore bleeding. Recently, new therapeutic strategies for hemophilia treatment, that do not rely on clotting factor replacement, have emerged. We propose an innovative approach consisting in targeting a natural and potent thrombin inhibitor, expressed by platelets and called protease nexin-1 (PN-1). Our results demonstrated that blocking PN-1 increased, in vitro, thrombin generation in plasma from patients with hemophilia, and reduced blood loss in hemophiliac mice. Our study provides proof-of-concept that PN-1 neutralizing can be a a novel approach for future clinical care in hemophilia. The potential role of PN-1 in regulating inflammatory processes is not known. Vascular cells, platelets and inflammatory cells express PN-1, but no data are available concerning its expression and potential function in neutrophils. For the first time, we demonstrated the presence of PN-1 in neutrophils. Our data have shown that neutrophil recruitment was much less important in peritoneal cavity of PN-1-/- mice than in those of WT mice. These novel findings suggest that PN-1 is a serpin regulating positively PMNs functions
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Books on the topic "SERPINH1":

1

Lucas, Alexandra, ed. Serpins. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8645-3.

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Macaryus, Sudartomo. Serpih-serpih pandangan Ki Hadjar Dewantara. Yogyakarta: Universitas Sarjanawiyata Tamansiswa bekerjasama dengan Penerbit Kepel Press, 2010.

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Kaswanti, Purwo Bambang, ed. Serpih-serpih telaah pasif bahasa Indonesia. Yogyakarta: Kanisius, 1989.

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Whisstock, James C. Biology of serpins. Amsterdam [u.a.]: Elsevier, Acad. Press, 2011.

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Geiger, Margarethe, Felix Wahlmüller, and Margareta Furtmüller, eds. The Serpin Family. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22711-5.

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Church, Frank C., Dennis D. Cunningham, David Ginsburg, Maureane Hoffman, Stuart R. Stone, and Douglas M. Tollefsen, eds. Chemistry and Biology of Serpins. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5391-5.

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C, Church Frank, and International Symposium on the Chemistry and Biology of Serpins (1996 : Chapel Hill, N.C.), eds. Chemistry and biology of serpins. New York: Plenum Press, 1997.

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Gettins, Peter G. W. Serpins: Structure, function, and biology. Austin: R.G. Landes, 1996.

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Potempa, Jan. Struktura, funkcja i ewolucja serpin. Kraków: Nakł. Uniwersytetu Jagiellońskiego, 1993.

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Carthy, Barry Mc. Ovalbumin, gene Y and serpin inhibitory function. Dublin: University College Dublin, 1998.

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Book chapters on the topic "SERPINH1":

1

Czekay, Ralf-Peter, Tessa M. Simone, and Paul J. Higgins. "SerpinE1." In Encyclopedia of Signaling Molecules, 4902–13. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101828.

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Czekay, Ralf Peter, Tessa M. Simone, and Paul J. Higgins. "SerpinE1." In Encyclopedia of Signaling Molecules, 1–11. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101828-1.

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Travis, James. "Serpins." In Advances in Experimental Medicine and Biology, 1–4. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5391-5_1.

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Stone, Stuart R., James C. Whisstock, Stephen P. Bottomley, and Paul C. R. Hopkins. "Serpins." In Advances in Experimental Medicine and Biology, 5–15. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5391-5_2.

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Johnson, Tierra A., Marguerite S. Buzza, Ekemini A. U. Riley, and Toni M. Antalis. "Plasminogen Activator Inhibitor Type-2 (PAI-2)/SerpinB2: A Unique Multifunctional Serpin." In The Serpin Family, 107–26. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22711-5_8.

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Metze, Dieter, Tam Nguyen, Birgit Haack, Alexander K. C. Leung, Noriko Miyake, Naomichi Matsumoto, A. J. Larner, et al. "Deficiency of AT-III SERPINC1." In Encyclopedia of Molecular Mechanisms of Disease, 499. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6346.

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Cierniewski, Czeslaw S., and Joanna Boncela. "Serpins in Angiogenesis." In Angiogenesis and Vascularisation, 101–18. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1428-5_5.

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Cohen, Maja, Thomas H. Roberts, and Robert Fluhr. "Serpins in Plants." In The Serpin Family, 15–28. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22711-5_2.

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Alberdi, Elena, and S. Patricia Becerra. "Inflammation and Noninhibitor Serpins." In Advances in Experimental Medicine and Biology, 307–39. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5391-5_25.

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Luke, Cliff J., Mark T. Miedel, Linda P. O’Reilly, Allyson Wyatt, Ryan R. Knoerdel, Stephen C. Pak, and Gary A. Silverman. "Serpins in Caenorhabditis elegans." In The Serpin Family, 253–68. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22711-5_15.

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Conference papers on the topic "SERPINH1":

1

Karelina, K. V., R. B. Bayandin, and V. A. . Ternovoi. "PRODUCTION OF A FRAGMENT OF RECOMBINANT TICK PROTECTIVE ANTIGEN SERPIN IPIS-1, RCL-LOOP DOMAIN, OF IXODES PERSULCATUS TICKS." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-87.

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Infections carried by ticks cause significant damage to livestock production, infections lead to loss of productivity, weakened immunity, allergic reactions, weight loss, and in severe cases death. When bitten, ticks produce a number of proteins — tick defense antigens — that facilitate the tick’s feeding on the host and thus facilitate the transmission of the infections they carry. Some of the tick protective antigens are serpins, a promising target for animal immunization and infection control. In studies, serpins from tick saliva have been shown to interact with host proteins while reducing the host immune response. In this study, we obtained a fragment of recombinant tick protective antigen serpin Ipis-1, an RCL-loop domain, from Ixodes Persulcatus ticks.
2

Pannekoek, H., M. Linders, J. Keijer, H. Veerman, H. Van Heerikhuizen, and D. J. Loskutoff. "THE STRUCTURE OF THE HUMAN ENDOTHELIAL PLASMINOGEN ACTIVATOR INHIBITOR (PAI-1) GENE: NON-RANDOM POSITIONING OF INTRONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644767.

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The endothelium plays a crucial role in the regulation of the fibrinolytic process, since it synthesizes and secretes tissue-type plasminogen activator (t-PA) as well as the fast-acting plasminogen activator inhibitor (PAI-1). Molecular cloning of full-length PAI-1 cDNA, employing a human endothelial cDNA expression library, and a subsequent determination of the complete nucleotide sequence, allowed a prediction of the amino-acid sequence of the PAI-1 glycoprotein. It was observed that the amino-acid sequence is significantly homologous to those of members of the serine protease inhibitor ("Serpin") family, e.g. αl-antitrypsin and antithrombin III. Serpins are regulators of various processes, such as coagulation, inflammatory reactions, complement activation and share a common functional principle and a similar structure, indicative for a common primordial gene. The intron-exon arrangement of Serpin genes may provide a record for the structure of a primordial gene. A comparison of the location of introns among members of the Serpin family reveals that some introns are indeed present at identical or almost identical positions, however in many other cases there is no correspondence between the intron positions among different Serpin genes.Obviously, more data on the chromosomal gene structure of members of this family are required to formulate a scheme for the evolutionary creation of the Serpins. To that end, we have established the number and the precise location of the introns in the PAI-1 gene and have compared these data with those reported on other Serpin genes. For that purpose a human genomic cosmid DNA library of about 340.000 independent colonies was screened with radiolabelled full-length PAI-1 cDNA as probe. Two clones were found which contain the entire PAI-1 gene. Restriction site mapping, electron microscopic inspection of heteroduplexes and nucleotide sequence analysis demonstrate that the PAI-1 gene comprises about 12.2kilo basepairs and consists of nine exons and eight introns. Intron-exon boundaries are all in accord with the "GT-AG" rule, including a cryptic acceptor splice site found in intron 7. Furthermore, it is observed that intron 3 of the PAI-1 gene occupies an identical position as intron E of chicken ovalbumin and intron E of the ovalbumin-related gene Y. The location of the other seven introns is unrelated to the known location of introns in the genes encoding the Serpins, rat angiotensin, chicken ovalbumin (and gene Y), human antithrombin III and human al-antitrypsin. The 3' untranslated region of the PAI-1 gene is devoid of introns, indicating that the two mRNA species detected in cultured endothelial cells which share an identical 5' untranslated segment and codogenic region, but differ in the length of the 3' untranslated region, arise by alternative polyadenylation. An extrapolation of the position of the introns to the amino-acid sequence of PAI-1, and adaption of the view that the subdomain structure of the Serpins is analogous, shows that the introns of PAI-1 are non-randomly distributed. Except for intron 7, the position of the other seven introns corresponds with randon-coil regions of the protein or with the borders of β-sheets and a-helices. Extrapolation of the position of introns in the genes of other Serpins to their respective amino-acid sequences and subdomain structures also reveals a preference for random-coil regions and borders of subdomains. These observations are reminiscent of an evolutionary model, called "intron sliding", that accounts for variations in surface loops of the same protein in different species by aberrant splicing (Craik et al., Science 220 (1983) 1125). The preferential presence of introns in gene segments, encoding these variable regions, and absence in regions determining the general folding of these proteins would explain conservation of the structure during the evolution of those genes.
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Ny, T., L. Hansson, and B. Åstedt. "ISOLATION OF cDNA FOR TYPE-2 PLASMINOGEN ACTIVATOR INHIBITOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642855.

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Abstract:
The placental type plasminogen activator inhibitor (PAI-2) has been purified from extracts of human placenta and from a histiocytic lymphoma cell line. It is mainly an uPA inhibitor but it also inhibits the two-chain form of tPA.In order to determine the factors regulating PAI-2 gene expression and thereby clarify the physiological role of PAI-2 we have undertaken the molecular cloning of PAI-2 cDNA. A λgt11 expression library prepared from placental mRNA, was screened, immunologically using a monoclonal antibody probe developed against PAI-2 purified from human placenta. When 1.7×105 recombinant phages were screened six positive clones were obtained. Hybridization experiments and comparison of restriction enzyme cleavege pattern revealed that the DNA inserts of the six clones were, related. To identify the clones as coding for PAI-2, a lysogen made from one of them was induced, and the proteins were separated by SDS-PAGE. In immuno-blotting wxperiments the recombinant fusion protein and purified PAI-2 were recognized by the monoclonal antibody and a monospecific polyclonal antibody against PAI-2, revealing an immunological similarity. The nucleotide sequence of the largest cDNA was determined. It was found to code for a protein with extensive sequence homology with members of the serine protease inhibitor family (serpins) Alignment of the active center region with other serpins indicates that PAI-2 is an arg-serpin, as expected for an inhibitor of plasminogen activators.
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Strandberg, L., D. Lawrence, and T. Ny. "ISOLATION OF THE GENOMIC REGION CODING FOR TYPE-1 PLASMINOGEN ACTIVATOR INHIBITOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644439.

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Abstract:
The type-1 Plasminogen Activator Inhibitor (PAI-1) has recently been identified as a member of the Serine Protease Inhibitor family (SERPINS). This family of proteins contain many serine protease inhibitors but also functionally unrelated proteins like ovalbumin and anginotensinogen. PAI-1 inhibits both u-PA and t-PA and might therefore be an important regulator of the fibrinolytic system.In order to study the evolution of the Serpin family as well as PAI-1 gene expression we have isolated the genomic region carrying the PAI-1 gene. A cDNA sequence for PAI-1 was used as probe to screen a human genomic library. When 2 million independent phages were screened, 13 positive clones were isolated. Characterisation of these clones showed that they could be divided into 3 overlapping groups covering a genomic region of approximately 30 kb. The gene was localized and characterized by restriction enzyme analysis, southern blotting using cDNA and oligomer probes, and DNA sequencing.
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Linja-Aho, Anna, Witold Mazur, Tuula Toljamo, Pentti Nieminen, Mikko Ronty, Steffen Ohlmeier, and Vuokko L. Kinnula. "Association Of SerpinA1 With Smoking And COPD." 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.a4362.

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Niemietz, C., S. Guttmann, V. Sandfort, and H. Schmidt. "SERPINA1 levels dictate TTR expression in HepG2 cells." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677092.

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Niemietz, C., and H. Schmidt. "Inverse Expression von SERPINA1 und TTR bei TTR Amyloidose." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695237.

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Ferrarotti, I., M. Zorzetto, I. Campo, S. Ottaviani, R. Scabini, M. Gorrini, and M. Luisetti. "SERPINA1 Gene Informative SNPs To Predict AAT Plasma Level." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3504.

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Rufino, M. C., T. Bartholo, A. P. Viana, B. Chaves, V. D´Elia, and C. Costa. "SERPINA1 Gene Polymorphism: Analysis of Patients Over 2 Years." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a3785.

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Vlasov, A. P., V. A. Trofimov, S. S. Al-Kubaysi, N. A. Myshkina, T. A. Muratova, L. N. Umnov, and M. Yu Khachaturov. "Personalized approach in optimizing the treatment of acute pancreatitis." In VIII Vserossijskaja konferencija s mezhdunarodnym uchastiem «Mediko-fiziologicheskie problemy jekologii cheloveka». Publishing center of Ulyanovsk State University, 2021. http://dx.doi.org/10.34014/mpphe.2021-60-62.

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Abstract:
In order to determine the effectiveness of the use of remaxol based on a personalized approach in patients with acute pancreatitis, based on the establishment of gene polymorphism of integrin beta-3 (T1565C, ITGB3), integrin alpha-2 (C807T, ITGA2), fibrinogen (G(-455)A, FGB) and plasminogen activator inhibitor (5G(-675)4G, SERPINE1), a study of 84 patients with acute pancreatitis of varying severity was conducted. As a result of the study, it was proved that in order to increase the effectiveness of treatment of patients with severe acute pancreatitis upon admission, in addition to clinical, laboratory and instrumental studies, it is necessary to conduct genetic testing of the genotypes of the polymorphism of the GPIIa gene (T1565C), ITGA2 (C807T), FGB (G(-455)A) and SERPINE1 (5G(-675)4G) to develop a personalized approach in the treatment of this severe category of patients. Key words: acute pancreatitis, genotype, DNA diagnostics, genetic testing of genotypes, personalized medicine.

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