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001-es BibID:BIBFORM036713
Első szerző:Bögel Gábor
Cím:Frank-ter Haar syndrome protein Tks4 regulates EGF-dependent cell migration / Gábor Böge, Annamária Gujdár, Miklós Geiszt, Árpád Lányi, Anna Fekete, Szabolcs Sipeki, Julian Downward, László Buday
Dátum:2012
ISSN:0021-9258
Megjegyzések:Mutations in the SH3PXD2B gene coding for the Tks4 protein are responsible for the autosomal-recessive Frank-ter Haar syndrome. Tks4, a substrate of Src tyrosine kinase is implicated in the regulation of podosome formation. Here, we report a novel role for Tks4 in the EGF signalling pathway. In EGF-treated cells, Tks4 is tyrosine phosphorylated and associated with the activated EGF receptor. This association is not direct but requires the presence of Src tyrosine kinase. In addition, treatment of cells with LY294002, an inhibitor of PI 3-kinase, or mutations of the PX domain reduces tyrosine phosphorylation and membrane translocation of Tks4. Furthermore, a PX domain mutant (R43W) Tks4 carrying a reported point mutation in a Frank-ter Haar syndrome patient showed aberrant intracellular expression and reduced phosphoinositide binding. Finally, silencing of Tks4 was shown to markedly inhibit HeLa cell migration in a Boyden chamber assay in response to EGF or serum. Our results therefore reveal a new function for Tks4 in the regulation of growth factor-dependent cell migration.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
EGF receptor
Tks4
cell migration
Frank-ter Haar syndrome
PX domain
Molekuláris Medicina
Megjelenés:Journal Of Biological Chemistry. - 287 : 37 (2012), p. 31321-31329. -
További szerzők:Gujdár Annamária Geiszt Miklós Lányi Árpád (1962-) (biológus, immunológus) Fekete Anna Sipeki Szabolcs Downward, Julian Buday László
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A HOFI/SH3PXD2B aktin citoszkeletont szabályozó új adaptor fehérje funkcionális vizsgálata
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

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
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM028890
Első szerző:Lányi Árpád (biológus, immunológus)
Cím:The homolog of the five SH3-domain protein (HOFI/SH3PXD2B) regulates lamellipodia formation and cell spreading / Lányi Á., Baráth M., Péterfi Z., Bogel G., Orient A., Simon T., Petrovszki E., Kis-Tóth K., Sirokmány G., Rajnavölgyi É., Terhorst C., Buday L., Geiszt M.
Dátum:2011
ISSN:1932-6203
Megjegyzések:Motility of normal and transformed cells within and across tissues requires specialized subcellular structures, e. g. membrane ruffles, lamellipodia and podosomes, which are generated by dynamic rearrangements of the actin cytoskeleton. Because the formation of these sub-cellular structures is complex and relatively poorly understood, we evaluated the role of the adapter protein SH3PXD2B [HOFI, fad49, Tks4], which plays a role in the development of the eye, skeleton and adipose tissue. Surprisingly, we find that SH3PXD2B is requisite for the development of EGF-induced membrane ruffles and lamellipodia, as well as for efficient cellular attachment and spreading of HeLa cells. Furthermore, SH3PXD2B is present in a complex with the non-receptor protein tyrosine kinase Src, phosphorylated by Src, which is consistent with SH3PXD2B accumulating in Src-induced podosomes. Furthermore, SH3PXD2B closely follows the subcellular relocalization of cortactin to Src-induced podosomes, EGF-induced membrane ruffles and lamellipodia. Because SH3PXD2B also forms a complex with the C-terminal region of cortactin, we propose that SH3PXD2B is a scaffold protein that plays a key role in regulating the actin cytoskeleton via Src and cortactin.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
lamellipodia, podosome
scaffold protein
Megjelenés:PLoS One. - 6 : 8 (2011), p. e23653. -
További szerzők:Baráth Mónika Péterfi Zalán Bogel Gábor Orient Anna Simon Tünde (1984-) (biokémikus, molekuláris biológus) Petrovszki Enikő Kis-Tóth Katalin (1975-) (immunológus) Sirokmány Gábor Rajnavölgyi Éva (1950-) (immunológus) Terhorst, Cox Buday László Geiszt Miklós
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Molekuláris immunológia
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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