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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. | |||||||
| ACACA_HUMAN | LIG_BRCT_BRCA1_1 | 1262 | 1266 | Phosphorylation of S1263 in the BRCT-binding motif of Acetyl-CoA carboxylase 1 (ACACA) induces binding to the Breast cancer type 1 susceptibility protein (BRCA1) protein. | |||
| F175A_HUMAN | LIG_BRCT_BRCA1_1 | 405 | 409 | Phosphorylation of S406 in the BRCT-binding motif of BRCA1-A complex subunit Abraxas (FAM175A) induces binding to the Breast cancer type 1 susceptibility protein (BRCA1) protein. | |||
| ATRIP_HUMAN | LIG_BRCT_BRCA1_1 | 238 | 242 | Phosphorylation of S239 in the BRCT-binding motif of ATR-interacting protein (ATRIP) induces binding to the Breast cancer type 1 susceptibility protein (BRCA1) protein. | |||
| COM1_HUMAN | LIG_BRCT_BRCA1_1 | 326 | 330 | Phosphorylation of S327 in the BRCT-binding motif of DNA endonuclease RBBP8 (RBBP8) induces binding to the Breast cancer type 1 susceptibility protein (BRCA1) protein. | |||
| FANCJ_HUMAN | LIG_BRCT_BRCA1_1 | 989 | 993 | Phosphorylation of S990 in the BRCT-binding motif of Fanconi anemia group J protein (BRIP1) induces binding to the Breast cancer type 1 susceptibility protein (BRCA1) protein. | |||
| FANCJ_HUMAN | LIG_BRCT_BRCA1_2 | 989 | 995 | Phosphorylation of S990 in the BRCT-binding motif of Fanconi anemia group J protein (BRIP1) induces binding to the Breast cancer type 1 susceptibility protein (BRCA1) protein. | |||
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. | |||||||
| BRCA1_HUMAN | TRG_NLS_MonoExtN_4 | 501 | 508 | Alternative splicing removes the nuclear localisation signal (NLS) of Breast cancer type 1 susceptibility protein (BRCA1), abrogating binding to Importin subunit alpha-1 (KPNA1) and import into the nucleus. The study compared the full-length Brca1 splice variant (Isoform 1 of Breast cancer type 1 susceptibility protein (BRCA1)) to the Delta11b isoform (Isoform Delta11b of Breast cancer type 1 susceptibility protein (BRCA1)). The shorter isoform is missing exon 11b and differs in a number of ways. Firstly, it lacks an NLS and therefore has a cytoplasmic localisation. Also, when over-expressed, the Delta11b isoform was not toxic, suggesting nuclear localisation is important for Brca1's toxic behaviour. | |||