Provisionen im Fussball

Der Spielervermittlungsbegriff wird vom Sportlermanagerbegriff differenziert. Der Begriff „Spielervermittlung“ umfasst die Vermittlung von Spielerkontrakten zwischen Fußballvereinen und Fußballspielern. Der Sportlermanagerbegriff tangiert Dienstleistungen der Privatsphäre. Der Arbeitsvermittlungsbegriff behandelt die Vermittlung von Arbeitskontrakten zwischen Arbeitnehmern und Arbeitgebern. Die Arbeit setzt sich mit der Frage der Zulässigkeit von Vermittlungsprovisionen im Rahmen der Arbeitsvermittlung auseinander. Es wird die Zulässigkeit des Prinzips der „unentgeltlichen Arbeitsvermittlung gegenüber Arbeitnehmern“ für den Fußballbereich an Hand der Erwerbsausübungsfreiheit und der Dienstleistungsfreiheit geprüft. Die Spielervermittlungsregulative knüpfen an die Ausübung der Spielervermittlungstätigkeit Voraussetzungen, wie Lizenzpflicht, Bankgarantie bzw Haftpflichtversicherung. Die Arbeit umfasst die Thematik, ob diese Voraussetzungen mit der österreichischen Erwerbsausübungsfreiheit, der Dienstleistungsfreiheit und dem Europäischen Wettbewerbsrecht vereinbar sind. Die Provision ist eine in Prozentsätzen formulierte Wertbeteiligung bzw konkrete Summe ohne prozentuellen Bezug (Fixbetrag) an den Verträgen des Dienstgebers für Vermittlung. Es wird die Entgeltform der Provision behandelt. Vor allem wird die Einordnung der Provision als „Erfolgslohn“, „Leistungslohn“ respektive „Mischform“ behandelt. Der Begriff der „Schlüsselkraft“ setzt einen Mindestlohn, eine bestimmte Qualifikation und nicht bloße Individualinteressen des Arbeitgebers voraus. Die Einordnung des Fußballspielers als Schlüsselkraft wird in der Arbeit dargestellt. Der Ausbildungskostenbegriff wird vom Einschulungskostenbegriff differenziert. Der Begriff der Ausbildungskosten setzt vor allem eine „erfolgreich absolvierte Ausbildung“ voraus. Es wird dargestellt wie diese Tatbestandsvoraussetzung zu verstehen ist und wie sie bei Fußballspielern gegeben sein kann. Der Sonderfall der Ausbildungskostenvereinbarung bei „mündig Minderjährigen“ wird analysiert. Das Gesetz fordert die Zustimmung des „gesetzlichen Vertreters“. Es wird die Problematik aufgeworfen wie diese Tatbestandsvoraussetzung zu verstehen ist und ob es auch der Genehmigung des Pflegschaftgerichtes bedarf

A DR4:tBID axis drives the p53 apoptotic response by promoting oligomerization of poised BAX

The cellular response to p53 activation varies greatly in a stimulus‐ and cell type‐specific manner. Dissecting the molecular mechanisms defining these cell fate choices will assist the development of effective p53‐based cancer therapies and also illuminate fundamental processes by which gene networks control cellular behaviour. Using an experimental system wherein stimulus‐specific p53 responses are elicited by non‐genotoxic versus genotoxic agents, we discovered a novel mechanism that determines whether cells undergo proliferation arrest or cell death. Strikingly, we observe that key mediators of cell‐cycle arrest (p21, 14‐3‐3σ) and apoptosis (PUMA, BAX) are equally activated regardless of outcome. In fact, arresting cells display strong translocation of PUMA and BAX to the mitochondria, yet fail to release cytochrome C or activate caspases. Surprisingly, the key differential events in apoptotic cells are p53‐dependent activation of the DR4 death receptor pathway, caspase 8‐mediated cleavage of BID, and BID‐dependent activation of poised BAX at the mitochondria. These results reveal a previously unappreciated role for DR4 and the extrinsic apoptotic pathway in cell fate choice following p53 activation.Fil: Henry, Ryan E. State University Of Colorado-boulder; Estados UnidosFil: Andrysik, Zdenek. State University Of Colorado-boulder; Estados UnidosFil: Paris, Ramiro. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Mar del Plata. Instituto de Investigaciones Biológicas; Argentina. Universidad Nacional de Mar del Plata. Facultad de Ciencias Exactas y Naturales. Instituto de Investigaciones Biológicas; Argentina. State University Of Colorado-boulder; Estados UnidosFil: Galbraith, Matthew D.. State University Of Colorado-boulder; Estados UnidosFil: Espinosa, Joaquín M.. State University Of Colorado-boulder; Estados Unido

po 077 identification of dhx30 as an inhibitor of the translation of pro apoptotic mrnas after p53 activation by nutlin

Introduction The transcription factor p53 can be efficiently activated by the small molecule Nutlin-3 without inducing genotoxic stress. Treatment of different cell lines with this small molecule can result in different phenotypes, ranging from cell cycle arrest to apoptosis. HCT116 (colon cancer-derived cells) and SJSA1 (osteosarcoma-derived cells) were used to model the opposite behaviour respectively, by analysing the transcriptional and translational responses after Nutlin-3 treatment. Material and methods Total and polysomal-bound mRNAs were collected and sequenced after 12 hour of 10 uM Nutlin-3 treatment. A bioinformatics analysis of the polysome-enriched mRNAs using Weeder allowed the identification of a 3'UTR motif ('CG-rich') which is enriched in the translationally upregulated genes of SJSA1. The effect of the motif on translation was evaluated after cloning its consensus sequence in the 3'UTR of the b-globin gene, which was put downstream the luciferase reporter. The activity of the construct was evaluated after 12 or 24 hours of Nutlin-3. The same consensus was used for a pull-down experiment followed by mass spectrometry to identify proteins interacting with it. Results and discussions RNA-seq data indicate that HCT116 and SJSA1, although sharing almost completely the transcriptional program lead by p53, show almost no overlap at a translation level. SJSA1 present different pro-apoptotic translationally-upregulated genes after Nutlin-3, which have one or more instances of a CG-rich motif in the 3'UTR. The impact of the motif is to enhance the activity of the luciferase reported when cloned in two copies flanking the 3'UTR of the b-globin gene, but only in SJSA1. A pull-down experiment using an RNA bait with the consensus motif was used to identify interactors, among which DHX30 was deeply studied. DHX30 silencing in HCT116 causes: 1) enhanced the activity of the reporter construct after Nutlin; 2) polysomal association of selected mRNAs containing the motif; 3) induction of apoptosis as assessed by Annexin-V staining. In addition, silencing of DHX30 in U2OS cells decreased their survival after Nutlin-3 treatment. Conclusion We show how a p53-dependent transcriptional program can be shaped at a translational level thanks to the action of a CG-rich motif which is enriched in the 3'UTR of some pro-apoptotic mRNAs and that can be bound by DHX30. This protein acts as a translational repressor of mRNAs containing the motif. The exact mechanism and the generalisation of the model are currently being investigated

The novel mouse Polo-like kinase 5 responds to DNA damage and localizes in the nucleolus

Polo-like kinases (Plk1-4) are emerging as an important class of proteins involved in many aspects of cell cycle regulation and response to DNA damage. Here, we report the cloning of a fifth member of the polo-like kinase family named Plk5. DNA and protein sequence analyses show that Plk5 shares more similarities with Plk2 and Plk3 than with Plk1 and Plk4. Consistent with this observation, we show that mouse Plk5 is a DNA damage inducible gene. Mouse Plk5 protein localizes predominantly to the nucleolus, and deletion of a putative nucleolus localization signal (NoLS) within its N-terminal moiety disrupts its nucleolar localization. Ectopic expression of Plk5 leads to cell cycle arrest in G1, decreased DNA synthesis, and to apoptosis, a characteristic it shares with Plk3. Interestingly, in contrast to mouse Plk5 gene, the sequence of human Plk5 contains a stop codon that produces a truncated protein lacking part of the kinase domain

Bekämpfung der Schwarzarbeit und illegaler Beschäftigung in Europa am Beispiel der Rechtsordnungen Österreichs, Deutschlands und Polens

nicht angegebe

A Genetic Screen Identifies TCF3/E2A and TRIAP1 as Pathway-Specific Regulators of the Cellular Response to p53 Activation

The p53 transcription factor participates in diverse cellular responses to stress, including cell-cycle arrest, apoptosis, senescence, and autophagy. The molecular mechanisms defining the ultimate outcome of p53 activation remain poorly characterized. We performed a genome-wide genetic screen in human cells to identify pathway-specific coregulators of the p53 target gene CDKN1A (p21), an inhibitor of cell-cycle progression, versus BBC3 (PUMA), a key mediator of apoptosis. Our screen identified numerous factors whose depletion creates an imbalance in the p21:PUMA ratio upon p53 activation. The transcription factor TCF3, also known as E2A, drives p21 expression while repressing PUMA across cancer cell types of multiple origins. Accordingly, TCF3/E2A depletion impairs the cell-cycle-arrest response and promotes apoptosis upon p53 activation by chemotherapeutic agents. In contrast, TRIAP1 is a specific repressor of p21 whose depletion slows down cell-cycle progression. Our results reveal strategies for driving cells toward specific p53-dependent responses