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Dive into the research topics where András Falus is active.

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Featured researches published by András Falus.


FEBS Letters | 2001

Mice lacking histidine decarboxylase exhibit abnormal mast cells

Hiroshi Ohtsu; Satoshi Tanaka; Tadashi Terui; Yoshio Hori; Yoko Makabe-Kobayashi; Gunnar Pejler; Elena Tchougounova; Lars Hellman; Marina Gertsenstein; Noriyasu Hirasawa; Eiko Sakurai; Edit I. Buzás; Péter Kovács; G. Csaba; Ágnes Kittel; Mikiko Okada; Masahiro Hara; Lynn Mar; Keiko Numayama-Tsuruta; Satsuki Ishigaki-Suzuki; Kazuo Ohuchi; Atsushi Ichikawa; András Falus; Takehiko Watanabe; Andras Nagy

Histidine decarboxylase (HDC) synthesizes histamine from histidine in mammals. To evaluate the role of histamine, we generated HDC‐deficient mice using a gene targeting method. The mice showed a histamine deficiency and lacked histamine‐synthesizing activity from histidine. These HDC‐deficient mice are viable and fertile but exhibit a decrease in the numbers of mast cells while the remaining mast cells show an altered morphology and reduced granular content. The amounts of mast cell granular proteases were tremendously reduced. The HDC‐deficient mice provide a unique and promising model for studying the role of histamine in a broad range of normal and disease processes.


Blood | 2011

Detection and isolation of cell-derived microparticles are compromised by protein complexes resulting from shared biophysical parameters

Bence György; Károly Módos; Éva Pállinger; Krisztina Pálóczi; Mária Pásztói; Petra Misják; Mária A. Deli; Áron Sipos; Anikó Szalai; István Voszka; Anna Polgár; K. Tóth; Mária Csete; György Nagy; András Falus; Ágnes Kittel; Edit I. Buzás

Numerous diseases, recently reported to associate with elevated microvesicle/microparticle (MP) counts, have also long been known to be characterized by accelerated immune complex (IC) formation. The goal of this study was to investigate the potential overlap between parameters of protein complexes (eg, ICs or avidin-biotin complexes) and MPs, which might perturb detection and/or isolation of MPs. In this work, after comprehensive characterization of MPs by electron microscopy, atomic force microscopy, dynamic light-scattering analysis, and flow cytometry, for the first time, we drive attention to the fact that protein complexes, especially insoluble ICs, overlap in biophysical properties (size, light scattering, and sedimentation) with MPs. This, in turn, affects MP quantification by flow cytometry and purification by differential centrifugation, especially in diseases in which IC formation is common, including not only autoimmune diseases, but also hematologic disorders, infections, and cancer. These data may necessitate reevaluation of certain published data on patient-derived MPs and contribute to correct the clinical laboratory assessment of the presence and biologic functions of MPs in health and disease.


Nature Reviews Rheumatology | 2014

Emerging role of extracellular vesicles in inflammatory diseases

Edit I. Buzás; Bence György; György Nagy; András Falus

The discovery that submicron-sized extracellular vesicles (EVs) are generated by both prokaryotic and eukaryotic cells might have a profound effect on experimental and clinical sciences, and could pave the way for new strategies to combat various diseases. EVs are carriers of pathogen-associated and damage-associated molecular patterns, cytokines, autoantigens and tissue-degrading enzymes. In addition to a possible role in the pathogenesis of a number of inflammatory conditions, such as infections and autoimmune diseases, EVs, including microvesicles (also known as microparticles), exosomes and apoptotic vesicles, have therapeutic potential and might be used as biomarkers for inflammatory diseases. Therefore, molecular diagnostics and targeted therapy could benefit from expanding knowledge in the field. In this Review, we summarize important developments and propose that extracellular vesicles could be used as therapeutic vehicles and as targets for the treatment and prevention of inflammatory diseases.


Inflammation Research | 2009

The major inflammatory mediator interleukin-6 and obesity.

Katalin Éder; Noemi Baffy; András Falus; András Fülöp

Adipose tissue is one of the main sources of inflammatory mediators, with interleukin-6 (IL-6) among them. Although high systemic levels of inflammatory mediators are cachectogenic and/or anorexic, today it is a widely propagated thesis that in the background of obesity, a low level of chronic inflammation can be found, with IL-6 being one of the many suggested mediators. This paper reviews the studies describing elevated IL-6 levels in obese patients and the role of adipocytes and adipose-tissue macrophages in the production of IL-6. The secretion of IL-6 is regulated by several physiologic or pathologic factors: hormones, cytokines, diet, physical activity, stress, hypoxia, and others. Adipose tissue-derived IL-6 may have an effect on metabolism through several mechanisms, including adipose tissue-specific gene expression, triglyceride release, lipoprotein lipase downregulation, insulin sensitivity, and so on. Having a better understanding of these mechanisms may contribute to the prevention and treatment of obesity.


Cell Biology International | 2004

Leptin-induced signal transduction pathways

Krisztina Hegyi; Kristóf A. Fülöp; Krisztina Kovács; Sára Tóth; András Falus

Leptin is a multifunctional cytokine and hormone that primarily acts in the hypothalamus and plays a key role in the regulation of food intake and energy expenditure. In addition, it has direct effects on many cell types on the periphery. Leptin acts through its receptor, the product of the db gene, which has six isoforms. Only one of them (OB‐Rb) has full signalling capabilities and is able to activate the Jak/STAT pathway, the major pathway used by leptin to exert its effects. However, some signalling events can be initiated by the short isoforms. Besides Jak/STAT, other pathways, such as MAPK and the 5′‐AMP‐activated protein kinase (AMPK) pathway, are also involved in leptin signalling. Leptin also interacts with insulin signalling. In this paper, we give an overview of the signal transduction mechanisms that are related to the actions of leptin.


Inflammation Research | 2009

Highlights of a new type of intercellular communication: microvesicle-based information transfer

Erna Pap; Éva Pállinger; Mária Pásztói; András Falus

Abstract.Microvesicles (MVs) are membrane-covered cell fragments released by most cell types during apoptosis or activation. They are increasingly considered to play a pivotal role in information transfer between cells. Their presence and role have been proven in several physiological and pathological processes, such as immune modulation in inflammation and pregnancy, or blood coagulation and cancer. MVs represent a newly recognized system of intercellular communications. They not only may serve as prognostic markers in different diseases, but could also hold the potential to be new therapeutic targets or drug delivery systems.The present overview aims to highlight some aspects of this new means of cellular communication: “microvesicular communication”.


Endocrine-related Cancer | 2009

Integrative molecular bioinformatics study of human adrenocortical tumors: microRNA, tissue-specific target prediction, and pathway analysis

Zsófia Tömböl; Péter Szabó; Viktor Molnár; Zoltán Wiener; Gergely Tölgyesi; János Horányi; Péter Riesz; Péter Reismann; Attila Patócs; István Likó; Rolf C. Gaillard; András Falus; Károly Rácz

MicroRNAs (miRs) are involved in the pathogenesis of several neoplasms; however, there are no data on their expression patterns and possible roles in adrenocortical tumors. Our objective was to study adrenocortical tumors by an integrative bioinformatics analysis involving miR and transcriptomics profiling, pathway analysis, and a novel, tissue-specific miR target prediction approach. Thirty-six tissue samples including normal adrenocortical tissues, benign adenomas, and adrenocortical carcinomas (ACC) were studied by simultaneous miR and mRNA profiling. A novel data-processing software was used to identify all predicted miR-mRNA interactions retrieved from PicTar, TargetScan, and miRBase. Tissue-specific target prediction was achieved by filtering out mRNAs with undetectable expression and searching for mRNA targets with inverse expression alterations as their regulatory miRs. Target sets and significant microarray data were subjected to Ingenuity Pathway Analysis. Six miRs with significantly different expression were found. miR-184 and miR-503 showed significantly higher, whereas miR-511 and miR-214 showed significantly lower expression in ACCs than in other groups. Expression of miR-210 was significantly lower in cortisol-secreting adenomas than in ACCs. By calculating the difference between dCT(miR-511) and dCT(miR-503) (delta cycle threshold), ACCs could be distinguished from benign adenomas with high sensitivity and specificity. Pathway analysis revealed the possible involvement of G2/M checkpoint damage in ACC pathogenesis. To our knowledge, this is the first report describing miR expression patterns and pathway analysis in sporadic adrenocortical tumors. miR biomarkers may be helpful for the diagnosis of adrenocortical malignancy. This tissue-specific target prediction approach may be used in other tumors too.


Nature Medicine | 2011

Histamine deficiency promotes inflammation-associated carcinogenesis through reduced myeloid maturation and accumulation of CD11b + Ly6G + immature myeloid cells

Xiang Dong Yang; Walden Ai; Samuel Asfaha; Govind Bhagat; Richard A. Friedman; Guangchun Jin; Heuijoon Park; Benjamin Shykind; Thomas G. Diacovo; András Falus; Timothy C. Wang

Histidine decarboxylase (HDC), the unique enzyme responsible for histamine generation, is highly expressed in myeloid cells, but its function in these cells is poorly understood. Here we show that Hdc-knockout mice show a high rate of colon and skin carcinogenesis. Using Hdc-EGFP bacterial artificial chromosome (BAC) transgenic mice in which EGFP expression is controlled by the Hdc promoter, we show that Hdc is expressed primarily in CD11b+Ly6G+ immature myeloid cells (IMCs) that are recruited early on in chemical carcinogenesis. Transplant of Hdc-deficient bone marrow to wild-type recipients results in increased CD11b+Ly6G+ cell mobilization and reproduces the cancer susceptibility phenotype of Hdc-knockout mice. In addition, Hdc-deficient IMCs promote the growth of tumor allografts, whereas mouse CT26 colon cancer cells downregulate Hdc expression through promoter hypermethylation and inhibit myeloid cell maturation. Exogenous histamine induces the differentiation of IMCs and suppresses their ability to support the growth of tumor allografts. These data indicate key roles for Hdc and histamine in myeloid cell differentiation and CD11b+Ly6G+ IMCs in early cancer development.


Inflammation Research | 2001

Biological and clinical significance of the JAK-STAT pathway; lessons from knockout mice.

Szabolcs Tóth; András Falus

Abstract. Originally described as the signal-transducing pathway of interferons, the JAK-STAT pathway soon turned out to participate in the signalling of numerous other immune and even non-immune mediators. Several murine knockout models have been described that underline the biological significance of this signalling system. Some human diseases (mainly neoplastic) are also known where malfunctioning of the JAK-STAT pathway is considered to participate in the pathogenesis. In this brief review article we will try to make a synopsis of its biological and clinical significance.


PLOS ONE | 2012

Improved flow cytometric assessment reveals distinct microvesicle (cell-derived microparticle) signatures in joint diseases.

Bence György; Tamás Szabó; Lilla Turiák; Matthew Wright; Petra Herczeg; Zsigmond Lédeczi; Ágnes Kittel; Anna Polgár; K. Tóth; Beáta Dérfalvi; Gergő Zelenák; István Böröcz; Bob Carr; György Nagy; Károly Vékey; András Falus; Edit I. Buzás

Introduction Microvesicles (MVs), earlier referred to as microparticles, represent a major type of extracellular vesicles currently considered as novel biomarkers in various clinical settings such as autoimmune disorders. However, the analysis of MVs in body fluids has not been fully standardized yet, and there are numerous pitfalls that hinder the correct assessment of these structures. Methods In this study, we analyzed synovial fluid (SF) samples of patients with osteoarthritis (OA), rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA). To assess factors that may confound MV detection in joint diseases, we used electron microscopy (EM), Nanoparticle Tracking Analysis (NTA) and mass spectrometry (MS). For flow cytometry, a method commonly used for phenotyping and enumeration of MVs, we combined recent advances in the field, and used a novel approach of differential detergent lysis for the exclusion of MV-mimicking non-vesicular signals. Results EM and NTA showed that substantial amounts of particles other than MVs were present in SF samples. Beyond known MV-associated proteins, MS analysis also revealed abundant plasma- and immune complex-related proteins in MV preparations. Applying improved flow cytometric analysis, we demonstrate for the first time that CD3+ and CD8+ T-cell derived SF MVs are highly elevated in patients with RA compared to OA patients (p = 0.027 and p = 0.009, respectively, after Bonferroni corrections). In JIA, we identified reduced numbers of B cell-derived MVs (p = 0.009, after Bonferroni correction). Conclusions Our results suggest that improved flow cytometric assessment of MVs facilitates the detection of previously unrecognized disease-associated vesicular signatures.

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