| The FXYD1 protein plays a protective role against pulmonary hypertension and arterial remodeling via redox and inflammatory mechanisms. | The FXYD1 protein plays a protective role against pulmonary hypertension and arterial remodeling via redox and inflammatory mechanisms.
Hansen TS, Karimi Galougahi K, Tang O, Tsang M, Scherrer-Crosbie M, Arystarkhova E, Sweadner K, Bursill C, Bubb KJ, Figtree GA. | 02/22/2024 |
| FXYD1 Is Protective Against Vascular Dysfunction. | FXYD1 Is Protective Against Vascular Dysfunction.
Bubb KJ, Tang O, Gentile C, Moosavi SM, Hansen T, Liu CC, Di Bartolo BA, Figtree GA. | 01/15/2022 |
| Total FXYD1 subunit (modulates Na,K-ATPase activity) abundance was decreased in both mouse models | Isoform-specific Na,K-ATPase and membrane cholesterol remodeling in motor endplates in distinct mouse models of myodystrophy.
Kravtsova VV, Bouzinova EV, Chibalin AV, Matchkov VV, Krivoi II. | 08/13/2020 |
| Authors studied the male progeny of Fxyd1 null males bred to heterozygous Mecp2 female mice. Maximal NKA enzymatic activity was not altered by the loss of MeCP2, but it increased in mice lacking one Fxyd1 allele, suggesting that NKA activity is under Fxyd1 inhibitory control. | Correcting deregulated Fxyd1 expression rescues deficits in neuronal arborization and potassium homeostasis in MeCP2 deficient male mice.
Matagne V, Wondolowski J, Frerking M, Shahidullah M, Delamere NA, Sandau US, Budden S, Ojeda SR., Free PMC Article | 09/28/2019 |
| It was proposed that FXYD1 plays a role in regulating AQP2 retention in apical membrane, and that this involves transfers between raft-like membrane domains in endosomes and plasma membranes. | Impaired AQP2 trafficking in Fxyd1 knockout mice: A role for FXYD1 in regulated vesicular transport.
Arystarkhova E, Bouley R, Liu YB, Sweadner KJ., Free PMC Article | 12/23/2017 |
| Both the extracellular PFXYD motif and the transmembrane domain of PLM but not the cytoplasmic tail were necessary for regulation of peak L-type Ca(2+) current amplitude. | Regulation of L-type calcium channel by phospholemman in cardiac myocytes.
Zhang XQ, Wang J, Song J, Rabinowitz J, Chen X, Houser SR, Peterson BZ, Tucker AL, Feldman AM, Cheung JY., Free PMC Article | 04/9/2016 |
| Decreased phosphorylation of PLM reduces Na/K pump activity and exacerbates Na overload, contractile dysfunction, and adverse remodelling following aortic constriction in mice. | Cardiac hypertrophy in mice expressing unphosphorylatable phospholemman.
Boguslavskyi A, Pavlovic D, Aughton K, Clark JE, Howie J, Fuller W, Shattock MJ., Free PMC Article | 06/20/2015 |
| Nitric oxide activates Na/K-ATPase via phospholemman phosphorylation. | Nitric oxide regulates cardiac intracellular Na⁺ and Ca²⁺ by modulating Na/K ATPase via PKCε and phospholemman-dependent mechanism.
Pavlovic D, Hall AR, Kennington EJ, Aughton K, Boguslavskyi A, Fuller W, Despa S, Bers DM, Shattock MJ., Free PMC Article | 02/15/2014 |
| The results of this study indicated that reducing FXYD1 levels improves a specific cognitive impairment in MECP2-deficient mice. | Correcting deregulated Fxyd1 expression ameliorates a behavioral impairment in a mouse model of Rett syndrome.
Matagne V, Budden S, Ojeda SR, Raber J., Free PMC Article | 08/31/2013 |
| Alterations in PLM expression and phosphorylation are important adaptations post-myocardial infarction. | Phospholemman deficiency in postinfarct hearts: enhanced contractility but increased mortality.
Mirza MA, Lane S, Yang Z, Karaoli T, Akosah K, Hossack J, McDuffie M, Wang J, Zhang XQ, Song J, Cheung JY, Tucker AL., Free PMC Article | 10/6/2012 |
| Constitutive overexpression of S68E mutant was detrimental, both in terms of depressed cardiac function and increased arrhythmogenesis. | Constitutive overexpression of phosphomimetic phospholemman S68E mutant results in arrhythmias, early mortality, and heart failure: potential involvement of Na+/Ca2+ exchanger.
Song J, Gao E, Wang J, Zhang XQ, Chan TO, Koch WJ, Shang X, Joseph JI, Peterson BZ, Feldman AM, Cheung JY., Free PMC Article | 03/24/2012 |
| Exercise induces FXYD1 phosphorylation at multiple sites in human muscle; in mice, contraction-induced changes in FXYD1 phosphorylation are fiber-type specific and dependent on protein kinase Calpha activity. | Protein kinase Cα activity is important for contraction-induced FXYD1 phosphorylation in skeletal muscle.
Thomassen M, Rose AJ, Jensen TE, Maarbjerg SJ, Bune L, Leitges M, Richter EA, Bangsbo J, Nordsborg NB. | 02/18/2012 |
| The results of this study showed the involvement of epigenetic mechanisms in the manifestation of brain region-specific differences in Fxyd1 expression. | Brain region-specific expression of Fxyd1, an Mecp2 target gene, is regulated by epigenetic mechanisms.
Banine F, Matagne V, Sherman LS, Ojeda SR., Free PMC Article | 08/27/2011 |
| Under catecholamine stress when [Na+]i is high, phospholemman minimizes [Na+]i overload by relieving its inhibition of Na+-K+-ATPase and preserves inotropy by simultaneously inhibiting Na+/Ca2+ exchanger. | Regulation of in vivo cardiac contractility by phospholemman: role of Na+/Ca2+ exchange.
Wang J, Gao E, Rabinowitz J, Song J, Zhang XQ, Koch WJ, Tucker AL, Chan TO, Feldman AM, Cheung JY., Free PMC Article | 05/28/2011 |
| Under stressful conditions in which [Na(+)](i) was high, beta-adrenergic agonist-mediated phosphorylation of phospholemman resulted in time-dependent reduction in inotropy due to relief of inhibition of Na(+)-K(+)-ATPase. | Phospholemman and beta-adrenergic stimulation in the heart.
Wang J, Gao E, Song J, Zhang XQ, Li J, Koch WJ, Tucker AL, Philipson KD, Chan TO, Feldman AM, Cheung JY., Free PMC Article | 04/12/2010 |
| It was concluded that the potassium affinity of 2 Slc12a2 isozymes differed in cardiac myocytes, FXYD1 decreased the apparent potassium affinity, phosphorylation of phospholemman does not alter the potassium affinity of Slc12a2. | Extracellular potassium dependence of the Na+-K+-ATPase in cardiac myocytes: isoform specificity and effect of phospholemman.
Han F, Tucker AL, Lingrel JB, Despa S, Bers DM., Free PMC Article | 01/21/2010 |
| These results suggest that FXYD1 contributes to facilitating the advent of puberty by maintaining GnRH neuronal excitability to incoming transsynaptic stimulatory inputs. | FXYD1, a modulator of Na,K-ATPase activity, facilitates female sexual development by maintaining gonadotrophin-releasing hormone neuronal excitability.
Garcia-Rudaz C, Deng V, Matagne V, Ronnekleiv OK, Bosch M, Han V, Percy AK, Ojeda SR., Free PMC Article | 01/21/2010 |
| Myocytes swelled equally in both genotypes, indicating that phospholemman, when expressed at physiological levels in cardiomyocytes, is not essential to limit water accumulation in response to a hyposmotic challenge. | Cell volume control in phospholemman (PLM) knockout mice: do cardiac myocytes demonstrate a regulatory volume decrease and is this influenced by deletion of PLM?
Bell JR, Lloyd D, Curl CL, Delbridge LM, Shattock MJ. | 01/21/2010 |
| Phospholemman does not participate in forskolin-induced swine carotid artery relaxation. | Phospholemman does not participate in forskolin-induced swine carotid artery relaxation.
Meeks MK, Han S, Tucker AL, Rembold CM., Free PMC Article | 01/21/2010 |
| Phospholemman phosphorylation and SERCA stimulation are an integral part of the sympathetic fight-or-flight response, tempering the rise in [Na](i) and cellular Ca loading and perhaps limiting Ca overload-induced arrhythmias. | Phospholemman-mediated activation of Na/K-ATPase limits [Na]i and inotropic state during beta-adrenergic stimulation in mouse ventricular myocytes.
Despa S, Tucker AL, Bers DM., Free PMC Article | 01/21/2010 |
| PLM plays an important role in the contractile function of the normoxic mouse heart | Characterization of the phospholemman knockout mouse heart: depressed left ventricular function with increased Na-K-ATPase activity.
Bell JR, Kennington E, Fuller W, Dighe K, Donoghue P, Clark JE, Jia LG, Tucker AL, Moorman JR, Marber MS, Eaton P, Dunn MJ, Shattock MJ. | 01/21/2010 |
| PLM mediates the PKC-dependent activation of Na+/K+ pump function in cardiac myocytes | Phospholemman phosphorylation mediates the protein kinase C-dependent effects on Na+/K+ pump function in cardiac myocytes.
Han F, Bossuyt J, Despa S, Tucker AL, Bers DM. | 01/21/2010 |
| unphosphorylated FXYD1 inhibits Na/K ATPase, whereas S68 phosphorylated FXYD1 stimulates Na/K ATPase to a level above that seen in the absence of FXYD1 | The intracellular region of FXYD1 is sufficient to regulate cardiac Na/K ATPase.
Pavlović D, Fuller W, Shattock MJ. | 01/21/2010 |
| study reports that FXYD1 is elevated in frontal cortex neurons of Rett syndrome patients and Mecp2-null mice; FXYD1 is identified as a MeCP2 target gene whose de-repression may directly contribute to RTT neuronal pathogenesis | FXYD1 is an MeCP2 target gene overexpressed in the brains of Rett syndrome patients and Mecp2-null mice.
Deng V, Matagne V, Banine F, Frerking M, Ohliger P, Budden S, Pevsner J, Dissen GA, Sherman LS, Ojeda SR. | 01/21/2010 |
| a primary effect of phospholemman is to modulate the Na-K-ATPase and that its reduced activity initiates compensatory responses in heart hypertrophy | Hypertrophy, increased ejection fraction, and reduced Na-K-ATPase activity in phospholemman-deficient mice.
Jia LG, Donnet C, Bogaev RC, Blatt RJ, McKinney CE, Day KH, Berr SS, Jones LR, Moorman JR, Sweadner KJ, Tucker AL. | 01/21/2010 |