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WNK lysine deficient protein kinase 2

WNK2, mitogen-activated protein kinase kinase
The protein encoded by this gene is a cytoplasmic serine-threonine kinase that contains cysteine in place of the lysine found at the conserved ATP-binding location in subdomain II of protein kinases. Since this protein does have kinase activity, it is possible that another lysine in the kinase subdomain I can substitute for the missing conserved lysine. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ERK, V1a, MAPK, AP-1, Akt
Papers on WNK2
QTL mapping of temperature sensitivity reveals candidate genes for thermal adaptation and growth morphology in the plant pathogenic fungus Zymoseptoria tritici.
McDonald et al., Zürich, Switzerland. In Heredity (edinb), Feb 2016
One QTL had a logarithm of odds score >11 and contained only six candidate genes, including PBS2, encoding a mitogen-activated protein kinase kinase associated with low temperature tolerance in Saccharomyces cerevisiae.
MEK/ERK pathway activation by insulin receptor isoform alteration is associated with the abnormal proliferation and differentiation of intestinal epithelial cells in diabetic mice.
Chen et al., Guangzhou, China. In Mol Cell Biochem, Feb 2016
The insulin receptor (IR) and its downstream mitogen-activated protein kinase kinase (MAPKK also known as MEK)/extracellular-regulated protein kinase (ERK) pathway is a classic pathway associated with cell proliferation and differentiation.
Regulator of G-Protein Signaling 10 Negatively Regulates Cardiac Remodeling by Blocking Mitogen-Activated Protein Kinase-Extracellular Signal-Regulated Protein Kinase 1/2 Signaling.
Yuan et al., Changsha, China. In Hypertension, Jan 2016
Mechanistically, cardiac remodeling improvement elicited by RGS10 was associated with the abrogation of mitogen-activated protein kinase kinase 1/2-extracellular signal-regulated protein kinase 1/2 signaling.
Kv1.3 potassium channel mediates macrophage migration in atherosclerosis by regulating ERK activity.
Wang et al., Jinan, China. In Arch Biochem Biophys, Jan 2016
U-0126, the mitogen-activated protein kinase kinase inhibitors, could reverse macrophage migration induced by Kv1.3 channel overexpression.
Overexpression of miR-199a-5p decreases esophageal cancer cell proliferation through repression of mitogen-activated protein kinase kinase kinase-11 (MAP3K11).
Donahue et al., Baltimore, United States. In Oncotarget, Jan 2016
MiR-199a-5p is predicted to bind mitogen-activated protein kinase kinase kinase 11 (MAP3K11) mRNA with high affinity.
Poly(I:C) increases the expression of mPGES-1 and COX-2 in rat primary microglia.
Fiebich et al., Belo Horizonte, Brazil. In J Neuroinflammation, Dec 2015
Protein levels of COX-2 and mPGES-1 were reduced by SB203580, SP600125, and SC514 (p38 mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK), and IκB kinase (IKK) inhibitors, respectively), as well as by PD98059 and PD0325901 (mitogen-activated protein kinase kinase (MEK) inhibitors).
Ocular Toxicity in Metastatic Melanoma Patients Treated With Mitogen-Activated Protein Kinase Kinase Inhibitors: A Case Series.
Guida et al., Bari, Italy. In Am J Ophthalmol, Nov 2015
PURPOSE: To report the clinical features and management of mitogen-activated protein kinase kinase inhibitor-associated ocular side effects in 4 patients with advanced melanoma and a review of literature.
The Far Side of Vascular Injury: Nonconventional Vasoconstrictors, DNA-targeting Agents, and Agents Toxic to Vascular Smooth Muscle.
Guionaud, Cambridge, United Kingdom. In Toxicol Pathol, Oct 2015
Anticancer drugs, immunosuppressants, and heavy metals are targeting primarily ECs while allylamine, β-aminopropionitrile, and mitogen-activated protein kinase kinase inhibitors affect mainly SMCs.
Low-grade epithelial ovarian cancer: a number of distinct clinical entities?
Gourley et al., Edinburgh, United Kingdom. In Curr Opin Oncol, Sep 2015
A prospective study of the mitogen-activated protein kinase kinase inhibitor selumetinib (response rate 15%) and retrospective bevacizumab studies suggest that these may be more effective approaches.Limited retrospective clinical data and even more sparse molecular data suggest that similar distinctions may exist between low-grade endometrioid and mucinous ovarian cancers and their respective high-grade counterparts, but more research is required in order to clarify the biological differences and the implications that these have for management.
Long-term survival as a treatment benchmark in melanoma: latest results and clinical implications.
Margolin et al., Salt Lake City, United States. In Ther Adv Med Oncol, May 2015
Fortunately, since the approval by the US Food and Drug Administration of agents targeting the cytotoxic T lymphocyte antigen-4 (CTLA-4) receptor, as well as those targeting B-raf and mitogen-activated protein kinase kinase (MEK) in the mitogen-activated protein kinase (MAPK) pathway for patients whose melanoma is 'driven' by a BRAF mutation, long-term survival of stage IV melanoma is increasing substantially.
Ptpn11 deletion in a novel progenitor causes metachondromatosis by inducing hedgehog signalling.
Neel et al., Providence, United States. In Nature, 2013
Shp2-deficient chondroprogenitors had decreased fibroblast growth factor-evoked ERK activation and enhanced Ihh and Pthrp expression, whereas fibroblast growth factor receptor (FGFR) or mitogen-activated protein kinase kinase (MEK) inhibitor treatment of chondroid cells increased Ihh and Pthrp expression.
Oncogenic NRAS signaling differentially regulates survival and proliferation in melanoma.
Chin et al., Boston, United States. In Nat Med, 2012
Here, leveraging an inducible mouse model of NRAS-mutant melanoma, we show that pharmacological inhibition of mitogen-activated protein kinase kinase (MEK) activates apoptosis but not cell-cycle arrest, which is in contrast to complete genetic neuroblastoma RAS homolog (NRAS) extinction, which triggers both of these effects.
Profiling of residual breast cancers after neoadjuvant chemotherapy identifies DUSP4 deficiency as a mechanism of drug resistance.
Arteaga et al., Nashville, United States. In Nat Med, 2012
Finally, inhibition of mitogen-activated protein kinase kinase (MEK) synergized with docetaxel treatment in BLBC xenografts.
Control of nonapoptotic developmental cell death in Caenorhabditis elegans by a polyglutamine-repeat protein.
Shaham et al., New York City, United States. In Science, 2012
pqn-41 expression is controlled by the mitogen-activated protein kinase kinase SEK-1, which functions in parallel to the zinc-finger protein LIN-29 to promote cellular demise.
A MEK-independent role for CRAF in mitosis and tumor progression.
Cheresh et al., San Diego, United States. In Nat Med, 2011
The role of RAF in cell proliferation has been linked to its ability to activate mitogen-activated protein kinase kinase 1 (MEK) and mitogen-activated protein kinase 1 (ERK).
WNK2 kinase is a novel regulator of essential neuronal cation-chloride cotransporters.
Lifton et al., New Haven, United States. In J Biol Chem, 2011
a role for WNK2 in the regulation of CCCs in the mammalian brain, with implications for both cell volume regulation and/or GABAergic signaling.
Epigenetic silencing of the kinase tumor suppressor WNK2 is tumor-type and tumor-grade specific.
Costello et al., San Francisco, United States. In Neuro Oncol, 2009
Epigenetic silencing of the kinase tumor suppressor WNK2 is tumor-type and tumor-grade specific.
WNK2 modulates MEK1 activity through the Rho GTPase pathway.
Jordan et al., Lisbon, Portugal. In Cell Signal, 2008
WNK2 controls a RhoA-mediated cross-talk mechanism that regulates the efficiency with which MEK1 can activate ERK1/2 upon growth factor stimulation.
Protein kinase WNK2 inhibits cell proliferation by negatively modulating the activation of MEK1/ERK1/2.
Jordan et al., Lisbon, Portugal. In Oncogene, 2007
WNK2 is involved in the modulation of growth factor-induced cancer cell proliferation through the MEK1/ERK1/2 pathway.
Epigenome scans and cancer genome sequencing converge on WNK2, a kinase-independent suppressor of cell growth.
Costello et al., San Francisco, United States. In Proc Natl Acad Sci U S A, 2007
epigenetic silencing, occasional deletion and point mutation, and functional assessment suggest that aberrations of WNK2 may contribute to unregulated tumor cell growth
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