LIVIVO - Search results -

Search results

Result 1 - 10 of total 33

Search options

Article ; Online: Lipocalin-2 induces mitochondrial dysfunction in renal tubular cells via mTOR pathway activation.

Marques, Eloïse / Alves Teixeira, Maraiza / Nguyen, Clément / Terzi, Fabiola / Gallazzini, Morgan

2023 Volume 42, Issue 9, Page(s) 113032

Abstract: Mitochondrial dysfunction is a critical process in renal epithelial cells upon kidney injury. While its implication in kidney disease progression is established, the mechanisms modulating it remain unclear. Here, we describe the role of Lipocalin-2 (LCN2) ...

Abstract	Mitochondrial dysfunction is a critical process in renal epithelial cells upon kidney injury. While its implication in kidney disease progression is established, the mechanisms modulating it remain unclear. Here, we describe the role of Lipocalin-2 (LCN2), a protein expressed in injured tubular cells, in mitochondrial dysfunction. We show that LCN2 expression decreases mitochondrial mass and function and induces mitochondrial fragmentation. Importantly, while LCN2 expression favors DRP1 mitochondrial recruitment, DRP1 inhibition antagonizes LCN2's effect on mitochondrial shape. Remarkably, LCN2 promotes mitochondrial fragmentation independently of its secretion or transport iron activity. Mechanistically, intracellular LCN2 expression increases mTOR activity, and rapamycin inhibits LCN2's effect on mitochondrial shape. In vivo, Lcn2 gene inactivation prevents mTOR activation and mitochondrial length decrease observed upon ischemia-reperfusion-induced kidney injury (IRI) in Lcn2
MeSH term(s)	Mice ; Animals ; Lipocalin-2/genetics ; Lipocalin-2/metabolism ; Kidney/metabolism ; Reperfusion Injury/metabolism ; Epithelial Cells/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Mitochondria/metabolism
Chemical Substances	Lipocalin-2 ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2023-08-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113032
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article ; Online: Endoplasmic reticulum stress and kidney dysfunction.

Gallazzini, Morgan / Pallet, Nicolas

Biology of the cell

2018 Volume 110, Issue 9, Page(s) 205–216

Abstract: Chronic kidney disease (CKD) affects millions of persons worldwide and constitutes a major public health problem. Therefore, understanding the molecular basis of CKD is a key challenge for the development of preventive and therapeutic strategies. A major ...

Abstract	Chronic kidney disease (CKD) affects millions of persons worldwide and constitutes a major public health problem. Therefore, understanding the molecular basis of CKD is a key challenge for the development of preventive and therapeutic strategies. A major contributor to chronic histological damage associated with CKD is acute kidney injury (AKI). At the cellular level, kidney injuries are associated with microenvironmental alterations, forcing cells to activate adaptive biological processes that eliminate the stressor and generate alarm signals. These signalling pathways actively participate in tissue remodelling by promoting inflammation and fibrogenesis, ultimately leading to CKD. Many stresses that are encountered upon kidney injury are prone to trigger endoplasmic reticulum (ER) stress. In the kidney, ER stress both participates in acute and chronic histological damages, but also promotes cellular adaptation and nephroprotection. In this review, we will discuss the implication of ER stress in the pathophysiology of AKI and CKD progression, and we will give a critical analysis of the current experimental and clinical evidence that support ER stress as a mediator of kidney damage.
MeSH term(s)	Animals ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Stress ; Humans ; Kidney/metabolism ; Kidney/physiopathology ; Kidney Diseases/metabolism ; Kidney Diseases/physiopathology ; Stress, Physiological ; Unfolded Protein Response
Language	English
Publishing date	2018-08-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	245745-3
ISSN	1768-322X ; 0399-0311 ; 0248-4900
ISSN (online)	1768-322X
ISSN	0399-0311 ; 0248-4900
DOI	10.1111/boc.201800019
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 758: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Lipocalin-2 Regulates Epidermal Growth Factor Receptor Intracellular Trafficking.

Yammine, Lucie / Zablocki, Aniela / Baron, William / Terzi, Fabiola / Gallazzini, Morgan

Cell reports

2019 Volume 29, Issue 7, Page(s) 2067–2077.e6

Abstract: Epidermal growth factor receptor (EGFR) activation and lipocalin-2 (Lcn2) expression are frequently observed in the same pathological contexts, such as cancers or chronic kidney disease (CKD). However, the significance of this association is unknown. ... ...

Abstract	Epidermal growth factor receptor (EGFR) activation and lipocalin-2 (Lcn2) expression are frequently observed in the same pathological contexts, such as cancers or chronic kidney disease (CKD). However, the significance of this association is unknown. Here, we describe the role of Lcn2 in regulating EGFR trafficking. We show that Lcn2 increases EGFR cell surface abundance and is required for transforming growth factor α (TGF-α)-induced EGFR recycling to the plasma membrane and sustained activation. Lcn2 binds to the intracellular domain of EGFR in late endosomal compartments and inhibits its lysosomal degradation. Consistently, Lcn2 enhances EGFR-induced cell migration after TGF-α stimulation. In vivo, Lcn2 gene inactivation prevents EGFR recycling to the plasma membrane in an experimental model of CKD. Remarkably, this is associated with a dramatic decrease of renal lesions. Together, our data identify Lcn2 as a key mediator of EGFR trafficking processes. Hence, therapeutic inhibition of Lcn2 may counteract the deleterious effect of EGFR activation.
MeSH term(s)	Animals ; Cell Membrane/genetics ; Cell Membrane/metabolism ; Cell Movement/drug effects ; Cell Movement/genetics ; Endosomes/genetics ; Endosomes/metabolism ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; Female ; Lipocalin-2/genetics ; Lipocalin-2/metabolism ; Mice ; Mice, Knockout ; Protein Transport/drug effects ; Protein Transport/genetics ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/pathology ; Transforming Growth Factor alpha/pharmacology
Chemical Substances	Lipocalin-2 ; Transforming Growth Factor alpha ; Lcn2 protein, mouse (126469-30-5) ; EGFR protein, mouse (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2019-11-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2019.10.015
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Lipocalin-2 Regulates Epidermal Growth Factor Receptor Intracellular Trafficking

Lucie Yammine / Aniela Zablocki / William Baron / Fabiola Terzi / Morgan Gallazzini

Cell Reports, Vol 29, Iss 7, Pp 2067-2077.e

2019 Volume 6

Abstract: Summary: Epidermal growth factor receptor (EGFR) activation and lipocalin-2 (Lcn2) expression are frequently observed in the same pathological contexts, such as cancers or chronic kidney disease (CKD). However, the significance of this association is ... ...

Abstract	Summary: Epidermal growth factor receptor (EGFR) activation and lipocalin-2 (Lcn2) expression are frequently observed in the same pathological contexts, such as cancers or chronic kidney disease (CKD). However, the significance of this association is unknown. Here, we describe the role of Lcn2 in regulating EGFR trafficking. We show that Lcn2 increases EGFR cell surface abundance and is required for transforming growth factor α (TGF-α)-induced EGFR recycling to the plasma membrane and sustained activation. Lcn2 binds to the intracellular domain of EGFR in late endosomal compartments and inhibits its lysosomal degradation. Consistently, Lcn2 enhances EGFR-induced cell migration after TGF-α stimulation. In vivo, Lcn2 gene inactivation prevents EGFR recycling to the plasma membrane in an experimental model of CKD. Remarkably, this is associated with a dramatic decrease of renal lesions. Together, our data identify Lcn2 as a key mediator of EGFR trafficking processes. Hence, therapeutic inhibition of Lcn2 may counteract the deleterious effect of EGFR activation. : Yammine et al. propose lipocalin-2 (Lcn2) as a regulator of EGFR activity. By binding to TGF-α-activated EGFR intracellular domain, cytosolic Lcn2 enhances its recycling to the cell surface. This accounts for EGFR sustained activation leading to chronic kidney disease and makes Lcn2 a potential therapeutic target in this context. Keywords: EGFR, lipocalin-2, recycling, trafficking, chronic kidney disease
Keywords	Biology (General) ; QH301-705.5
Subject code	616
Language	English
Publishing date	2019-11-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article: What's new about osmotic regulation of glycerophosphocholine.

Gallazzini, Morgan / Burg, Maurice B

Physiology (Bethesda, Md.)

2009 Volume 24, Page(s) 245–249

Abstract: Glycerophosphocholine is an abundant renal medullary organic osmolyte that protects renal medullary cells from the high interstitial concentrations of NaCl and urea to which they are normally exposed. We consider the metabolism of glycerophosphocholine, ... ...

Abstract	Glycerophosphocholine is an abundant renal medullary organic osmolyte that protects renal medullary cells from the high interstitial concentrations of NaCl and urea to which they are normally exposed. We consider the metabolism of glycerophosphocholine, its osmotic regulation, and the recently discovered molecular identity of the enzymes that osmoregulate its abundance.
MeSH term(s)	Animals ; Glycerylphosphorylcholine/physiology ; Humans ; Kidney Medulla/cytology ; Kidney Medulla/physiology ; Sodium Chloride/metabolism ; Urea/metabolism ; Water-Electrolyte Balance/physiology
Chemical Substances	Sodium Chloride (451W47IQ8X) ; Glycerylphosphorylcholine (60M22SGW66) ; Urea (8W8T17847W)
Language	English
Publishing date	2009-08-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2158667-6
ISSN	1548-9221 ; 1548-9213
ISSN (online)	1548-9221
ISSN	1548-9213
DOI	10.1152/physiol.00009.2009
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2164: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Molecular pathways of chronic kidney disease progression.

Bienaimé, Frank / Canaud, Guillaume / El Karoui, Khalil / Gallazzini, Morgan / Terzi, Fabiola

Nephrologie & therapeutique

2016 Volume 12 Suppl 1, Page(s) S35–8

Abstract: Chronic kidney disease is characterized by the progressive loss of functional nephrons. This loss means that the remaining nephrons are put under stress and are forced to adapt in order to maintain kidney function. Over the time, the strains imposed by ... ...

Abstract	Chronic kidney disease is characterized by the progressive loss of functional nephrons. This loss means that the remaining nephrons are put under stress and are forced to adapt in order to maintain kidney function. Over the time, the strains imposed by these adaptations result in a vicious circle in which the loss of damaged nephrons results in the damage of the so far healthy nephrons. Hence, the rate of chronic kidney disease progression depends on the ability of the remaining nephrons to cope with stress. This article reviews the molecular pathways involved in the compensation and deterioration process after nephron reduction. In particular, we examine the role of mammalian target of rapamycin complex (mTORC)/serine-threonine protein kinase AKT, epidermal growth factor receptor (EGFR) and unfolded protein response pathways, as well as the pleiotropic function of Lipocalin 2. We also discuss the dual role played by some of these pathways in acute and chronic kidney disease. Finally, the relevance of these experimental finding to human chronic kidney disease is discussed.
Language	English
Publishing date	2016-04
Publishing country	France
Document type	Journal Article
ZDB-ID	2229575-6
ISSN	1872-9177 ; 1769-7255
ISSN (online)	1872-9177
ISSN	1769-7255
DOI	10.1016/j.nephro.2016.02.009
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6298: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: The costimulatory receptor B7-1 is not induced in injured podocytes.

Baye, Emilie / Gallazzini, Morgan / Delville, Marianne / Legendre, Christophe / Terzi, Fabiola / Canaud, Guillaume

Kidney international

2016 Volume 90, Issue 5, Page(s) 1037–1044

Abstract: Recent research on podocytes has proposed B7-1 as an important player in podocyte biology and as a potential new therapeutic target. B7-1 was upregulated in injured podocytes and described as a biomarker to identify patients who may benefit from ... ...

Abstract	Recent research on podocytes has proposed B7-1 as an important player in podocyte biology and as a potential new therapeutic target. B7-1 was upregulated in injured podocytes and described as a biomarker to identify patients who may benefit from abatacept, a B7-1 blocker. However, after this initial enthusiasm, several reports have not confirmed the efficiency of abatacept at inducing proteinuria remission in patients. In order to resolve these discrepancies, we explored the role of B7-1 in the injured podocyte. Both primary cultured and immortalized podocytes were exposed to lipopolysaccharides, but this failed to induce B7-1 expression at the mRNA and protein levels. Importantly, TLR-4 engagement confirmed lipopolysaccharide efficacy. We then evaluated B7-1 expression in several mouse models of podocyte injury including treatment with lipopolysaccharide or Adriamycin, a lupus prone model (NZB/W F1) and subtotal nephrectomy. Using 3 commercially available anti-B7-1 antibodies and appropriate controls, we could not find B7-1 expression in podocytes, whereas some infiltrating cells were positive. Thus, our findings do not support a role for B7-1 in podocyte biology. Hence, further studies are mandatory before treating proteinuric patients with B7-1 blockers.
MeSH term(s)	Animals ; B7-1 Antigen/metabolism ; Glomerulosclerosis, Focal Segmental/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Podocytes/metabolism ; Primary Cell Culture
Chemical Substances	B7-1 Antigen
Language	English
Publishing date	2016-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2016.06.022
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 797: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: CRISPR/Cas9-Engineered HLA-Deleted Glomerular Endothelial Cells as a Tool to Predict Pathogenic Non-HLA Antibodies in Kidney Transplant Recipients.

Journal of the American Society of Nephrology : JASN

2022 Volume 32, Issue 12, Page(s) 3231–3251

Abstract: Background: After kidney transplantation, donor-specific antibodies against human leukocyte antigen donor-specific antibodies (HLA-DSAs) drive antibody-mediated rejection (ABMR) and are associated with poor transplant outcomes. However, ABMR histology ( ... ...

Abstract	Background: After kidney transplantation, donor-specific antibodies against human leukocyte antigen donor-specific antibodies (HLA-DSAs) drive antibody-mediated rejection (ABMR) and are associated with poor transplant outcomes. However, ABMR histology (ABMRh) is increasingly reported in kidney transplant recipients (KTRs) without HLA-DSAs, highlighting the emerging role of non-HLA antibodies (Abs). Methods: W e designed a non-HLA Ab detection immunoassay (NHADIA) using HLA class I and II-deficient glomerular endothelial cells (CiGEnC Results: W e sequentially applied CRISPR/Cas9 to delete the Conclusion: The NHADIA identifies non-HLA Abs and strongly predicts graft endothelial injury independent of HLA-DSAs.
MeSH term(s)	Adult ; Aged ; CRISPR-Cas Systems/genetics ; Cells, Cultured ; Endothelial Cells/immunology ; Female ; Gene Deletion ; Graft Rejection/etiology ; HLA Antigens/genetics ; HLA Antigens/immunology ; Humans ; Isoantibodies/immunology ; Kidney Glomerulus/immunology ; Kidney Transplantation/adverse effects ; Male ; Middle Aged ; Nuclear Proteins/genetics ; Reoperation ; Retrospective Studies ; Tissue Donors ; Trans-Activators/genetics ; beta 2-Microglobulin/genetics
Chemical Substances	B2M protein, human ; HLA Antigens ; Isoantibodies ; MHC class II transactivator protein ; Nuclear Proteins ; Trans-Activators ; beta 2-Microglobulin
Language	English
Publishing date	2022-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2021050689
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3344: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Signaling pathways predisposing to chronic kidney disease progression.

Zaidan, Mohamad / Burtin, Martine / Zhang, Jitao David / Blanc, Thomas / Barre, Pauline / Garbay, Serge / Nguyen, Clément / Vasseur, Florence / Yammine, Lucie / Germano, Serena / Badi, Laura / Gubler, Marie-Claire / Gallazzini, Morgan / Friedlander, Gérard / Pontoglio, Marco / Terzi, Fabiola

JCI insight

2020 Volume 5, Issue 9

Abstract: The loss of functional nephrons after kidney injury triggers the compensatory growth of the remaining ones to allow functional adaptation. However, in some cases, these compensatory events activate signaling pathways that lead to pathological alterations ...

Abstract	The loss of functional nephrons after kidney injury triggers the compensatory growth of the remaining ones to allow functional adaptation. However, in some cases, these compensatory events activate signaling pathways that lead to pathological alterations and chronic kidney disease. Little is known about the identity of these pathways and how they lead to the development of renal lesions. Here, we combined mouse strains that differently react to nephron reduction with molecular and temporal genome-wide transcriptome studies to elucidate the molecular mechanisms involved in these events. We demonstrated that nephron reduction led to 2 waves of cell proliferation: the first one occurred during the compensatory growth regardless of the genetic background, whereas the second one occurred, after a quiescent phase, exclusively in the sensitive strain and accompanied the development of renal lesions. Similarly, clustering by coinertia analysis revealed the existence of 2 waves of gene expression. Interestingly, we identified type I interferon (IFN) response as an early (first-wave) and specific signature of the sensitive (FVB/N) mice. Activation of type I IFN response was associated with G1/S cell cycle arrest, which correlated with p21 nuclear translocation. Remarkably, the transient induction of type I IFN response by poly(I:C) injections during the compensatory growth resulted in renal lesions in otherwise-resistant C57BL6 mice. Collectively, these results suggest that the early molecular and cellular events occurring after nephron reduction determine the risk of developing late renal lesions and point to type I IFN response as a crucial event of the deterioration process.
MeSH term(s)	Animals ; Cell Proliferation ; Disease Progression ; Disease Susceptibility ; Female ; G1 Phase Cell Cycle Checkpoints ; Interferon Type I/metabolism ; Kidney/metabolism ; Kidney/pathology ; Mice ; Mice, Inbred C57BL ; Nephrons/metabolism ; Nephrons/pathology ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/pathology ; Signal Transduction
Chemical Substances	Interferon Type I
Language	English
Publishing date	2020-05-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.126183
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: GDPD5 is a glycerophosphocholine phosphodiesterase that osmotically regulates the osmoprotective organic osmolyte GPC.

Gallazzini, Morgan / Ferraris, Joan D / Burg, Maurice B

Proceedings of the National Academy of Sciences of the United States of America

2008 Volume 105, Issue 31, Page(s) 11026–11031

Abstract: Glycerophosphocholine (GPC) is an abundant osmoprotective renal medullary organic osmolyte. We previously found that its synthesis from phosphatidylcholine is catalyzed by tonicity-regulated activity of the phospholipase B, neuropathy target esterase. We ...

Abstract	Glycerophosphocholine (GPC) is an abundant osmoprotective renal medullary organic osmolyte. We previously found that its synthesis from phosphatidylcholine is catalyzed by tonicity-regulated activity of the phospholipase B, neuropathy target esterase. We also found that its degradation is catalyzed by glycerophosphocholine phosphodiesterase (GPC-PDE) activity and that elevating osmolality from 300 to 500 mosmol/kg by adding NaCl or urea, inhibits GPC-PDE activity, which contributes to the resultant increase of GPC. In the present studies we identify GDPD5 (glycerophosphodiester phosphodiesterase domain containing 5) as a GPC-PDE that is rapidly inhibited by high NaCl or urea. Recombinant GDPD5 colocalizes with neuropathy target esterase in the perinuclear region of HEK293 cells, and immuno-precipitated recombinant GDPD5 degrades GPC in vitro. The in vitro activity is reduced when the cells from which the GDPD5 is immuno-precipitated have been exposed to high NaCl or urea. In addition, high NaCl decreases mRNA abundance of GDPD5 via an increase of its degradation rate, although high urea does not. At 300 mosmol/kg siRNA knockdown of GDPD5 increases GPC in mouse inner medullary collecting duct-3 cells, and over expression of recombinant GDPD5 increases cellular GPC-PDE activity, accompanied by decreased GPC. We conclude that GDPD5 is a GPC-PDE that contributes to osmotic regulation of cellular GPC.
MeSH term(s)	Analysis of Variance ; Animals ; Blotting, Western ; Cell Line ; DNA Primers ; Glycerylphosphorylcholine/metabolism ; Humans ; Immunoprecipitation ; Kidney/metabolism ; Mice ; Microscopy, Fluorescence ; Phosphoric Diester Hydrolases/genetics ; Phosphoric Diester Hydrolases/metabolism ; RNA Interference ; RNA, Small Interfering/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Sodium Chloride/pharmacology ; Urea/pharmacology ; Water-Electrolyte Balance/physiology
Chemical Substances	DNA Primers ; RNA, Small Interfering ; Sodium Chloride (451W47IQ8X) ; Glycerylphosphorylcholine (60M22SGW66) ; Urea (8W8T17847W) ; Phosphoric Diester Hydrolases (EC 3.1.4.-) ; glycerophosphocholine phosphodiesterase (EC 3.1.4.2)
Language	English
Publishing date	2008-07-30
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.0805496105
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1148: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito