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| Untersuchte Arbeit: Seite: 80, Zeilen: 8-11 |
Quelle: Wouters et al 2007 Seite(n): 693, Zeilen: left col. 2-10 |
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Figure 26: Overview of the influence of hypoxia on the cell in culture (adopted by (Wouters et al. 2007) Abbreviations: ASK-1, apoptosis signal-regulating kinase 1; ERK, extracellular signal–regulated kinase; HIF-1, hypoxia inducible factor 1; IAP-2, inhibitor of apoptosis protein 2; JNK, c-Jun N-terminal kinase; MAPK, mitogen-activated protein kinase; PI3K, phosphatidylinositol 3-kinase; ROS, reactive oxygen species Hypoxia mediates a striking effect on cell cycle progression (Amellem and Pettersen 1991;Amellem et al. 1998) revealed that mammalian cells in general tend to accumulate in the G1 phase of the cell cycle during prolonged hypoxia. It has been reported that this accumulation results from three processes: [(a) retinoblastoma protein (pRb)- mediated cell cycle arrest in mid-G1; (b) activation of an oxygen-sensitive restriction point in late G1, close to the G1/S border; and (c) inhibition of DNA replication.] Amellem O, Pettersen EO (1991) The role of protein accumulation on the kinetics of entry into S phase following extreme hypoxia. Anticancer Res 11:1083-1087 Amellem O, Sandvik JA, Stokke T, Pettersen EO (1998) The retinoblastoma protein-associated cell cycle arrest in S-phase under moderate hypoxia is disrupted in cells expressing HPV18 E7 oncoprotein. Br J Cancer 77:862-872 Wouters A, Pauwels B, Lardon F, Vermorken JB (2007) Review: implications of in vitro research on the effect of radiotherapy and chemotherapy under hypoxic conditions. Oncologist 12:690-712 |
Figure 1. Overview of the influence of hypoxia on the cell in culture. Abbreviations: ASK-1, apoptosis signal-regulating kinase 1; ERK, extracellular signal–regulated kinase; HIF-1, hypoxia inducible factor 1; IAP-2, inhibitor of apoptosis protein 2; JNK, c-Jun N-terminal kinase; MAPK, mitogen-activated protein kinase; PI3K, phosphatidylinositol 3-kinase; ROS, reactive oxygen species. As mentioned above, exposure to hypoxia mediates a striking effect on cell cycle progression. Amellem et al. [43, 44] revealed that mammalian cells in general tend to accumulate in the G1 phase of the cell cycle during prolonged hypoxia. It has been reported that this accumulation results from three processes: (a) retinoblastoma protein (pRb)- mediated cell cycle arrest in mid-G1; (b) activation of an oxygen- sensitive restriction point in late G1, close to the G1/S border; and (c) inhibition of DNA replication. 43 Amellem O, Pettersen E. Cell inactivation and cell cycle inhibition as induced by extreme hypoxia: The possible role of cell cycle arrest as a protection against hypoxia-induced lethal damage. Cell Prolif 1991;24:127–141. 44 Amellem O, Sandvik JA, Stokke T et al. The retinoblastoma protein-associated cell cycle arrest in S-phase under moderate hypoxia is disrupted in cells expressing HPV18 E7 oncoprotein. Br J Cancer 1998;77:862– 872. |
From the final chapter of Iam's thesis ("Discussion"): Nothing has been marked as a citation, though the texts and the list of the references are identical. The source is mentioned in the legend to the accompanying figure 26. |
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