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| Domain hiding | Altered binding specificity | Motif hiding | Composite binding site formation |
| Uncategorised | Rheostatic | Allostery | Avidity-sensing |
| Physicochemical compatibility | Pre-translational | Competition |
| Protein | Motif | Start | End | Switch description | Information |
Type: Binary Subtype: Physicochemical compatibility | |||||||
| PTM of a residue in a motif or in its flanking regions alters the physicochemical and/or structural compatibility of the motif with its binding partner. This can either induce or enhance an interaction, or result in inhibition or even abrogation of an interaction. | |||||||
| DPOD3_HUMAN | LIG_PCNA_PIPBox_1 | 456 | 465 | Phosphorylation of S458 in the PCNA-binding motif of DNA polymerase delta subunit 3 (POLD3) by cAMP subfamily reduces the affinity of binding to the Proliferating cell nuclear antigen (PCNA) and decreases the processivity of the polymerase complex. | |||
| CDN1A_HUMAN | LIG_PCNA_PIPBox_1 | 144 | 153 | Phosphorylation of T145 in the PCNA-binding motif of Cyclin-dependent kinase inhibitor 1 (CDKN1A) by RAC-alpha serine/threonine-protein kinase (AKT1) inhibits binding to Proliferating cell nuclear antigen (PCNA). As a result, Cyclin-dependent kinase inhibitor 1 (CDKN1A) no longer inhibits Proliferating cell nuclear antigen (PCNA) and blocking of DNA replication is relieved. | |||
| CDN1A_HUMAN | LIG_PCNA_PIPBox_1 | 144 | 153 | Phosphorylation of S146 in the PCNA-binding motif of Cyclin-dependent kinase inhibitor 1 (CDKN1A) by PKC subfamily inhibits binding to Proliferating cell nuclear antigen (PCNA). As a result, Cyclin-dependent kinase inhibitor 1 (CDKN1A) no longer inhibits Proliferating cell nuclear antigen (PCNA) and blocking of DNA replication is relieved. | |||
Type: Binary Subtype: Pre‑translational | |||||||
| Pre-translational mechanisms such as alternative splicing, alternative promoter-usage and/or RNA editing result in inclusion or removal of exons that contain an entire or partial motif. | |||||||
| ING1_HUMAN | LIG_PCNA_2 | 9 | 15 | Alternative splicing removes the PCNA-binding motif of Isoform Variant A of Inhibitor of growth protein 1 (ING1), abrogating binding to Proliferating cell nuclear antigen (PCNA). P33-ING1b (also known as Isoform Variant A of Inhibitor of growth protein 1 (ING1)) binds specially to PCNA, resulting in a major change in subcellular localisation and the import of this isoform into the nucleus. This is theorised to act by limiting access to the PCNA-binding domain but eventually it promotes apoptosis (though this may not be its physiological effect). | |||