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FXYD domain containing ion transport regulator 2

This gene encodes a member of the FXYD family of transmembrane proteins. This particular protein encodes the sodium/potassium-transporting ATPase subunit gamma. Mutations in this gene have been associated with Renal Hypomagnesemia-2. Alternatively spliced transcript variants have been described. Read-through transcripts have been observed between this locus and the upstream FXYD domain-containing ion transport regulator 6 (FXYD6, GeneID 53826) locus.[provided by RefSeq, Feb 2011] (from NCBI)
Top mentioned proteins: ATPase, Phospholamban, CAN, Alpha-1, HAD
Papers on FXYD2
The organic osmolyte betaine induces keratin 2 expression in rat epidermal keratinocytes - A genome-wide study in UVB irradiated organotypic 3D cultures.
Pasonen-Seppänen et al., Kuopio, Finland. In Toxicol In Vitro, Jan 2016
Expression of Egr1, a transcription factor, and Purkinje cell protein 4, a regulator of Ca(2+)/calmodulin metabolism, also increased, while downregulated genes included several ion-channel components, such as Fxyd2.
Functional Studies of Na(+),K(+)-ATPase Using Transfected Cell Cultures.
Sweadner et al., Boston, United States. In Methods Mol Biol, Dec 2015
Renal Na,K-ATPase is tightly bound to a small single-span membrane protein, the γ subunit, or FXYD2.
Development of a peptide-functionalized imaging nanoprobe for the targeting of (FXYD2)γa as a highly specific biomarker of pancreatic beta cells.
Muller et al., Mons, Belgium. In Contrast Media Mol Imaging, Sep 2015
Our work describes a phage display-derived peptide (P88) that is highly specific to (FXYD2)γa expressed by human beta cells and is proposed as a molecular vector for the development of functionalized imaging probes.
Recurrent FXYD2 p.Gly41Arg mutation in patients with isolated dominant hypomagnesaemia.
Knoers et al., Nijmegen, Netherlands. In Nephrol Dial Transplant, Jun 2015
In 2000, mutations in FXYD2, encoding the γ-subunit of the Na(+)-K(+)-ATPase, were identified to cause isolated dominant hypomagnesaemia (IDH) in a large Dutch family suffering from hypomagnesaemia, hypocalciuria and chondrocalcinosis.
FXYD2, a γ subunit of Na⁺, K⁺-ATPase, maintains persistent mechanical allodynia induced by inflammation.
Zhang et al., Shanghai, China. In Cell Res, Mar 2015
Nociceptive afferent neurons express not only the α and β subunits of NKA but also the γ subunit FXYD2.
Structure of the Na,K-ATPase regulatory protein FXYD2b in micelles: implications for membrane-water interfacial arginines.
Marassi et al., Los Angeles, United States. In Biochim Biophys Acta, 2015
FXYD2 is a membrane protein responsible for regulating the function of the Na,K-ATPase in mammalian kidney epithelial cells.
Paradoxical activation of the sodium chloride cotransporter (NCC) without hypertension in kidney deficient in a regulatory subunit of Na,K-ATPase, FXYD2.
Sweadner et al., Boston, United States. In Physiol Rep, 2015
In kidney FXYD2 is the most abundant: it is an inhibitory subunit expressed in almost every nephron segment.
Mutations in PCBD1 cause hypomagnesemia and renal magnesium wasting.
Bindels et al., Nijmegen, Netherlands. In J Am Soc Nephrol, 2014
Overexpression in a human kidney cell line showed that wild-type PCBD1 binds HNF1B to costimulate the FXYD2 promoter, the activity of which is instrumental in Mg(2+) reabsorption in the DCT.
Tissue-specific expression and in vivo regulation of zebrafish orthologues of mammalian genes related to symptomatic hypomagnesemia.
Hoenderop et al., Nijmegen, Netherlands. In Pflugers Arch, 2013
In humans, mutations related to hypomagnesemia are located in the genes TRPM6 and CNNM2, encoding for a Mg(2+) channel and transporter, respectively; EGF (epidermal growth factor); SLC12A3, which encodes for the Na(+)-Cl(-) co-transporter NCC; KCNA1 and KCNJ10, encoding for the K(+) channels Kv1.1 and Kir4.1, respectively; and FXYD2, which encodes for the γ-subunit of the Na(+),K(+)-ATPase.
Identification of a crab gill FXYD2 protein and regulation of crab microsomal Na,K-ATPase activity by mammalian FXYD2 peptide.
Fontes et al., Brazil. In Biochim Biophys Acta, 2012
findings confirm the presence of an FXYD2 peptide in the crab gill Na,K-ATPase and demonstrate that this peptide plays an important role in regulating enzyme activity
Regulation of the Na,K-ATPase gamma-subunit FXYD2 by Runx1 and Ret signaling in normal and injured non-peptidergic nociceptive sensory neurons.
Carroll et al., Montpellier, France. In Plos One, 2011
The transcription factor Runx1 controls FXYD2 expression during the maturation of the somato-sensory system, partly through regulation of the tyrosine kinase receptor Ret.
Post-transcriptional control of Na,K-ATPase activity and cell growth by a splice variant of FXYD2 protein with modified mRNA.
Arystarkhova et al., Boston, United States. In J Biol Chem, 2011
Post-transcriptional control of Na,K-ATPase activity and cell growth by a splice variant of FXYD2 protein with modified mRNA.
HNF-1B specifically regulates the transcription of the γa-subunit of the Na+/K+-ATPase.
Bindels et al., Nijmegen, Netherlands. In Biochem Biophys Res Commun, 2011
wild type HNF1B specifically induces FXYD2A transcription whereas all HNF1B mutants partially prevented it.
A genomic-based approach identifies FXYD domain containing ion transport regulator 2 (FXYD2)gammaa as a pancreatic beta cell-specific biomarker.
Eizirik et al., Brussels, Belgium. In Diabetologia, 2010
Datab propose human FXYD2gammaa as a novel beta cell-specific biomarker.
Hereditary tubular transport disorders: implications for renal handling of Ca2+ and Mg2+.
Bindels et al., Nijmegen, Netherlands. In Clin Sci (lond), 2010
In the distal convolutions, several proteins involved in Mg2+ transport have been identified [TRPM6 (transient receptor potential melastatin 6), proEGF (pro-epidermal growth factor) and FXYD2 (Na+/K+-ATPase gamma-subunit)].
[FXYD proteins: novel regulators of Na,K-ATPase].
Geering et al., Lausanne, Switzerland. In Med Sci (paris), 2006
Recent evidence suggests that 6 out of 7 FXYD proteins, FXYD1 (phospholemman), FXYD2 (gamma subunit of Na,K-ATPase), FXYD3 (Mat-8), FXYD4 (CHIF), FXYD5 (Ric) and FXYD7 associate with Na,K-ATPase and modulate its transport properties e.g. its Na+ and/or its K+ affinity in a distinct way.
FXYD proteins: new regulators of Na-K-ATPase.
Geering, Lausanne, Switzerland. In Am J Physiol Renal Physiol, 2006
Recent experimental evidence suggests that at least five of the seven members of this family, FXYD1 (phospholemman), FXYD2 (gamma-subunit of Na-K-ATPase), FXYD3 (Mat-8), FXYD4 (CHIF), and FXYD7, are auxiliary subunits of Na-K-ATPase and regulate Na-K-ATPase activity in a tissue- and isoform-specific way.
Function of FXYD proteins, regulators of Na, K-ATPase.
Geering, Lausanne, Switzerland. In J Bioenerg Biomembr, 2005
FXYD2 or gamma subunit and FXYD4 or CHIF modulate the apparent affinity for Na(+) of Na, K-ATPase in an opposite way, adapted to the physiological needs of Na(+) reabsorption in different segments of the renal tubule.
Splice variants of the gamma subunit (FXYD2) and their significance in regulation of the Na, K-ATPase in kidney.
Sweadner et al., Boston, United States. In J Bioenerg Biomembr, 2005
At least six members of the family have been shown to associate with the Na, K-ATPase in a cell- and tissue-specific manner, while four of them, namely the gamma subunit (FXYD2), CHIF (FXYD4), phospholemman (FXYD1), and dysadherin (FXYD5) have been identified in kidney.
Dominant isolated renal magnesium loss is caused by misrouting of the Na(+),K(+)-ATPase gamma-subunit.
Knoers et al., Nijmegen, Netherlands. In Nat Genet, 2000
We identified a putative dominant-negative mutation in the gene encoding the Na(+), K(+)-ATPase gamma-subunit (FXYD2), leading to defective routing of the protein in a family with dominant renal hypomagnesaemia.
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