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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. | |||||||
| MPIP3_HUMAN | TRG_NES_CRM1_1 | 189 | 203 | Phosphorylation of S198 in the NES of M-phase inducer phosphatase 3 (CDC25C) by Serine/threonine-protein kinase PLK1 (PLK1) inhibits binding to Exportin-1 (XPO1), thus promoting nuclear localization of M-phase inducer phosphatase 3 (CDC25C). | |||
| ACE2_YEAST | TRG_NES | 122 | 150 | Phosphorylation of S137 in the NES of Metallothionein expression activator (ACE2) inhibits binding to Exportin-1 (CRM1). Phosphorylation of S137, and to a lesser extent S122, by Cbk1 directly antagonizes the interaction of Ace2 with nuclear export machinery. | |||
| ACE2_YEAST | TRG_NES | 122 | 150 | Phosphorylation of S122 in the NES of Metallothionein expression activator (ACE2) inhibits binding to Exportin-1 (CRM1). Phosphorylation of S137, and to a lesser extent S122, by Cbk1 directly antagonizes the interaction of Ace2 with nuclear export machinery. | |||
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. | |||||||
| P53_HUMAN | TRG_NES_CRM1_1 | 339 | 352 | Alternative splicing removes the nuclear export signal (NES) of Cellular tumor antigen p53 (TP53), abrogating binding to Exportin-1 (XPO1) and export from the nucleus. | |||
| FBXW7_HUMAN | TRG_NES_CRM1_2 | 19 | 26 | Alternative splicing removes the nuclear export signal (NES) of Isoform Archipelago beta of F-box/WD repeat-containing protein 7 (FBXW7), abrogating binding to Exportin-1 (XPO1) and export from nucleus. The presence of the NES produces an isoform with a cytoplasmic localisation. The two other isoforms of FBXW7 localise to the nucleus and the nucleolus, respectively. | |||
| SMAD4_HUMAN | TRG_NES_CRM1_2 | 142 | 149 | Alternative splicing removes the nuclear export signal (NES) motif of Mothers against decapentaplegic homolog 4 (SMAD4), thereby inhibiting binding to Exportin-1 (XPO1) and export from the nucleus. A splice variant lacking the NES does not shuttle back and forth between nucleus and cytosol. At present, this particular splice variant is not annotated in UniProtKB. | |||
| PML_HUMAN | TRG_NES_CRM1_1 | 702 | 716 | Alternative splicing removes the nuclear export signal (NES) of Protein PML (PML), abrogating binding to Exportin-1 (XPO1) and export from the nucleus. | |||
| MDM2_HUMAN | TRG_NES_CRM1_2 | 190 | 202 | Alternative splicing removes the nuclear export signal (NES) of E3 ubiquitin-protein ligase Mdm2 (MDM2), abrogating binding to Exportin-1 (XPO1). | |||
| CTND1_HUMAN | TRG_NES_CRM1_1 | 942 | 956 | Alternative splicing removes the nuclear export signal (NES) of Catenin delta-1 (CTNND1), abrogating binding to Exportin-1 (XPO1). Despite demonstration of the importance of the NES for removing Catenin delta-1 (CTNND1) from the nucleus, those isoforms without NES are rarely found in the nucleus. | |||
| NF2L1_HUMAN | TRG_NES_CRM1_2 | 251 | 259 | Alternative splicing removes the nuclear export signal (NES) of Nuclear factor erythroid 2-related factor 1 (NFE2L1), abrogating binding to Exportin-1 (XPO1). Only the full-length variant of NFE2L1 (Isoform 1 of Nuclear factor erythroid 2-related factor 1 (NFE2L1)) contains an NES and shows cytoplasmic localisation. The two other naturally occuring isoforms (of which at present only 1 is annotated in UniProtKB) lack the NES and show exclusive nuclear staining. | |||