human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: The molecular mechanism mediating expression of senescent cell antigen-aggregated or cleaved band 3 and externalized phosphatidylserine ( PS ) on the surface of aged erythrocytes and their premature expression in certain anemias is not completely elucidated . The erythrocytes with these surface modifications undergo macrophage-mediated phagocytosis . In this study , the role of protein kinase C ( PKC ) isoforms in the expression of these surface modifications was investigated . Inhibition of PKC Î± by 30âÎ¼M rottlerin ( R30 ) and 2.3ânM Gï¿½ 6976 caused expression of both the senescent cell marker-externalized PS measured by FACS analysis and aggregated band 3 detected by western blotting . In contrast to this observation , but in keeping with literature , PKC activation by phorbol-12-myristate-13-acetate ( PMA ) also led to the expression of senescence markers . We explain this antithesis by demonstrating that PMA-treated cells show reduction in the activity of PKC Î± , thereby simulating inhibition . The reduction in PKC Î± activity may be attributed to the known downregulation of PMA-activated PKC Î± , caused by its membrane translocation and proteolysis . We demonstrate membrane translocation of PKC Î± in PMA-treated cells to substantiate this inference . Thus loss of PKC Î± activity either by inhibition or downregulation can cause surface modifications which can trigger erythrophagocytosis .
    OUTPUT:

agent
enabling replicative immortality
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: The molecular mechanism mediating expression of senescent cell antigen-aggregated or cleaved band 3 and externalized phosphatidylserine ( PS ) on the surface of aged erythrocytes and their premature expression in certain anemias is not completely elucidated . The erythrocytes with these surface modifications undergo macrophage-mediated phagocytosis . In this study , the role of protein kinase C ( PKC ) isoforms in the expression of these surface modifications was investigated . Inhibition of PKC Î± by 30âÎ¼M rottlerin ( R30 ) and 2.3ânM Gï¿½ 6976 caused expression of both the senescent cell marker-externalized PS measured by FACS analysis and aggregated band 3 detected by western blotting . In contrast to this observation , but in keeping with literature , PKC activation by phorbol-12-myristate-13-acetate ( PMA ) also led to the expression of senescence markers . We explain this antithesis by demonstrating that PMA-treated cells show reduction in the activity of PKC Î± , thereby simulating inhibition . The reduction in PKC Î± activity may be attributed to the known downregulation of PMA-activated PKC Î± , caused by its membrane translocation and proteolysis . We demonstrate membrane translocation of PKC Î± in PMA-treated cells to substantiate this inference . Thus loss of PKC Î± activity either by inhibition or downregulation can cause surface modifications which can trigger erythrophagocytosis .
    OUTPUT:
