Cell cycle | G1/S DNA Damage Checkpoints | Neurotrophin signaling pathway |
PI3K-Akt signaling pathway | Wnt signaling pathway | p53 signaling pathway |
p53-Dependent G1/S DNA damage checkpoint |
Motif | Protein | Start | End | Switch Type | Switch Subtype | Switch description | Information | Evidence |
Cell cycle (KEGG - hsa04110) | ||||||||
MOD_GSK3_1 | P53_HUMAN | 30 | 37 | Binary | Physicochemical compatibility | Phosphorylation of Cellular tumor antigen p53 (TP53) at S37 primes the protein for phosphorylation at S33 by Glycogen synthase kinase-3 beta (GSK3B). | Inferred | |
DEG_MDM2_1 | P53_HUMAN | 19 | 26 | Binary | Physicochemical compatibility | Phosphorylation of Cellular tumor antigen p53 (TP53) on T18 (in vitro by Casein kinase I subfamily, requiring prior phosphorylation of S15) inhibits its binding to E3 ubiquitin-protein ligase Mdm2 (MDM2). In vivo, T18 is phosphorylated in response to DNA damage. | Curated | |
LIG_TAZ2 | P53_HUMAN | 19 | 25 | Cumulative | Rheostatic | Multisite phosphorylation of S15 and T18 and S20 and S33 and S37 and S46 in the TAD region of Cellular tumor antigen p53 (TP53) additively enhances its affinity for CREB-binding protein (CREBBP). | Curated | |
DEG_MDM2_1 | P53_HUMAN | 19 | 26 | Binary | Pre‑translational | Alternative promoter usage and alternative splicing removes the E3 ubiquitin ligase MDM2-binding motif of Cellular tumor antigen p53 (TP53), abrogating binding to E3 ubiquitin-protein ligase Mdm2 (MDM2). The splice variant without this motif is resistant to MDM2-mediated degradation, leading to a longer half-life. | Curated | |
G1/S DNA Damage Checkpoints (Reactome - 69615) | ||||||||
LIG_TAZ2 | P53_HUMAN | 19 | 25 | Cumulative | Rheostatic | Multisite phosphorylation of S15 and T18 and S20 and S33 and S37 and S46 in the TAD region of Cellular tumor antigen p53 (TP53) additively enhances its affinity for CREB-binding protein (CREBBP). | Curated | |
Neurotrophin signaling pathway (KEGG - hsa04722) | ||||||||
MOD_GSK3_1 | P53_HUMAN | 30 | 37 | Binary | Physicochemical compatibility | Phosphorylation of Cellular tumor antigen p53 (TP53) at S37 primes the protein for phosphorylation at S33 by Glycogen synthase kinase-3 beta (GSK3B). | Inferred | |
PI3K-Akt signaling pathway (KEGG - hsa04151) | ||||||||
MOD_GSK3_1 | P53_HUMAN | 30 | 37 | Binary | Physicochemical compatibility | Phosphorylation of Cellular tumor antigen p53 (TP53) at S37 primes the protein for phosphorylation at S33 by Glycogen synthase kinase-3 beta (GSK3B). | Inferred | |
Wnt signaling pathway (KEGG - hsa04310) | ||||||||
MOD_GSK3_1 | P53_HUMAN | 30 | 37 | Binary | Physicochemical compatibility | Phosphorylation of Cellular tumor antigen p53 (TP53) at S37 primes the protein for phosphorylation at S33 by Glycogen synthase kinase-3 beta (GSK3B). | Inferred | |
p53 signaling pathway (KEGG - hsa04115) | ||||||||
DEG_MDM2_1 | P53_HUMAN | 19 | 26 | Binary | Physicochemical compatibility | Phosphorylation of Cellular tumor antigen p53 (TP53) on T18 (in vitro by Casein kinase I subfamily, requiring prior phosphorylation of S15) inhibits its binding to E3 ubiquitin-protein ligase Mdm2 (MDM2). In vivo, T18 is phosphorylated in response to DNA damage. | Curated | |
DEG_MDM2_1 | P53_HUMAN | 19 | 26 | Binary | Pre‑translational | Alternative promoter usage and alternative splicing removes the E3 ubiquitin ligase MDM2-binding motif of Cellular tumor antigen p53 (TP53), abrogating binding to E3 ubiquitin-protein ligase Mdm2 (MDM2). The splice variant without this motif is resistant to MDM2-mediated degradation, leading to a longer half-life. | Curated | |
p53-Dependent G1/S DNA damage checkpoint (Reactome - 69580) | ||||||||
DEG_MDM2_1 | P53_HUMAN | 19 | 26 | Binary | Physicochemical compatibility | Phosphorylation of Cellular tumor antigen p53 (TP53) on T18 (in vitro by Casein kinase I subfamily, requiring prior phosphorylation of S15) inhibits its binding to E3 ubiquitin-protein ligase Mdm2 (MDM2). In vivo, T18 is phosphorylated in response to DNA damage. | Curated | |
DEG_MDM2_1 | P53_HUMAN | 19 | 26 | Binary | Pre‑translational | Alternative promoter usage and alternative splicing removes the E3 ubiquitin ligase MDM2-binding motif of Cellular tumor antigen p53 (TP53), abrogating binding to E3 ubiquitin-protein ligase Mdm2 (MDM2). The splice variant without this motif is resistant to MDM2-mediated degradation, leading to a longer half-life. | Curated |