Редактирование: WNK1

Serine/threonine-protein kinase WNK1 (EC 2.7.11.1) (Erythrocyte 65 kDa protein) (p65) (Kinase deficient protein) (Protein kinase lysine-deficient 1) (Protein kinase with no lysine 1) (hWNK1) [HSN2] [KDP] [KIAA0344] [PRKWNK1]

==Publications==

{{medline-entry
|title=Overexpression of [[WNK1]] in [[POMC]]-expressing neurons reduces weigh gain via [[WNK4]]-mediated degradation of Kir6.2.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29392534
|abstract="With no lysine" (WNK) kinases have been shown to regulate various ion transporters in various tissues, but studies on the function of WNK kinases in the brain have been limited. In this study, we discovered that [[WNK1]] and [[WNK4]] in [[POMC]]-expressing neuronal cells in [[WNK1]] overexpressed transgenic mice ([[WNK1]] [[TG]]) decrease appetite via degradation of Kir6.2. Weight gain after 20 weeks of age was delayed in [[WNK1]] [[TG]] mice as a result of reduced food intake. Expression of [[WNK1]] and proopiomelanocortin ([[POMC]]) was higher in [[POMC]]-expressing neurons in the hypothalamus of [[WNK1]] [[TG]] mice than in WT mice. Immunostaining of serial sections of the hypothalamus revealed that [[POMC]]-expressing neurons were smaller in [[WNK1]] [[TG]] mice than in WT mice. In addition, expression of Kir6.2 was significantly reduced in [[WNK1]] [[TG]] mice. Overexpression and knockdown of [[WNK4]] demonstrated that [[WNK4]] regulates protein expression of Kir6.2 via protein-protein interaction. Accordingly, reduced age-dependent weight gain of [[WNK1]] [[TG]] mice seems to be related with the decreased Kir6.2 expression via [[WNK1]]- and [[WNK4]]-regulated protein stability of Kir6.2.
|mesh-terms=* Aging
* Animals
* Gene Expression Regulation
* HEK293 Cells
* Humans
* Hypothalamus
* KATP Channels
* Mice
* Mice, Transgenic
* Neurons
* Pro-Opiomelanocortin
* Protein Stability
* Protein-Serine-Threonine Kinases
* Proteolysis
* Rats
* WNK Lysine-Deficient Protein Kinase 1
|keywords=* Appetite
* Kir6.2
* POMC-expressing neuron
* Protein degradation
* Transgenic mice
* WNK1
* WNK4
|full-text-url=https://sci-hub.do/10.1007/s11010-018-3301-4
}}