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WNK3 encodes a protein belonging to the 'with no lysine' family of serine-threonine protein kinases. Additionally we are shipping WNK3 Antibodies (68) and and many more products for this protein.
Data show that WNK lysine deficient protein kinase 3 protein (WNK3) interacts with NCC (show SLC12A3 ELISA Kits) and increases the Na-Cl cotransporter (NCC (show SLC12A3 ELISA Kits)) expression on the cell membrane and in cytoplasm together.
WNK3 enhances NCC (show SLC12A3 ELISA Kits) protein expression by increasing NCC (show SLC12A3 ELISA Kits) synthesis via an ERK 1 (show MAPK3 ELISA Kits)/2-dependent signaling pathway
WNK3 knockout mice exhibited significantly decreased infarct volume in a transgenic model of stroke and brain damage.
There may be a novel role for WNK3 on the renal Na+-Cl-cotransporter (NCC (show SLC12A3 ELISA Kits)) expression at the plasma membrane, an effect apparently independent of the SPAK (show STK39 ELISA Kits) kinase and the aldosterone-SGK1 (show SGK1 ELISA Kits) pathway.
LINGO-1 potentiates neuronal apoptosis, likely by inhibiting WNK3 kinase activity.
WNK3 modulates intracellular Cl(-) concentration and regulatory volume decrease in HEK293 cells.
The Wnk3 protein isoforms have a similar effect on SLC12 cotransporters. NKCC1 (show SLC12A2 ELISA Kits)/2 and NCC (show SLC12A3 ELISA Kits) were inhibited, even in hypertonicity, while KCCs were activated, even in isotonic conditions.
Analysis of the data showed that WNK3 is an essential regulator of NKCC1 (show SLC12A2 ELISA Kits) and that WNK3 activates NKCC1 (show SLC12A2 ELISA Kits)-mediated ion transport necessary for cell volume changes associated with cell invasion.
OXSR1 (show OXSR1 ELISA Kits) and WNK3 transcripts were substantially overexpressed in subjects with schizophrenia relative to comparison subjects.
Data find that expression of the N termini of all four WNKs results in modest to strong activation of SGK1 (show SGK1 ELISA Kits).
WNK3 knockout mice show faster neurological functional recovery after occlusion of the left middle cerebral artery.
angiotensin II activates the WNK-SPAK (show STK39 ELISA Kits)-NKCC1 (show SLC12A2 ELISA Kits) phosphorylation cascade through the angiotensin II type 1 receptor (show AGTR1 ELISA Kits). activation of the WNK-SPAK (show STK39 ELISA Kits)-NKCC1 (show SLC12A2 ELISA Kits) phosphorylation cascade induced by a low-salt diet and angiotensin II is dependent on WNK3.
WNK3 may serve as a member of a kinase network that facilitates the fine-tuning of renal transepithelial NaCl transport.
WNK3 increases the cytoplasmic localization of Fox-1 (show A2BP1 ELISA Kits), thereby suppressing Fox-1 (show A2BP1 ELISA Kits)-dependent mrna splicing.
suggest that WNK3 is part of the Cl(-)/volume-sensing mechanism necessary for the maintenance of cell volume during osmotic stress and the dynamic modulation of GABA neurotransmission
effects of WNK3 on these transporters and their coexpression in renal epithelia implicate WNK3 in NaCl, water, and blood pressure homeostasis, perhaps via signaling downstream of vasopressin (show AVP ELISA Kits)
WNK3 is likely a component of one of the mechanisms that determines the balance between renal NaCl reabsorption and K+ secretion.
This gene encodes a protein belonging to the 'with no lysine' family of serine-threonine protein kinases. These family members lack the catalytic lysine in subdomain II, and instead have a conserved lysine in subdomain I. This family member functions as a positive regulator of the transcellular Ca2+ transport pathway, and it plays a role in the increase of cell survival in a caspase-3-dependent pathway. Alternative splicing results in multiple transcript variants.
, WNK lysine deficient protein kinase 3
, protein kinase with no lysine 3
, serine/threonine-protein kinase WNK3
, WNK lysine deficient protein kinase 3, pseudogene
, protein kinase lysine-deficient 3