|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Structural and functional interaction sites between Na, K-ATPase and FXYD proteins显示文摘 | Li C Grosdidier A Crambert G | 2004 | J Biol Chem2004，279，38： | 1 |
| 2 | FXYD7 is a brainspecific regulator of Na^+ , K^+ATPase alpha 1-beta isozymes 显示文摘 | Beguin P Crambert G Monnet-Tschudi F | 2002 | EMBO J2002，21，13： | 1 |
| 3 | FXYD proteins: new tissue-specific regulators of the ubiquitous Na+, K+-ATPase显示文摘 | Crambert G Geering K | 2003 | Sci STKE2003，2003，166： | 1 |
| 4 | FXYD proteins:new tissue-specific regul-ators of the ubiquitous Na+,K+-ATPase显示文摘 | Crambert G Geering K | | 0，，166： | 1 |
| 5 | Structural and functional interaction sites between Na,K-ATPase and FXYD proteins显示文摘 | Li C Gresdidier A Crambert G | | 0，，37： | 1 |
| 6 | Transport and pharmacological properties of nine different human Na, K - ATPase isozymes 显示文摘 | Crambert G Hasler U Beggab AT | 2000 | J Biol Chem2000，275，3： | 1 |
| 7 | CHIF,a member of the FXYD protein family,is a regulator of Na,K-ATPase distinct from the γ-subunit显示文摘 | Bèguin P Crambert G Guennoun S | 2001 | The EMBO Journal2001，20，13： | 1 |
| 8 | FXYD7 is a brain-specific regulator of Na,KATPase α1-β isozymes 显示文摘 | Beguin P Crambert G Monnet-Tschudi F | 2002 | The EMBO Journal2002，21，13： | 1 |
| 9 | FXYD proteins: new tissue-specific regulators of the ubiquitous Na, K-ATPase 显示文摘 | Crambert G Geering K | 2003 | Sci STKE2003，2003，166： | 1 |
| 10 | Phespholemman (FXYD1) associates with Na,K-ATPase and regulates its transport properties显示文摘 | Crambert G Fiizesi M Garry H | | 0，，： | 1 |
| 11 | FXYD7 is a brain-specific regulator of Na,K-ATPase alpha 1-beta isozymes显示文摘 | Béguin P Crambert G Monnet-Tschudi F | | 0，，13： | 1 |
| 12 | Structural and functional interactionsites between Na^+-K^+-ATPase and FXYD 显示文摘 | Li C Grosdidier A Crambert G | 2004 | J Biol Chem2004，279，38： | 1 |
| 13 | New insights into sodium transport regulation in the distal nephron:Role of G-protein coupled receptors显示文摘The renal handling of Na^+ balance is a major determinant of the blood pressure(BP) level. The inability of the kidney to excrete the daily load of Na+ represents the primary cause of chronic hypertension. Among the different segments that constitute the nephron, those present in the distal part(i.e., the cortical thick ascending limb, the distal convoluted tubule, the connecting and collecting tubules) play a central role in the fine-tuning of renal Na^+ excretion and are the target of many different regulatory processes that modulate Na^+ retention more or less efficiently. G-protein coupled receptors(GPCRs) are crucially involved in this regulation and could represent efficient pharmacological targets to control BP levels. In this review, we describe both classical and novel GPCR-dependent regulatory systems that have been shown to modulate renal Na^+ absorption in the distal nephron. In addition to the multiplicity of the GPCR that regulate Na^+ excretion, this review also highlights the complexity of these different pathways, and the connections between them. | Luciana Morla Aurélie Edwards Gilles Crambert | 2016 | World Journal of Biological Chemistry2016，7，1： | 1 |
| 14 | FXYD3 ( Mat-8), a new regulator of Na^+-K^+-ATPase 显示文摘 | Crambert G Li C Claeys D | 2005 | Mol Biol Cell2005，16，5： | 1 |
| 15 | Human nongastric H^+-K^+-ATPase:transport properties of ATP1al1 assembled with different beta-subunits显示文摘 | Crambert G Horisberger JD Modyanov NN | 2002 | Am J Physiol Cell Physiol2002，283，1： | 1 |
| 16 | FXYD7 is a brain-specific regulator of Na^+ ,K^+-ATPase alpha 1-beta isozymes显示文摘 | Beguin P Crambert G Monnet-Tschudi F | 2002 | EMBO J2002，21，13： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员