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. 2021 Jun 12;22:26–39. doi: 10.1016/j.omtm.2021.06.002

Table 1.

Altered biological pathways in immortalized erythroid cell lines compared to equivalent primary cells

Pathway name
Oncogene-Induced Senescence
Diseases of Cellular Response to Stress
Diseases of Cellular Senescence
Cellular Senescence
Evasion of Oxidative Stress-Induced Senescence Due to p16INK4A Defects
Evasion of Oncogene-Induced Senescence Due to p16INK4A Defects
Evasion of Oxidative Stress-Induced Senescence Due to Defective p16INK4A Binding to CDK4 and CDK6
Evasion of Oncogene-Induced Senescence Due to Defective p16INK4A Binding to CDK4 and CDK6
Oxidative Stress-Induced Senescence
Cyclin D-Associated Events in G1
G1 Phase
Evasion of Oxidative Stress Induced Senescence Due to Defective p16INK4A Binding to CDK4
Evasion of Oncogene-Induced Senescence Due to Defective p16INK4A Binding to CDK4
Aberrant Regulation of Mitotic G1/S Transition in Cancer Due to RB1 Defects
Defective Binding of RB1 Mutants to E2F1,(E2F2, E2F3)
Formation of Senescence-Associated Heterochromatin Foci (SAHF)
Apoptotic Execution Phase
Cellular Responses to External Stimuli
Mitotic G1 Phase and G1/S Transition
Diseases of Mitotic Cell Cycle

Pathways generated by input of proteins where abundance differed by ≥2-fold in all of the BEL-C, BEL-P, BEL-A, and BM cell line datasets into the Reactome Pathway Knowledgebase. The top 20 pathways with false discovery rate of Q < 0.05 are shown.