Alterations in H+-ATPase Gene Expression in Response to Salt

1994 ◽  
pp. 429-442 ◽  
Author(s):  
Marla L. Binzel
Keyword(s):  
Gene Expression ◽  
Atpase Gene

Plasma Membrane Calcium ATPase Gene Expression in Bovine Lens Epithelium

2000 ◽  
Vol 32 (2-3) ◽  
pp. 100-105 ◽  
Author(s):  
Lijun Bian ◽  
Junwen Zeng ◽  
Douglas Borchman ◽  
Christopher A. Paterson
Keyword(s):  
Gene Expression ◽  
Plasma Membrane ◽  
Calcium Atpase ◽  
Lens Epithelium ◽  
Plasma Membrane Calcium Atpase ◽  
Bovine Lens ◽  
Atpase Gene

Plasma-membrane H+-ATPase gene expression is regulated by NaCl in cells of the halophyte Atriplex nummularia L.

Planta ◽  
1993 ◽  
Vol 190 (4) ◽  
Author(s):  
Xiaomu Niu ◽  
Jian-Kang Zhu ◽  
MeenaL. Narasimhan ◽  
RayA. Bressan ◽  
PaulM. Hasegawa
Keyword(s):  
Gene Expression ◽  
Plasma Membrane ◽  
Atpase Gene ◽  
Atriplex Nummularia ◽  
In Cells

Cadmium effect on vacuolar H+-ATPase gene expression in the roots of barley seedlings of different age

2012 ◽  
Vol 60 (1) ◽  
pp. 55-59 ◽  
Author(s):  
N. M. Kaznina ◽  
A. F. Titov ◽  
L. V. Topchieva ◽  
G. F. Laidinen ◽  
Yu. V. Batova
Keyword(s):  
Gene Expression ◽  
Atpase Gene

Skeletal Muscle Sarcoplasmic Reticulum Ca 2+ -ATPase Gene Expression in Congestive Heart Failure

1997 ◽  
Vol 81 (5) ◽  
pp. 703-710 ◽  
Author(s):  
David G. Peters ◽  
Heather L. Mitchell ◽  
Sylvia A. McCune ◽  
Sonhee Park ◽  
Jay H. Williams ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Congestive Heart Failure ◽  
Sarcoplasmic Reticulum ◽  
Atpase Gene

Dexamethasone stimulates transcription of the Na+-K+-ATPase β1gene in adult rat lung epithelial cells

2003 ◽  
Vol 285 (3) ◽  
pp. L593-L601 ◽  
Author(s):  
Hong Hao ◽  
Christine H. Wendt ◽  
Gurpreet Sandhu ◽  
David H. Ingbar
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Regulatory Elements ◽  
Lung Epithelial Cells ◽  
Mrna Levels ◽  
Rat Lung ◽  
Alveolar Epithelial ◽  
Adult Rat ◽  
Atpase Gene ◽  
Lung Epithelial

Na+-K+-ATPase plays an essential role in active alveolar epithelial fluid resorption. In fetal and adult alveolar epithelial cells, glucocorticoids (GC) increase Na+-K+-ATPase activity and mRNA levels. We sought to define the mechanism of Na+-K+-ATPase gene upregulation by GC. In a rat alveolar epithelial cell line (RLE), dexamethasone (Dex) increased β1-subunit Na+-K+-ATPase mRNA expression two- to threefold within 3 h after exposure to the GC. The increased gene expression was due to increased transcription as demonstrated by nuclear run-on assays, whereas mRNA stability remained unchanged. Transient transfection of 5′ deletion mutants of a β1promoter-reporter construct demonstrated a 1.5- to 2.2-fold increase in promoter activity by Dex. All of the 5′ deletion constructs contained partial or palindromic GC regulatory elements (GRE) and responded to GC. The increased expression of promoter reporter was inhibited by RU-486, a GC receptor (GR) antagonist, suggesting the involvement of GR. The palindromic GRE at -631 demonstrated Dex induction in a heterologous promoter construct. Gel mobility shift assays using RLE nuclear extracts demonstrated specific binding to this site and the presence of GR. We conclude that GC directly stimulate transcription of Na+-K+-ATPase β1gene expression in adult rat lung epithelial cells through a GR-dependent mechanism that can act at multiple sites.

Phorbol 12-myristate 13-acetate alters SR Ca(2+)-ATPase gene expression in cultured neonatal rat heart cells

1996 ◽  
Vol 271 (3) ◽  
pp. H1031-H1039 ◽  
Author(s):  
M. Qi ◽  
J. W. Bassani ◽  
D. M. Bers ◽  
A. M. Samarel
Keyword(s):  
Gene Expression ◽  
Sarcoplasmic Reticulum ◽  
Mrna Stability ◽  
Primary Cultures ◽  
Neonatal Rat ◽  
Response To Treatment ◽  
Similar Degree ◽  
Heart Cells ◽  
Mrna Levels ◽  
Atpase Gene

Primary cultures of neonatal rat ventricular myocytes were used to examine how the cardiac myocyte cytoplasmic Ca2+ ([Ca2+]i) transient and sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2) gene expression change in response to treatment with the protein kinase C activator phorbol 12-myristate 13-acetate (PMA). Exposure of neonatal myocytes to PMA (200 nM, 48-72 h) produced myocyte growth and a 70% prolongation of the half-time for [Ca2+]i decline induced by potassium depolarization in the absence of extracellular Na+ (in which the sarcoplasmic reticulum Ca2+ pump is the main mechanism responsible for [Ca2+]i decline). The reduced rate of [Ca2+]i transient decline corresponded to a 53% reduction in SERCA2 protein levels and a 43% reduction in SERCA2 mRNA levels as compared with control myocytes. Exposure to PMA for as little as 30 min or for as long as 48 h produced a similar degree of SERCA2 mRNA downregulation over time. PMA-induced downregulation of SERCA2 mRNA levels was blocked by either 10 nM staurosporine or 4 microM chelerythrine, whereas treatment with either agent alone increased SERCA2 mRNA levels as compared with control cells. Actinomycin D mRNA stability assays revealed that PMA treatment appeared to markedly destabilize the relatively long-lived SERCA2 mRNA transcript. Taken together, these results indicate that downregulation of SERCA2 gene by PMA in cultured neonatal myocytes occurs at least in part by alterations in mRNA stability and results in functional alterations in [Ca2+]i decline that are similar to that observed in the hypertrophied and failing adult myocardium.

scholarly journals Oxidant effects on epithelial Na,K-ATPase gene expression and promoter function.

1998 ◽  
Vol 106 (suppl 5) ◽  
pp. 1213-1217 ◽  
Author(s):  
C H Wendt ◽  
R Sharma ◽  
R Bair ◽  
H Towle ◽  
D H Ingbar
Keyword(s):  
Gene Expression ◽  
Promoter Function ◽  
Atpase Gene
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