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Group by :Switch typeMotif classProteinEnzymePathway            Group Index    Colouring Info              Filtered: UNIPROT:Q969H0 (10 hits) x
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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

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Type: Binary Subtype: Physicochemical compatibilityType: Binary Subtype: Pre‑translationalType: Specificity Subtype: Altered binding specificity


ProteinMotifStartEndSwitch descriptionInformation

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.
LT_SV40DEG_SCF_FBW7_2699705Phosphorylation of T701 in the degron of Large T antigen induces binding to the F-box/WD repeat-containing protein 7 (FBXW7) protein, which recruits it to the SCF ubiquitin ligase complex where it is marked for degradation.
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NOTC1_HUMANDEG_SCF_FBW7_225082515Phosphorylation of T2511 in the degron of Neurogenic locus notch homolog protein 1 (NOTCH1) induces binding to the F-box/WD repeat-containing protein 7 (FBXW7) protein, which recruits it to the SCF ubiquitin ligase complex where it is marked for degradation.
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FBXW7_HUMANDOC_WW_Pin1_4202207Phosphorylation of T205 in the Pin1-binding motif of F-box/WD repeat-containing protein 7 (FBXW7) induces binding to the Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (PIN1) protein. Pin1 interacts with Fbw7 in a phoshorylation-dependent manner and promotes Fbw7 self-ubiquitination and protein degradation by disrupting Fbw7 dimerization. Paper also shows the over-expression of Pin1 suppresses the ability of Fbw7 to inhibit cell transformation and proliferation, suggesting a link between Pin1 overexpression and cancer.
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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.
FBXW7_HUMANTRG_NLS_MonoCore_21015Alternative splicing removes the nuclear localisation signal (NLS) of F-box/WD repeat-containing protein 7 (FBXW7), abrogating binding to Importin subunit alpha-1 (KPNA1). There are two other NLS motifs in the protein, meaning the isoform can still enter the nucleus.
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FBXW7_HUMANTRG_NES_CRM1_21926Alternative 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.
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Type: Specificity Subtype: Altered binding specificity
The balance of the competition for overlapping or adjacent, mutually exclusive interaction interfaces is tipped in favor of one of the interactors by PTM-dependent modulation of the intrinsic affinity of a binding region. Multiple, successive PTMs allow sequential switching of different binding partners in an ordered manner by step-wise alteration of binding specificity.
CCNE1_HUMANDEG_SCF_FBW7_1378384Phosphorylation of Isoform E-S of G1/S-specific cyclin-E1 (CCNE1) at S384 by CDK2 primes CCNE1 for phosphorylation by Glycogen synthase kinase-3 beta (GSK3B) at T380, which creates a recognition site for F box proteins of the SCF ubiquitin ligase complex (F-box/WD repeat-containing protein 7 (FBXW7)) that target CCNE1 for degradation.
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MYC_HUMANDEG_SCF_FBW7_15562Phosphorylation of Myc proto-oncogene protein (MYC) at S62 by Mitogen-activated protein kinase 1 (MAPK1) primes MYC for phosphorylation by Glycogen synthase kinase-3 beta (GSK3B), which targets MYC to the SCF ubiquitin ligase complex, F-box/WD repeat-containing protein 7 (FBXW7) that marks MYC for degradation.
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JUN_HUMANDEG_SCF_FBW7_1236243Transcription factor AP-1 (JUN) is primed by an unknown kinase for phosphorylation by Glycogen synthase kinase-3 beta (GSK3B), which targets JUN to the SCF ubiquitin ligase complex, F-box/WD repeat-containing protein 7 (FBXW7) that marks JUN for degradation. In v-Jun (Viral jun-transforming protein (JUN)) the residue corresponding to S243 is mutated to phenylalanine, which protects v-Jun (JUN) from degradation.
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CCNE1_HUMANDEG_SCF_FBW7_1393399Phosphorylation of G1/S-specific cyclin-E1 (CCNE1) at S399 generates a docking site for Glycogen synthase kinase-3 beta (GSK3B). Subsequent phosphorylation of CCNE1 by Glycogen synthase kinase-3 beta (GSK3B) at T395 switches the specificity of CCNE1 to the F-box/WD repeat-containing protein 7 (FBXW7), which recruits CCNE1 to the SCF ubiquitin ligase complex to mark CCNE1 for degradation.
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SRBP1_HUMANDEG_SCF_FBW7_1425430Phosphorylation of SREBP-1 (Sterol regulatory element-binding protein 1 (SREBF1)) at S430 generates a docking site for Glycogen synthase kinase-3 beta (GSK3B). Subsequent phosphorylation of SREBP-1 (SREBF1) by GSK3B at T426 switches the specificity of SREBP-1 (SREBF1) to the F-box/WD repeat-containing protein 7 (FBXW7), which recruits SREBP-1 (SREBF1) to the SCF ubiquitin ligase complex to mark SREBP-1 (SREBF1) for degradation.
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