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1.

001-es BibID:BIBFORM089348
035-os BibID:(cikkazonosító)1581 (WoS)000592983700001 (Scopus)85096519824
Első szerző:Aladdin, Azzam (molekuláris biológus)
Cím:The Proteasome Activators Blm10/PA200 Enhance the Proteasomal Degradation of N-Terminal Huntingtin / Aladdin Azzam, Yao Yanhua, Yang Ciyu, Kahlert Günther, Ghani Marvi, Király Nikolett, Boratkó Anita, Uray Karen, Dittmar Gunnar, Tar Krisztina
Dátum:2020
ISSN:2218-273X
Megjegyzések:The Blm10/PA200 family of proteasome activators modulates the peptidase activity of the core particle (20S CP). They participate in opening the 20S CP gate, thus facilitating the degradation of unstructured proteins such as tau and Dnm1 in a ubiquitin- and ATP-independent manner. Furthermore, PA200 also participates in the degradation of acetylated histones. In our study, we use a combination of yeast and human cell systems to investigate the role of Blm10/PA200 in the degradation of N-terminal Huntingtin fragments (N-Htt). We demonstrate that the human PA200 binds to N-Htt. The loss of Blm10 in yeast or PA200 in human cells results in increased mutant N-Htt aggregate formation and elevated cellular toxicity. Furthermore, Blm10 in vitro accelerates the proteasomal degradation of soluble N-Htt. Collectively, our data suggest N-Htt as a new substrate for Blm10/PA200-proteasomes and point to new approaches in Huntington's disease (HD) research.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Biomolecules. - 10 : 11 (2020), p. 1-33. -
További szerzők:Yao, Yanhua Yang, Ciyu Kahlert, Günther Ghani, Marvi (1990-) (PhD hallgató) Király Nikolett (1992-) (molekuláris biológus, biokémikus) Boratkó Anita (1985-) (biokémikus, molekuláris biológus) Uray Karen (1964-) (biokémikus) Dittmar, Gunnar Tar Krisztina (1975-) (biokémikus, molekuláris biológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM092840
035-os BibID:(cikkazonosító)347 (WoS)000633434800001 (Scopus)85101254453
Első szerző:Bagoly Zsuzsa (orvos)
Cím:Incorporation of [alfa]2-Plasmin Inhibitor into Fibrin Clots and Its Association with the Clinical Outcome of Acute Ischemic Stroke Patients / Bagoly Zsuzsa, Baráth Barbara, Orbán-Kálmándi Rita, Szegedi István, Bogáti Réka, Sarkady Ferenc, Csiba László, Katona Éva
Dátum:2021
ISSN:2218-273X
Megjegyzések:Cross-linking of ?2-plasmin inhibitor (?2-PI) to fibrin by activated factor XIII (FXIIIa) is essential for the inhibition of fibrinolysis. Little is known about the factors modifying ?2-PI incorporation into the fibrin clot and whether the extent of incorporation has clinical consequences. Herein we calculated the extent of ?2-PI incorporation by measuring ?2-PI antigen levels from plasma and serum obtained after clotting the plasma by thrombin and Ca2+. The modifying effect of FXIII was studied by spiking of FXIII-A-deficient plasma with purified plasma FXIII. Fibrinogen, FXIII, ?2-PI incorporation, in vitro clot-lysis, soluble fibroblast activation protein and ?2-PI p.Arg6Trp polymorphism were measured from samples of 57 acute ischemic stroke patients obtained before thrombolysis and of 26 healthy controls. Increasing FXIII levels even at levels above the upper limit of normal increased ?2-PI incorporation into the fibrin clot. ?2-PI incorporation of controls and patients with good outcomes did not differ significantly (49.4 ? 4.6% vs. 47.4 ? 6.7%, p = 1.000), however it was significantly lower in patients suffering post-lysis intracranial hemorrhage (37.3 ? 14.0%, p = 0.004). In conclusion, increased FXIII levels resulted in elevated incorporation of ?2-PI into fibrin clots. In stroke patients undergoing intravenous thrombolysis treatment, ?2-PI incorporation shows an association with the outcome of therapy, particularly with thrombolysis-associated intracranial hemorrhage.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Biomolecules. - 11 : 3 (2021), p. 1-13. -
További szerzők:Baráth Barbara (1991-) (orvosírnok) Orbán-Kálmándi Rita Angéla (1993-) (klinikai laboratóriumi kutató) Szegedi István (1992-) (orvos) Kissné Bogáti Réka (1988-) (tudományos segédmunkatárs) Sarkady Ferenc (1982-) (laboratóriumi analitikus) Csiba László (1952-) (neurológus, pszichiáter) Katona Éva (1961-) (klinikai biokémikus)
Pályázati támogatás:GINOP-2.2.1-15-2017-00043
GINOP
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM113505
035-os BibID:(cikkazonosító)795 (wos)000995540500001 (scopus)85160380650
Első szerző:Balogh Gábor (gyógyszerész)
Cím:The Interaction of Factor Xa and IXa with Non-Activated Antithrombin in Michaelis Complex : Insights from Enhanced-Sampling Molecular Dynamics Simulations / Balogh Gábor, Bereczky Zsuzsanna
Dátum:2023
ISSN:2218-273X
Megjegyzések:The interaction between coagulation factors Xa and IXa and the activated state of their inhibitor, antithrombin (AT),have been investigated using X-ray diffraction studies. However, only mutagenesis data are available for non-activated AT. Our aim was to propose a model based on docking and advanced-sampling molecular dynamics simulations that can reveal the conformational behavior of the systems when AT is not binding a pentasaccharide. We built the initial structure for non-activated AT-FXa and AT-FIXa complexes using HADDOCK 2.4. The conformational behavior was studied using Gaussian accelerated molecular dynamics simulations. In addition to the docked complexes, two systems based on the X-ray structures were also simulated, with and without the ligand. The simulations revealed large variability in conformation for both factors. In the docking-based complex of AT-FIXa, conformations with stable Arg150?AT interactions can exist for longer time periods but the system also has a higher tendency for reaching states with very limited interaction with the "exosite" of AT. By comparing simulations with or without the pentasaccharide, we were able to gain insights into the effects of conformational activation on the Michaelis complexes. RMSF analysis and correlation calculations for the alpha-carbon atoms revealed important details of the allosteric mechanisms. Our simulations provide atomistic models for better understanding the conformational activation mechanism of AT against its target factors.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Biomolecules. - 13 : 5 (2023), p. 1-21. -
További szerzők:Bereczky Zsuzsanna (1974-) (orvosi laboratóriumi diagnosztika szakorvos)
Pályázati támogatás:OTKA-139293
OTKA
OTKA-106294
OTKA
OTKA-116228
OTKA
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM099490
035-os BibID:(WoS)000747614400001 (Scopus)85121503950 (cikkazonosító)19
Első szerző:Bencze János (orvos)
Cím:Comparison of Semi-Quantitative Scoring and Artificial Intelligence Aided Digital Image Analysis of Chromogenic Immunohistochemistry / János Bencze, Máté Szarka, Balázs Kóti, Woosung Seo, Tibor G. Hortobágyi, Viktor Bencs, László V. Módis, Tibor Hortobágyi
Dátum:2021
ISSN:2218-273X
Megjegyzések:Semi-quantitative scoring is a method that is widely used to estimate the quantity of proteins on chromogen-labelled immunohistochemical (IHC) tissue sections. However, it suffers from several disadvantages, including its lack of objectivity and the fact that it is a time-consuming process. Our aim was to test a recently established artificial intelligence (AI)-aided digital image analysis platform, Pathronus, and to compare it to conventional scoring by five observers on chromogenic IHC-stained slides belonging to three experimental groups. Because Pathronus operates on grayscale 0-255 values, we transformed the data to a seven-point scale for use by pathologists and scientists. The accuracy of these methods was evaluated by comparing statistical significance among groups with quantitative fluorescent IHC reference data on subsequent tissue sections. The pairwise inter-rater reliability of the scoring and converted Pathronus data varied from poor to moderate with Cohen's kappa, and overall agreement was poor within every experimental group using Fleiss' kappa. Only the original and converted that were obtained from Pathronus original were able to reproduce the statistical significance among the groups that were determined by the reference method. In this study, we present an AI-aided software that can identify cells of interest, differentiate among organelles, protein specific chromogenic labelling, and nuclear counterstaining after an initial training period, providing a feasible and more accurate alternative to semi-quantitative scoring.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Biomolecules. - 12 : 1 (2021), p. 1-14. -
További szerzők:Szarka Máté (1990-) Kóti Balázs Seo, Woosung Hortobágyi Tibor G. (1998-) (orvostanhallgató) Bencs Viktor (1995-) (orvos) Módis László V. (neurológus) Hortobágyi Tibor (1965-) (patológus)
Pályázati támogatás:EFOP-3.6.2-16-2017-00009
EFOP
ÚNKP-21-3
Egyéb
Nemzeti Agykutatási Program KTIA_13_NAP-A-II/7
Egyéb
NKFIH_SNN_132999
Egyéb
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM104120
035-os BibID:(cikkazonosító)1483 (WoS)000872311800001 (Scopus)85140443160
Első szerző:Czókolyová Mónika (molekuláris biológus)
Cím:Effects of One-Year Tofacitinib Therapy on Lipids and Adipokines in Association with Vascular Pathophysiology in Rheumatoid Arthritis / Monika Czókolyová, Attila Hamar, Anita Pusztai, Gábor Tajti, Edit Végh, Zsófia Pethő, Nóra Bodnár, Ágnes Horváth, Boglárka Soós, Szilvia Szamosi, Anita Szentpéteri, Ildikó Seres, Mariann Harangi, György Paragh, György Kerekes, Levente Bodoki, Andrea Domján, Katalin Hodosi, Tamás Seres, György Panyi, Zoltán Szekanecz, Gabriella Szűcs
Dátum:2022
ISSN:2218-273X
Megjegyzések:Background: Cardiovascular (CV) morbidity, mortality and metabolic syndrome are associated with rheumatoid arthritis (RA). A recent trial has suggested increased risk of major CV events (MACE) upon the Janus kinase (JAK) inhibitor tofacitinib compared with anti-tumor necrosis factor alpha (TNF-alpha) therapy. In our study, we evaluated lipids and other metabolic markers in relation to vascular function and clinical markers in RA patients undergoing one-year tofacitinib therapy. Patients and methods: Thirty RA patients treated with either 5 mg or 10 mg bid tofacitinib were included in a 12-month follow-up study. Various lipids, paraoxonase (PON1), myeloperoxidase (MPO), thrombospondin-1 (TSP-1) and adipokine levels, such as adiponectin, leptin, resistin, adipsin and chemerin were determined. In order to assess flow-mediated vasodilation (FMD), common carotid intima-media thickness (IMT) and arterial pulse-wave velocity (PWV) ultrasonography were performed. Assessments were carried out at baseline, and 6 and 12 months after initiating treatment. Results: One-year tofacitinib therapy significantly increased TC, HDL, LDL, APOA, APOB, leptin, adipsin and TSP-1, while significantly decreasing Lp(a), chemerin, PON1 and MPO levels. TG, lipid indices (TC/HDL and LDL/HDL), adiponectin and resistin showed no significant changes. Numerous associations were found between lipids, adipokines, clinical markers and IMT, FMD and PWV (p < 0.05). Regression analysis suggested, among others, association of BMI with CRP and PWV (p < 0.05). Adipokines variably correlated with age, BMI, CRP, CCP, FMD, IMT and PWV, while MPO, PON1 and TSP-1 variably correlated with age, disease duration, BMI, RF and PWV (p < 0.05). Conclusions: JAK inhibition by tofacitinib exerts balanced effects on lipids and other metabolic markers in RA. Various correlations may exist between metabolic, clinical parameters and vascular pathophysiology during tofacitinib treatment. Complex assessment of lipids, metabolic factors together with clinical parameters and vascular pathophysiology may be utilized in clinical practice to determine and monitor the CV status of patients in relation with clinical response to JAK inhibition.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Biomolecules. - 12 (2022), p. 1-22. -
További szerzők:Hamar Attila Béla (1990-) (általános orvos) Karancsiné Pusztai Anita (1989-) (tudományos segédmunkatárs) Tajti Gábor (1988-) (gyógyszerész, biofizikus, sejtbiológus) Végh Edit (1978-) (reumatológus, belgyógyász) Pethő Zsófia (1981-) (reumatológus, immunológus) Bodnár Nóra (1980-) (reumatológus) Horváth Ágnes (1985-) (reumatológus) Soós Boglárka (1988-) (általános orvos) Szamosi Szilvia (1975-) (belgyógyász, reumatológus) Szentpéteri Anita (1988-) (biológus) Seres Ildikó (1954-) (biokémikus) Harangi Mariann (1974-) (belgyógyász, endokrinológus) Paragh György (1953-) (belgyógyász) Kerekes György (1973-) (belgyógyász, kardiológus, angiológus) Bodoki Levente (1986-) (PhD hallgató) Domján Andrea (1979-) (reumatológus) Hódosi Katalin Seres Tamás Panyi György (1966-) (biofizikus) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Szűcs Gabriella (1963-) (belgyógyász, allergológus és klinikai immunológus, reumatológus)
Pályázati támogatás:4.2.4.A/2-11/1-2012-0001
TÁMOP
GINOP-2.3.2-15-2016-00050
GINOP
GINOP-2.3.2-15-2016-00015
GINOP
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

6.

001-es BibID:BIBFORM097590
035-os BibID:(WoS)000715101900001 (Scopus)85117088415
Első szerző:Czókolyová Mónika (molekuláris biológus)
Cím:Changes of Metabolic Biomarker Levels upon One-Year Anti-TNF-α Therapy in Rheumatoid Arthritis and Ankylosing Spondylitis : associations with Vascular Pathophysiology / Monika Czókolyová, Anita Pusztai, Edit Végh, Ágnes Horváth, Anita Szentpéteri, Attila Hamar, Szilvia Szamosi, Katalin Hodosi, Andrea Domján, Sándor Szántó, György Kerekes, Ildikó Seres, Mariann Harangi, György Paragh, Éva Szekanecz, Zoltán Szekanecz, Gabriella Szűcs
Dátum:2021
ISSN:2218-273X
Megjegyzések:Background: Cardiovascular (CV) morbidity, mortality, and metabolic syndrome are associated with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Here, lipids and other metabolic markers in relation to vascular function and clinical markers were evaluated in RA and AS patients undergoing one-year anti-TNF therapy. Patients and methods: Fifty-three patients including 36 RA patients treated with either etanercept (ETN) or certolizumab pegol (CZP) and 17 AS patients treated with ETN were included in a 12-month follow-up study. Various lipids, paraoxonase (PON) and arylesterase (ARE) activities, myeloperoxidase (MPO) and adipokine levels were determined overtime. Ultrasonography was performed to determine flow-mediated vasodilation (FMD), common carotid intima-media thickness (ccIMT), and arterial pulse-wave velocity (PWV) in all patients. All assessments were performed at baseline and 6 and 12 months after treatment initiation. Results: Anti-TNF therapy decreased ARE activity, MPO, adiponectin, and chemerin levels after 12 months (p < 0.05). Lipids, PON activity, and leptin remained unchanged. Regression analyses suggested variable associations of IMT, PWV, and FMD with ARE, MPO, leptin, and lipids (p < 0.05). On the other hand, these metabolic parameters were significantly associated with disease duration, CV history, CRP, obesity, PWV, and IMT (p < 0.05). One-year anti-TNF treatment together with baseline leptin (p = 0.039) or CRP (p = 0.016) levels determined 12 months of lipid changes overtime. TNF inhibition together with baseline disease activity determined ARE activity changes (p = 0.046). Anti TNF therapy and baseline chemerin levels determined IMT changes overtime (p = 0.003). Conclusions: Assessment of various metabolic parameters together with disease activity, CRP, and ultrasound based techniques may exert additional value in determining CV burden and in monitoring the effects of biologics on preclinical vascular pathophysiology.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
rheumatoid arthritis
ankylosing spondylitis
biologic therapy
metabolic biomarkers
lipids
adipokines
Megjelenés:Biomolecules. - 11 : 10 (2021), p. 1-15. -
További szerzők:Karancsiné Pusztai Anita (1989-) (tudományos segédmunkatárs) Végh Edit (1978-) (reumatológus, belgyógyász) Horváth Ágnes (1985-) (reumatológus) Szentpéteri Anita (1988-) (biológus) Hamar Attila Béla (1990-) (általános orvos) Szamosi Szilvia (1975-) (belgyógyász, reumatológus) Hódosi Katalin Domján Andrea (1979-) (reumatológus) Szántó Sándor (1968-) (belgyógyász, reumatológus) Kerekes György (1973-) (belgyógyász, kardiológus, angiológus) Seres Ildikó Harangi Mariann (1974-) (belgyógyász, endokrinológus) Paragh György (1953-) (belgyógyász) Szekanecz Éva (1968-) (onkológus szakorvos) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Szűcs Gabriella (1963-) (belgyógyász, allergológus és klinikai immunológus, reumatológus)
Pályázati támogatás:TÁMOP-4.2.4.A/2-11/1-2012-0001
TÁMOP
GINOP-2.3.2-15-2016-00050
GINOP
GINOP-2.3.2-15-2016-00005
GINOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

7.

001-es BibID:BIBFORM109052
035-os BibID:(cikkazonosító)401 (Scopus)85151113623 (WoS)000953989400001
Első szerző:Diószegi Ágnes (belgyógyász)
Cím:Role of Altered Metabolism of Triglyceride-Rich Lipoprotein Particles in the Development of Vascular Dysfunction in Systemic Lupus Erythematosus / Diószegi Ágnes, Lőrincz Hajnalka, Kaáli Eszter, Soltész Pál, Perge Bianka, Varga Éva, Harangi Mariann, Tarr Tünde
Dátum:2023
ISSN:2218-273X
Megjegyzések:Background: Impaired lipid metabolism contributes to accelerated inflammatory responses in addition to promoting the formation of atherosclerosis in systemic lupus erythematosus (SLE). We aimed to evaluate the lipid profile, inflammatory markers, and vascular diagnostic tests in active SLE patients to clarify the association between dyslipidemia and early vascular damage. Patients and Methods: 51 clinically active SLE patients and 41 age- and gender-matched control subjects were enrolled in the study. Lipoprotein subfractions were detected by Lipoprint. Brachial artery flow-mediated dilation and common carotid intima-media thickness were detected by ultrasonography. Arterial stiffness indicated by augmentation index (Aix) and pulse wave velocity was measured by arteriography. Results: We found significantly higher Aix, higher VLDL ratio, plasma triglyceride, ApoB100, and small HDL, as well as lower HDL-C, large HDL, and ApoA1 in patients with SLE. There was a significant positive correlation of Aix with triglyceride, VLDL, IDL-C, IDL-B, and LDL1. A backward stepwise multiple regression analysis showed IDL-C subfraction to be the best predictor of Aix. Conclusions: Our results indicate that in young patients with SLE, triglyceride-rich lipoproteins influence vascular function detected by Aix. These parameters may be assessed and integrated into the management plan for screening cardiovascular risk in patients with SLE.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
systemic lupus erythematosus
carotid intima-media thickness
augmentation index
flow-mediated dilation
triglyceride
very low-density lipoprotein
intermediate-density lipoprotein
triglyceride-rich lipoproteins
Megjelenés:Biomolecules. - 13 : 3 (2023), p. 1-13. -
További szerzők:Lőrincz Hajnalka (1986-) (biológus) Kaáli Eszter Soltész Pál (1961-) (belgyógyász, kardiológus) Perge Bianka Varga Éva (1982-) (belgyógyász) Harangi Mariann (1974-) (belgyógyász, endokrinológus) Tarr Tünde (1976-) (belgyógyász, allergológus és klinikai immunológus)
Pályázati támogatás:Tématerületi Kiválósági Program
Egyéb
K142273
NKFIH
TKP2021-EGA-18
Egyéb
TKP2021-EGA
Egyéb
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Intézményi repozitóriumban (DEA) tárolt változat
Borító:

8.

001-es BibID:BIBFORM107224
035-os BibID:(cikkazonosító)61 (WoS)000914513400001 (Scopus)85146601389
Első szerző:Gaál Zsuzsanna (csecsemő-és gyermekgyógyász központi gyakornok)
Cím:Targeted Epigenetic Interventions in Cancer with an Emphasis on Pediatric Malignancies / Gaál Zsuzsanna
Dátum:2023
ISSN:2218-273X
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Biomolecules. - 13 : 1 (2023), p. 1-25. -
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Intézményi repozitóriumban (DEA) tárolt változat
Borító:

9.

001-es BibID:BIBFORM099179
035-os BibID:(cikkazonosító)1531 (WoS)000714772300001 (Scopus)85117126323
Első szerző:Gaál Zsuzsanna (csecsemő-és gyermekgyógyász központi gyakornok)
Cím:MicroRNAs and Metabolism : revisiting the Warburg Effect with Emphasis on Epigenetic Background and Clinical Applications / Gaál Zsuzsanna
Dátum:2021
ISSN:2218-273X
Megjegyzések:Since the well-known hallmarks of cancer were described by Hanahan and Weinberg, fundamental advances of molecular genomic technologies resulted in the discovery of novel puzzle pieces in the multistep pathogenesis of cancer. MicroRNAs are involved in the altered epigenetic pattern and metabolic phenotype of malignantly transformed cells. They contribute to the initiation, progression and metastasis-formation of cancers, also interacting with oncogenes, tumor-suppressor genes and epigenetic modifiers. Metabolic reprogramming of cancer cells results from the dysregulation of a complex network, in which microRNAs are located at central hubs. MicroRNAs regulate the expression of several metabolic enzymes, including tumor-specific isoforms. Therefore, they have a direct impact on the levels of metabolites, also influencing epigenetic pattern due to the metabolite cofactors of chromatin modifiers. Targets of microRNAs include numerous epigenetic enzymes, such as sirtuins, which are key regulators of cellular metabolic homeostasis. A better understanding of reversible epigenetic and metabolic alterations opened up new horizons in the personalized treatment of cancer. MicroRNA expression levels can be utilized in differential diagnosis, prognosis stratification and prediction of chemoresistance. The therapeutic modulation of microRNA levels is an area of particular interest that provides a promising tool for restoring altered metabolism of cancer cells.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Biomolecules. - 11 : 10 (2021), p. 1-16. -
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

10.

001-es BibID:BIBFORM093898
035-os BibID:(cikkazonosító)544 (WoS)000642809000001 (Scopus)85103814901
Első szerző:Gindele Réka (molekuláris biológus)
Cím:Investigation of the Differences in Antithrombin to Heparin Binding among Antithrombin Budapest 3, Basel, and Padua Mutations by Biochemical and In Silico Methods / Gindele Réka, Pénzes-Daku Krisztina, Balogh Gábor, Kállai Judit, Bogáti Réka, Bécsi Bálint, Erdődi Ferenc, Katona Éva, Bereczky Zsuzsanna
Dátum:2021
ISSN:2218-273X
Megjegyzések:Antithrombin (AT) is a serine protease inhibitor, its activity is highly accelerated by heparin. Mutations at the heparin-binding region lead to functional defect, type II heparin-binding site (IIHBS) AT deficiency. The aim of this study was to investigate and compare the molecular background of AT Budapest 3 (p.Leu131Phe, ATBp3), AT Basel (p.Pro73Leu), and AT Padua (p.Arg79His) mutations. Advanced in silico methods and heparin-binding studies of recombinant AT proteins using surface plasmon resonance method were used. Crossed immunoelectrophoresis and Differential Scanning Fluorimetry (NanoDSF) were performed in plasma samples. Heparin affinity of AT Padua was the lowest (KD = 1.08 x 10(-6) M) and had the most severe consequences affecting the allosteric pathways of activation, moreover significant destabilizing effects on AT were also observed. KD values for AT Basel, ATBp3 and wild-type AT were 7.64 x 10(-7) M, 2.15 x 10(-8) M and 6.4 x 10(-10) M, respectively. Heparin-binding of AT Basel was slower, however once the complex was formed the mutation had only minor effect on the secondary and tertiary structures. Allosteric activation of ATBp3 was altered, moreover decreased thermostability in ATBp3 homozygous plasma and increased fluctuations in multiple regions of ATBp3 were observed by in silico methods suggesting the presence of a quantitative component in the pathogenicity of this mutation due to molecular instability.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Biomolecules. - 11 : 4 (2021), p. 1-18. -
További szerzők:Pénzes-Daku Krisztina (1978-) (biológus) Balogh Gábor (1991-) (gyógyszerész) Kállai Judit (1983-) (molekuláris biológus) Kissné Bogáti Réka (1988-) (tudományos segédmunkatárs) Bécsi Bálint (1981-) (vegyészmérnök) Erdődi Ferenc (1953-) (biokémikus) Katona Éva (1961-) (klinikai biokémikus) Bereczky Zsuzsanna (1974-) (orvosi laboratóriumi diagnosztika szakorvos)
Pályázati támogatás:GINOP-2.3.2-15-2016-00039
GINOP
GINOP-2.3.2-15-2016-00044
GINOP
GINOP-2.3.3-15-2016-00020
GINOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

11.

001-es BibID:BIBFORM086709
035-os BibID:(WoS)000557707400001 (Scopus)85087574382
Első szerző:Golda Mária (molekuláris biológus)
Cím:Biochemical characterization of human retroviral-like aspartic protease 1 (ASPRV1) / Mária Golda, János András Mótyán, Katalin Nagy, Krisztina Matúz, Tibor Nagy, József Tőzsér
Dátum:2020
ISSN:2218-273X
Megjegyzések:The human retroviral-like aspartic protease 1 (ASPRV1) is a mammalian retroviral-like enzyme that catalyzes a critical proteolytic step during epidermal differentiation; therefore, it is also referred as skin-specific aspartic protease (SASPase). Neutrophil granulocytes were also found recently to express ASPRV1 that is involved in the progression of acute chronic in?ammation in the central nervous system, especially in autoimmune encephalomyelitis. Thus, investigation of ASPRV1 is important due to its therapeutic or diagnostic potential. We investigated the structural characteristics of ASPRV1 by homology modeling; analysis of the proposed structure was used for interpretation of in vitro specificity studies. For in vitro characterization, activities of SASP28 and SASP14 enzyme forms were measured using synthetic oligopeptide substrates. We demonstrated that self-processing of SASP28 precursor causes autoactivation of the protease. Highest activity was measured for GST-SASP14 at neutral pH and at high ionic strength, and we proved that pepstatin A and acetyl-pepstatin can also inhibit the protease. In agreement with the structural characteristics, the relatively lower urea dissociation constant implied lower dimer stability of SASP14 compared to that of HIV-1 protease. The obtained structural and biochemical characteristics help better understanding of ASPRV1 function in skin and central nervous system
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
ASPRV1
SASPase
protease
retroviral-like protease
retroviral-like aspartic protease 1
skin-specific aspartic protease
homology modeling
protease inhibitor
Megjelenés:Biomolecules. - 10 : 7 (2020), p. 1-25. -
További szerzők:Mótyán János András (1981-) (biokémikus, molekuláris biológus) Nagy Katalin Matúz Krisztina (1980-) (vegyész, biokémikus) Nagy Tibor (1988-) (vegyész) Tőzsér József (1959-) (molekuláris biológus, biokémikus, vegyész)
Pályázati támogatás:GINOP-2.3.2-15-2016-00044
GINOP
TÁMOP 4.2.2.A-11/1/KONV-2012-0023
TÁMOP
TÁMOP-4.2.2.D-15/1/KONV-2015-0016
TÁMOP
GINOP-2.3.3-15-2016-00021
GINOP
NKFIH-1150-6/2019
Egyéb
K-101591
OTKA
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM099738
035-os BibID:(WoS)000748218100001 (Scopus)85122675323
Első szerző:Juhász Imre (belgyógyász)
Cím:Afamin Levels and Their Correlation with Oxidative and Lipid Parameters in Non-diabetic, Obese Patients / Imre Juhász, Szilvia Ujfalusi, Ildikó Seres, Hajnalka Lőrincz, Viktória Evelin Varga, György Paragh Jr., Sándor Somodi, Mariann Harangi, György Paragh
Dátum:2022
ISSN:2218-273X
Megjegyzések:Background: Afamin is a liver-produced bioactive protein and features α-and γ-tocopherol binding sites. Afamin levels are elevated in metabolic syndrome and obesity and correlate well with components of metabolic syndrome. Afamin concentrations, correlations between afamin and vitamin E, afamin and lipoprotein subfractions in non-diabetic, obese patients have not been fully examined. Methods: Fifty non-diabetic, morbidly obese patients and thirty-two healthy, normal-weight individuals were involved in our study. The afamin concentrations were measured by ELISA. Lipoprotein subfractions were determined with gel electrophoresis. Gas chromatography-mass spectrometry was used to measure α-and γ tocopherol levels. Results: Afamin concentrations were significantly higher in the obese patients compared to the healthy control (70.4 ± 12.8 vs. 47.6 ± 8.5 ?g/mL, p < 0.001). Positive correlations were found between afamin and fasting glucose, HbA1c, hsCRP, triglyceride, and oxidized LDL level, as well as the amount and ratio of small HDL subfractions. Negative correlations were observed between afamin and mean LDL size, as well as the amount and ratio of large HDL subfractions. After multiple regression analysis, HbA1c levels and small HDL turned out to be independent predictors of afamin. Conclusions: Afamin may be involved in the development of obesity-related oxidative stress via the development of insulin resistance and not by affecting alpha- and gamma-tocopherol levels.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Biomolecules. - 12 : 1 (2022), p. 1-11. -
További szerzők:Ujfalusi Szilvia (1990-) (belgyógyász) Seres Ildikó (1954-) (biokémikus) Lőrincz Hajnalka (1986-) (biológus) Varga Viktória Evelin (1988-) (biológus) Paragh György Jr. (1978-) (bőrgyógyász) Somodi Sándor (1977-) (belgyógyász) Harangi Mariann (1974-) (belgyógyász, endokrinológus) Paragh György (1953-) (belgyógyász)
Pályázati támogatás:NKFIH K115723
Egyéb
GINOP-2.3.2-15-2016-00005
GINOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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