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| Motif | Protein | Start | End | Switch Type | Switch Subtype | Switch description | Information | Evidence |
Calcium signaling pathway (KEGG - hsa04020) | ||||||||
| LIG_PDZ_Class_1 | AT2B4_HUMAN | 1236 | 1241 | Binary | Pre‑translational | Alternative splicing removes the PDZ-binding motif of Plasma membrane calcium-transporting ATPase 4 (ATP2B4), abrogating binding to Nitric oxide synthase, brain (NOS1). PMCA4b acts as a negative regulator of Nitric oxide synthase, brain (NOS1), reducing production of nitric oxide in heart tissue. This negative regulation was not dependent on a conformational change due to binding of the PDZ ligand, but on Ca2+ depletion in close proximity of the enzyme. Nitric oxide production by NOS1 is known to be important in the regulation of excitation-contraction (EC) coupling and subsequently contractility. | Inferred | |
Chemokine signaling pathway (KEGG - hsa04062) | ||||||||
| LIG_PDZ_Class_1 | PLCB1_HUMAN | 1211 | 1216 | Binary | Pre‑translational | Alternative splicing removes the PDZ-binding motif of 1-phosphatidylinositol 4,5-bisphosphate phosphodiesterase beta-1 (PLCB1), abrogating binding to Partitioning defective 3 homolog (PARD3). The G protein-activated PLCB1 can directly interact with cell polarity proteins Partitioning defective 3 homolog (PARD3) and Partitioning defective 6 homolog alpha (PARD6A) to form protein complexes in the cell, which potentially modulate G protein-activated PLCB1 activity in cell polarity formation and asymmetric cell division. | Inferred | |
Glutamatergic synapse (KEGG - hsa04724) | ||||||||
| LIG_PDZ_Class_1 | NMDZ1_HUMAN | 917 | 922 | Binary | Pre‑translational | Alternative splicing removes the PDZ-binding motif of Isoform 4 of Glutamate [NMDA] receptor subunit zeta-1 (GRIN1), abrogating binding to Disks large homolog 4 (DLG4). Binding of the PDZ domain of DLG4 suppresses an ER-retention motif in GRIN1, promoting its cell surface expression in a splice variant-specific manner. | Inferred | |
| LIG_PDZ_Class_1 | NMDZ1_HUMAN | 917 | 922 | Specificity | Motif hiding | Binding of the PDZ domain of Disks large homolog 4 (DLG4) suppresses the ER-retention motif of Isoform 4 of Glutamate receptor subunit zeta-1 (GRIN1) in a splice variant-specific manner, thereby promoting cell surface expression of this particular isoform. This supports the hypothesis that local regulation of receptor exit from neuronal ER plays a role in modifying discrete synaptic receptor number. | Inferred | |
| LIG_PDZ_Class_1 | NMDZ1_HUMAN | 917 | 922 | Binary | Pre‑translational | Alternative splicing removes the PDZ-binding motif of Isoform 4 of Glutamate [NMDA] receptor subunit zeta-1 (GRIN1), abrogating binding to Disks large homolog 4 (DLG4). Binding of the PDZ domain of DLG4 suppresses an ER-retention motif in GRIN1, promoting its cell surface expression in a splice variant-specific manner. | Inferred | |
| LIG_PDZ_Class_1 | NMDZ1_HUMAN | 917 | 922 | Specificity | Motif hiding | Binding of the PDZ domain of Disks large homolog 4 (DLG4) suppresses the ER-retention motif of Isoform 4 of Glutamate receptor subunit zeta-1 (GRIN1) in a splice variant-specific manner, thereby promoting cell surface expression of this particular isoform. This supports the hypothesis that local regulation of receptor exit from neuronal ER plays a role in modifying discrete synaptic receptor number. | Inferred | |
| LIG_PDZ_Class_1 | NMDZ1_HUMAN | 917 | 922 | Binary | Pre‑translational | Alternative splicing removes the PDZ-binding motif of Isoform 4 of Glutamate [NMDA] receptor subunit zeta-1 (GRIN1), abrogating binding to Disks large homolog 4 (DLG4). Binding of the PDZ domain of DLG4 suppresses an ER-retention motif in GRIN1, promoting its cell surface expression in a splice variant-specific manner. | Inferred | |
| LIG_PDZ_Class_1 | NMDZ1_HUMAN | 917 | 922 | Specificity | Motif hiding | Binding of the PDZ domain of Disks large homolog 4 (DLG4) suppresses the ER-retention motif of Isoform 4 of Glutamate receptor subunit zeta-1 (GRIN1) in a splice variant-specific manner, thereby promoting cell surface expression of this particular isoform. This supports the hypothesis that local regulation of receptor exit from neuronal ER plays a role in modifying discrete synaptic receptor number. | Inferred | |
Salivary secretion (KEGG - hsa04970) | ||||||||
| LIG_PDZ_Class_1 | AT2B4_HUMAN | 1236 | 1241 | Binary | Pre‑translational | Alternative splicing removes the PDZ-binding motif of Plasma membrane calcium-transporting ATPase 4 (ATP2B4), abrogating binding to Nitric oxide synthase, brain (NOS1). PMCA4b acts as a negative regulator of Nitric oxide synthase, brain (NOS1), reducing production of nitric oxide in heart tissue. This negative regulation was not dependent on a conformational change due to binding of the PDZ ligand, but on Ca2+ depletion in close proximity of the enzyme. Nitric oxide production by NOS1 is known to be important in the regulation of excitation-contraction (EC) coupling and subsequently contractility. | Inferred | |