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001-es BibID:	BIBFORM069283
035-os BibID:	(Cikkazonosító)34280 (WOS)000385169900001 (Scopus)84990245095
Első szerző:	Dülk, Metta
Cím:	The scaffold protein Tks4 is required for the differentiation of mesenchymal stromal cells (MSCs) into adipogenic and osteogenic lineages / Dülk Metta, Kudlik Gyöngyi, Fekete Anna, Ernszt Dávid, Kvell Krisztián, Pongrácz Judit E., Merő Balázs L., Szeder Bálint, Radnai László, Geiszt Miklós, Csécsy Dalma E., Kovács Tamás, Uher Ferenc, Lányi Árpád, Vas Virag, Buday László
Dátum:	2016
ISSN:	2045-2322
Megjegyzések:	The protein product of the SH3PXD2B gene is known as Tks4 (tyrosine kinase substrate with 4 SH3 domains)6,a scaffold protein. Upon phosphorylation by Src kinase, it has the ability to interact with signaling molecules toregulate the actin cytoskeleton7. Tks4 was also shown to play an important role in the formation of podosomes8,production of reactive oxygen species (ROS) by tumor cells9, and also involved in EGFR signaling10,11. Althoughwe have some knowledge of the possible function of Tks4, the detailed mechanism of how Tks4 impacts FTHSaffected tissues is less clear.Mesenchymal stromal cells (MSCs) as multipotent adult stem cells are able to form multiple cell types ofmesenchymal origin, e.g. adipocytes and osteoblasts12,13, therefore it is tempting to speculate that Tks4 may affectosteogenesis and lipogenesis of MSCs. Moreover, there are some hints for the possible role of Tks4 in MSC biology.For example, membrane type-1 matrix metalloproteinase (MT1-MMP), which is a binding partner of Tks4,is known to play a role in MSCs differentiation and trafficking14. Moreover, it has been described that Tks4 isinvolved in ROS production and ROS modulates several signaling pathways regulating MSC differentiation15.Therefore, we hypothesized that Tks4 may play a role in the process necessary for MSC differentiation and oneof the underlying mechanisms causing the FTHS phenotype could be the impaired stem cell functions of Tks4deficient MSCs.Here we present a novel Tks4?/? mouse strain on C57Bl/6 background with the complete loss of Tks4 protein.The adult Tks4 deficient mice have reduced fat tissue mass and altered craniofacial and skeletal bones. Wecompared the phenotype and differentiation potential of BM-MSCs (bone marrow mesenchymal stromal cells)isolated from Tks4?/? and wild type mice. Our data demonstrate that in the absence of Tks4, adipogenic and osteogenicdifferentiation of BM-MSCs is impaired; therefore, we concluded that Tks4 is necessary for the adipogenicand osteogenic mesenchymal differentiation pathways.
Tárgyszavak:	Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Tks4 adipogenesis osteogenesis mesenchymal differentiation
Megjelenés:	Scientific Reports. - 6 : 1 (2016), p. 1-9. -
További szerzők:	Kudlik Gyöngyi Fekete Anna Ernszt Dávid Kvell Krisztián Pongrácz Judit Merő Balázs L. Szeder Bálint Radnai László Geiszt Miklós Csécsy Dalma E. Kovács Tamás (Budapest) Uher Ferenc Lányi Árpád (1962-) (biológus, immunológus) Vas Virág Buday László
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM082984
035-os BibID:	(Cikkazonosító)14363 (WOS)000489011600008 (Scopus)85073077992
Első szerző:	Méhes Előd
Cím:	Enhanced endothelial motility and multicellular sprouting is mediated by the scaffold protein TKS4 / Elod Mehes, Monika Barath, Marton Gulyas, Edina Bugyik, Miklos Geiszt, Arpad Szoor, Arpad Lanyi, Andras Czirok
Dátum:	2019
ISSN:	2045-2322
Megjegyzések:	Endothelial cell motility has fundamental role in vasculogenesis and angiogenesis during developmental or pathological processes. Tks4 is a scaffold protein known to organize the cytoskeleton of lamellipodia and podosomes, and thus modulating cell motility and invasion. In particular, Tks4 is required for the localization and activity of membrane type 1-matrix metalloproteinase, a key factor for extracellular matrix (ECM) cleavage during cell migration. While its role in transformed cells is well established, little is known about the function of Tks4 under physiological conditions. In this study we examined the impact of Tks4 gene silencing on the functional activity of primary human umbilical vein endothelial cells (HUVEC) and used time-lapse videomicrosopy and quantitative image analysis to characterize cell motility phenotypes in culture. We demonstrate that the absence of Tks4 in endothelial cells leads to impaired ECM cleavage and decreased motility within a 3-dimensional ECM environment. Furthermore, absence of Tks4 also decreases the ability of HUVEC cells to form multicellular sprouts, a key requirement for angiogenesis. To establish the involvement of Tks4 in vascular development in vivo, we show that loss of Tks4 leads sparser vasculature in the fetal chorion in the Tks4-deficient 'nee' mouse strain.
Tárgyszavak:	Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk endothelial motility Tks4 podosome endothel sprouting
Megjelenés:	Scientific Reports. - 9 : 1 (2019), p. 1-13. -
További szerzők:	Baráth Mónika (1980-) (Phd hallgató) Gulyás Márton Bugyik Edina Geiszt Miklós Szöőr Árpád (1984-) (orvos) Lányi Árpád (1962-) (biológus, immunológus) Czirok András
Pályázati támogatás:	OTKA-109444 OTKA GINOP-2.3.2-15-2016-00050
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM072832
035-os BibID:	(Cikkazonosító)1765 (WOS)000423430000013 (Scopus)85041329100
Első szerző:	Szabó Attila (molekuláris biológus, immunológus, filozófus)
Cím:	Immunomodulatory capacity of the serotonin receptor 5-HT2B in a subset of human dendritic cells / Szabo Attila, Gogolak Peter, Koncz Gabor, Foldvari Zsofia, Pazmandi Kitti, Miltner Noemi, Poliska Szilard, Bacsi Attila, Djurovic Srdjan, Rajnavolgyi Eva
Dátum:	2018
ISSN:	2045-2322
Megjegyzések:	Serotonin is a monoamine neurotransmitter that signals through a wide array of receptors (5-HT1-7) many of which are also involved in immune processes. Dendritic cells (DCs) are crucial players in immune defense by bridging innate and adaptive immune responses via their vast repertoire of pattern recognition receptors and antigen-presenting capability. Although serotonin is known to influence immunity at many levels, cell type-specific expression and function of its receptors remains poorly understood. Here we aimed to study 5-HT1-7 expression and function in CD1a- and CD1a+ human monocyte-derived DCs (moDCs). We found that the 5-HT2B receptor-subtype is solely expressed by the inflammatory CD1a+ moDC subset. Specific 5-HT2B activation potently inhibited TLR2, TLR3, and TLR7/8-induced proinflammatory cytokine and chemokine (TNF-?, IL-6, IL-8, IP-10, IL-12) but not type I interferon-? responses. 5-HT2B agonism also interfered with the polarization of CD1a+ moDC-primed CD4+ T cells towards inflammatory Th1 and Th17 effector lymphocytes. Here we report the subset-specific expression and immunomodulatory function of 5-HT2B in human moDCs. Our results expand the biological role of 5-HT2B which may act not only as a neurotransmitter receptor, but also as an important modulator of both innate and adaptive immune responses.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Scientific Reports. - 8 (2018), p. 1-12. -
További szerzők:	Gogolák Péter (1968-) (biológus, immunológus) Koncz Gábor (1970-) (biológus, immunológus) Földvári Zsófia Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus) Miltner Noémi (1990-) (molekuláris biológus) Póliska Szilárd (1978-) (biológus) Bácsi Attila (1967-) (immunológus) Djurovic, Srdjan Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00050 GINOP PEOPLE-2013-COFUND FP7
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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