37 resultados para Mandioca - Fisiologia


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Errebisio bibliografiko honen bitartez erresistentziaren entrenamendurako erabiltzen diren metodo nagusien eragin fisiologikoak ezagutu nahi dira.Lana metodo ezberdinen aurkezpen eta sailkapen batekin hasiko da. Gero metodo jarraien errendimenduko eraginak ikusiko dira, eragin fisiologikoekin batera. Berdina egingo da metodo interbalikoarekin eta sprint metodoarekin. Jarraian erresistentzia entrenamenduaren periodizaziorako modelo ezberdinak ikusiko dira, bakoitzak dituen onura eta arazoekin. Seinale molekularren funtzionamenduaren azalpen labur bat egingo da jarraian, egokitzapen prozesuekin duen lotura handia dela eta. Bukatzeko, lanaren ondorioa nagusiak eta bertatik ateratako gomendio praktikoak ere eskuragarri dituzue.

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E2F1 and E2F2 transcription factors have an important role during the regulation of cell cycle. In experiments done with E2F1/E2F2 knockout mice, it has been described that bone-marrow-derived macrophages (BMDM) undergo an early rapid proliferation event related to DNA hyper-replication. As a consequence, DNA damage response (DDR) pathway is triggered and E2F1/E2F2 knockout macrophages enter premature senescence related to G2/M phase arrest. The exact mechanism trough which DNA hyper-replication leads to DDR in absence of E2F1 and E2F2 remains undiscovered. To determine whether the ATR/ATM pathway, the master regulator of G2/M checkpoint, might be the surveillance mechanism in order to regulate uncontrolled proliferation in the DKO model, we monitored and analysis biochemical properties of BMDM cultures in the presence of caffeine, a potent inhibitor of ATM/ATR activity. Our results show that the addition of caffeine abolishes premature senescence in DKO BMDM, stimulates γ-H2AX accumulation and decreases Mcm2 expression.

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In this work we wanted to study the mechanism of E2F2-mediated repression. Our hypothesis is that E2F2 activates the expression of one or more E2F members of the “repressor” subset of the family through the E2F motifs present in their promoters, and those repressor E2F(s) would subsequently repress the target promoters. To address this hypothesis, we focused on E2F7. E2F7 is a repressor that lacks the Rb binding domain, and associates with DNA through E2F binding sites (de Bruin et al., 2003). Furthermore, E2F7 itself is also regulated by E2F motifs on its own promoter, and it has been shown to repress DNA metabolism and replication genes in late S-phase (de Bruin et al., 2003; Westendorp et al., 2012). E2F7, together with E2F8 has been found to form heterodimers, being critical on cell proliferation and development, and both seem to have similar functions (Li et al., 2008). Preliminary results from Zubiaga’s group have indicated that E2F2 activates E2F7 transcription in U2OS cells, suggesting that E2F2’s repressor function could be mediated by E2F7. For this purpose, we focused on studying E2F7’s role on the target genes previously known to be repressed by E2F2: Chk1 and Mcm5. The specific aims for this work were the following: - Confirm that E2F2 induces E2F7 in HEK-293T cells - Assess whether E2F7 acts as a transcriptional repressor on E2F sites - Evaluate the role of E2F7 on E2F2-mediated transcriptional repression of Chk1 and Mcm5.

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Curso Educación Emancipadora: Acción y Transformación en la Sociedad Global. Hegoa 2013-2014.

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308 p.