Human With No Lysine Kinase 3 (WNK3)
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TEP details
Summary
Kinases WNK1-4 regulate cation-chloride cotransporters via phosphorylation of SPAK and OSR1 and thereby control salt homeostasis, cell volume and blood pressure. Gain of function mutations in WNK kinases are found in Gordon’s hypertension syndrome suggesting the WNK pathway as a therapeutic target. WNK3 inhibition in particular has also been shown to reduce cerebral injury after Ischemic stroke. Here we present assays and crystal structures that define (i) the molecular basis for disease mutations; (ii) the multiple functional domains of WNK kinases and their protein interactions; (iii) the binding of small molecule kinase inhibitors and a potential allosteric pocket.
Structures
Structures available in TEP:
- WNK1 CCT2 domain (PDB:5G3Q ): protein, ligand
- WNK2 CCT1 domain (PDB:6ELM ): protein, ligand
- WNK2 CCT1 domain + RFXV-containing peptide (PDB:6FKB ): protein, ligand
- WNK3 degron peptide + KLHL3 kelch domain (PDB:5NKP ): protein, ligand
- WNK4 degron peptide + KLHL2 kelch domain (PDB:4CHB ): protein, ligand
- WNK4 degron peptide + KLHL3 kelch domain (PDB:4CH9 ): protein, ligand
- WNK3 kinase monophosphorylated apo (PDB:5O23 ): protein, ligand
- WNK3 kinase A-loop exchange (PDB:5O1V ): protein, ligand
- WNK3 kinase + inhibitory Cl- ion (PDB:5O21 ): protein, ligand
- WNK3 kinase diphosphorylated + AMP-PNP (PDB:5O26 ): protein, ligand
- WNK3 kinase + PP121 inhibitor (PDB:5O2B ): protein, ligand
- WNK3 kinase-CCT1 fusion (PDB:5O2C ): protein, ligand