LIVIVO - Search results -

Search results

Result 1 - 10 of total 46

Search options

Book ; Online: Factors Influencing Mammalian Kidney Development: Implications for Health in Adult Life

Moritz, Karen M. / Bertram, John F. / Black, M. Jane / Caruana, Georgina / Wintour-Coghlan, Marelyn

2008

Author's details	by Karen M. Moritz, Marelyn Wintour-Coghlan, M. Jane Black, John F. Bertram, Georgina Caruana
Keywords	Human genetics ; Human physiology ; Nephrology
Language	English
Publisher	Springer-Verlag Berlin Heidelberg
Publishing place	Berlin, Heidelberg
Document type	Book ; Online
HBZ-ID	TT050387826
ISBN	978-3-540-77767-0 ; 978-3-540-77768-7 ; 3-540-77767-9 ; 3-540-77768-7
DOI	10.1007/978-3-540-77768-7
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

Full text online

Full text

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.

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.

Details ▾
- Full text online
- Order with fees

Article ; Online: Congenital anomalies of the kidney and urinary tract genetics in mice and men.

Caruana, Georgina / Bertram, John F

Nephrology (Carlton, Vic.)

2015 Volume 20, Issue 5, Page(s) 309–311

Abstract: The most common cause of paediatric end-stage kidney disease results from congenital anomalies of the kidney and urinary tract (CAKUT). Genetic manipulation in mice has provided insight into the developmental events that give rise to the broad spectrum ... ...

Abstract	The most common cause of paediatric end-stage kidney disease results from congenital anomalies of the kidney and urinary tract (CAKUT). Genetic manipulation in mice has provided insight into the developmental events that give rise to the broad spectrum of malformations associated with CAKUT. Despite the increase in the number of identified CAKUT-causing genes, the underlying genetic cause for the majority of patients with CAKUT remains unknown. In this mini-review, we provide an overview of the genetic causes of CAKUT based on current mouse mutant models, as well as next-generation sequencing approaches in humans that are helping to bridge the gaps in our understanding.
MeSH term(s)	Animals ; Disease Models, Animal ; Humans ; Kidney/abnormalities ; Mice ; Mutation/genetics ; Urogenital Abnormalities/genetics
Language	English
Publishing date	2015-05
Publishing country	Australia
Document type	Journal Article ; Review
ZDB-ID	1303661-0
ISSN	1440-1797 ; 1320-5358
ISSN (online)	1440-1797
ISSN	1320-5358
DOI	10.1111/nep.12402
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 4822: 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 ▾

Article: Genetic studies define MAGUK proteins as regulators of epithelial cell polarity.

Caruana, Georgina

The International journal of developmental biology

2002 Volume 46, Issue 4, Page(s) 511–518

Abstract: Polarized epithelial cells play critical roles during early embryonic development and organogenesis. Multi-domain scaffolding proteins belonging to the membrane associated guanylate kinase (MAGUK) family are commonly found at the plasma membrane of ... ...

Abstract	Polarized epithelial cells play critical roles during early embryonic development and organogenesis. Multi-domain scaffolding proteins belonging to the membrane associated guanylate kinase (MAGUK) family are commonly found at the plasma membrane of polarized epithelial cells. Genetic studies in Drosophila melanogaster and Caenorhabditis elegans have revealed that MAGUK proteins regulate various aspects of the polarized epithelial phenotype, including cell junction assembly, targeting of proteins to the plasma membrane and the organisation of polarized signalling complexes. This review will focus on the genetic studies that have contributed to our understanding of the MAGUK family members, Dlg and Lin-2/CASK, in controlling these processes. In addition, our recent genetic analysis of mouse Dlg, in combination with genetic and biochemical studies of Lin-2/CASK by others suggests a model placing Dlg and Lin-2/CASK within the same developmental pathway.
MeSH term(s)	Animals ; Caenorhabditis elegans/embryology ; Calcium-Calmodulin-Dependent Protein Kinases ; Drosophila Proteins ; Drosophila melanogaster/embryology ; Epithelial Cells/cytology ; Gene Expression Regulation, Developmental ; Genetic Linkage ; Guanylate Kinases ; Helminth Proteins/physiology ; Insect Proteins/genetics ; Insect Proteins/physiology ; Membrane Proteins/physiology ; Mice ; Models, Biological ; Models, Genetic ; Nucleoside-Phosphate Kinase/genetics ; Nucleoside-Phosphate Kinase/physiology ; Protein Structure, Tertiary ; Proteins/genetics ; Proteins/physiology ; Signal Transduction ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/physiology ; src Homology Domains
Chemical Substances	Drosophila Proteins ; Helminth Proteins ; Insect Proteins ; Lin-2 protein, C elegans ; Membrane Proteins ; Proteins ; Tumor Suppressor Proteins ; dlg1 protein, Drosophila (143513-41-1) ; CASK kinases (EC 2.7.11.1) ; Calcium-Calmodulin-Dependent Protein Kinases (EC 2.7.11.17) ; Nucleoside-Phosphate Kinase (EC 2.7.4.4) ; Guanylate Kinases (EC 2.7.4.8)
Language	English
Publishing date	2002-04-18
Publishing country	Spain
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1036070-0
ISSN	1696-3547 ; 0214-6282
ISSN (online)	1696-3547
ISSN	0214-6282
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3202: 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: The origin of renal fibroblasts/myofibroblasts and the signals that trigger fibrosis.

Sun, Yu Bo Yang / Qu, Xinli / Caruana, Georgina / Li, Jinhua

Differentiation; research in biological diversity

2016 Volume 92, Issue 3, Page(s) 102–107

Abstract: Renal fibrosis is a common characteristic of chronic kidney disease (CKD). Aberrant and excessive depositions of extracellular matrix (ECM) proteins in both glomeruli and interstitial regions are typical hallmarks of renal fibrosis and amplify the ... ...

Abstract	Renal fibrosis is a common characteristic of chronic kidney disease (CKD). Aberrant and excessive depositions of extracellular matrix (ECM) proteins in both glomeruli and interstitial regions are typical hallmarks of renal fibrosis and amplify the severity of kidney injury. To date, an approved therapy specifically targeted to renal fibrosis is needed to mitigate or even retard renal fibrosis. Recent findings have identified a unique population of myofibroblasts as a primary source of ECM in scar tissue formation. However, the origin of myofibroblasts in renal fibrosis remains the subject of controversial debates. The advancement in lineage tracing and immunofluorescent microscopy technologies have suggested that myofibroblasts may arise from a number of sources such as activated renal fibroblasts, pericytes, epithelial-to-mesenchymal transition (EMT), endothelial-to-mesenchymal transition (EndoMT), bone marrow derived cells and fibrocytes. Recent studies also indicate that multiple ligands of TGF-β/Smads are the direct mediators for renal fibrosis. Consistently, inhibition of the TGF-β/Smads signaling pathway using various strategies significantly reduce renal fibrotic lesions and ameliorate kidney injury, suggesting that targeting the TGF-β/Smads signaling pathway could be a new strategy for effective therapies. In this review, we will briefly discuss the diverse origins of myofibroblasts and molecular pathways triggering renal fibrosis. Prospective therapeutic approaches based on those molecular mechanisms will hopefully offer exciting insights in the development of new therapeutic interventions for patients in the near future.
MeSH term(s)	Animals ; Epithelial-Mesenchymal Transition/physiology ; Fibroblasts/metabolism ; Fibrosis/diagnosis ; Fibrosis/pathology ; Humans ; Kidney/metabolism ; Kidney/pathology ; Kidney Diseases/metabolism ; Kidney Diseases/pathology ; Myofibroblasts/pathology
Language	English
Publishing date	2016-09
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	184540-8
ISSN	1432-0436 ; 0301-4681
ISSN (online)	1432-0436
ISSN	0301-4681
DOI	10.1016/j.diff.2016.05.008
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1170: 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: Glomerular endothelial cell injury and damage precedes that of podocytes in adriamycin-induced nephropathy.

Sun, Yu Bo Yang / Qu, Xinli / Zhang, Xueming / Caruana, Georgina / Bertram, John F / Li, Jinhua

PloS one

2013 Volume 8, Issue 1, Page(s) e55027

Abstract: The role of podocytes in the development and progression of glomerular disease has been extensively investigated in the past decade. However, the importance of glomerular endothelial cells in the pathogenesis of proteinuria and glomerulosclerosis has ... ...

Abstract	The role of podocytes in the development and progression of glomerular disease has been extensively investigated in the past decade. However, the importance of glomerular endothelial cells in the pathogenesis of proteinuria and glomerulosclerosis has been largely ignored. Recent studies have demonstrated that endothelial nitric oxide synthatase (eNOS) deficiency exacerbates renal injury in anti-GBM and remnant kidney models and accelerates diabetic kidney damage. Increasing evidence also demonstrates the importance of the glomerular endothelium in preventing proteinuria. We hypothesize that endothelial dysfunction can initiate and promote the development and progression of glomerulopathy. Administration of adriamycin (ADR) to C57BL/6 mice, normally an ADR resistant strain, with an eNOS deficiency induced overt proteinuria, severe glomerulosclerosis, interstitial fibrosis and inflammation. We also examined glomerular endothelial cell and podocyte injury in ADR-induced nephropathy in Balb/c mice, an ADR susceptible strain, by immunostaining, TUNEL and Western blotting. Interestingly, down-regulation of eNOS and the appearance of apoptotic glomerular endothelial cells occurred as early as 24 hours after ADR injection, whilst synaptopodin, a functional podocyte marker, was reduced 7 days after ADR injection and coincided with a significant increase in the number of apoptotic podocytes. Furthermore, conditioned media from mouse microvascular endothelial cells over-expressing GFP-eNOS protected podocytes from TNF-α-induced loss of synaptopodin. In conclusion, our study demonstrated that endothelial dysfunction and damage precedes podocyte injury in ADR-induced nephropathy. Glomerular endothelial cells may protect podocytes from inflammatory insult. Understanding the role of glomerular endothelial dysfunction in the development of kidney disease will facilitate in the design of novel strategies to treat kidney disease.
MeSH term(s)	Animals ; Blotting, Western ; Culture Media, Conditioned ; Doxorubicin/toxicity ; Endothelium, Vascular/enzymology ; Endothelium, Vascular/pathology ; In Situ Nick-End Labeling ; Kidney/drug effects ; Kidney Glomerulus/pathology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Microscopy, Confocal ; Nitric Oxide Synthase Type III/metabolism ; Podocytes/pathology
Chemical Substances	Culture Media, Conditioned ; Doxorubicin (80168379AG) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
Language	English
Publishing date	2013-01-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0055027
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: Imaging the embryonic kidney.

Caruana, Georgina / Young, Richard J / Bertram, John F

Nephron. Experimental nephrology

2006 Volume 103, Issue 2, Page(s) e62–8

Abstract: The structural and functional development of the permanent mammalian kidney or metanephros is a complex process involving the actions of thousands of gene products, complex cell movements and tissue patterning in three dimensions (3D). This review ... ...

Abstract	The structural and functional development of the permanent mammalian kidney or metanephros is a complex process involving the actions of thousands of gene products, complex cell movements and tissue patterning in three dimensions (3D). This review focuses on the recent advances made in imaging technology, processing and analysis combined with mouse genetics and the generation of protein-reporter mice which has enabled us to monitor the development and movement of defined cell populations within the developing kidney in 3D and over time (4D).
MeSH term(s)	Animals ; Databases as Topic ; Diagnostic Imaging ; Embryonic Development ; Imaging, Three-Dimensional ; Kidney/embryology ; Microscopy, Electron ; Microscopy, Fluorescence, Multiphoton ; Microscopy, Phase-Contrast
Language	English
Publishing date	2006
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	207121-6
ISSN	1660-2129 ; 1423-0186 ; 2235-3186 ; 1660-8151 ; 0028-2766
ISSN (online)	1660-2129 ; 1423-0186 ; 2235-3186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000090618
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 169: 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 ▾

Article ; Online: High nephron endowment protects against salt-induced hypertension.

Walker, Kenneth A / Cai, Xiaochu / Caruana, Georgina / Thomas, Merlin C / Bertram, John F / Kett, Michelle M

American journal of physiology. Renal physiology

2012 Volume 303, Issue 2, Page(s) F253–8

Abstract: While low nephron number is associated with increased risk of developing cardiovascular and renal disease, the functional consequences of a high nephron number are unknown. We tested the hypothesis that a high nephron number provides protection against ... ...

Abstract	While low nephron number is associated with increased risk of developing cardiovascular and renal disease, the functional consequences of a high nephron number are unknown. We tested the hypothesis that a high nephron number provides protection against hypertensive and renal insults. Mean arterial pressure (MAP) and renal function were characterized in male wild-type (WT) and transforming growth factor-β2 heterozygous (Tgfb2(+/-)) mice under basal conditions and following a chronic high-salt diet. Kidneys were collected for unbiased stereological analysis. Baseline MAP and renal function were indistinguishable between genotypes. The chronic high-salt diet (5% NaCl for 4 wk followed by 8% NaCl for 4 wk) led to similar step-wise increases in urine volume, Na(+) excretion, and albuminuria in the genotypes. The 5% NaCl diet induced modest and similar increases in MAP (3.5 ± 1.6 and 3.4 ± 0.8 mmHg in WT and Tgfb2(+/-), respectively). After the step up to the 8% NaCl diet, MAP increased further in WT (+15.9 ± 5.1 mmHg), but not Tgfb2(+/-) (-0.1 ± 1.0 mmHg), mice. Nephron number was 30% greater in Tgfb2(+/-) than WT mice and was not affected by the chronic high-salt diet. Mean glomerular volume was lower in Tgfb2(+/-) than WT mice, and the chronic high-salt diet induced significant glomerular hypertrophy. In a separate cohort of mice, an acute, 7-day, 8% NaCl diet induced similar rises in MAP in the genotypes. This is the first study to examine the physiological characteristics of a model of high nephron number, and the findings are consistent with this phenotype providing protection against chronic, but not acute, hypertensive insults.
MeSH term(s)	Animals ; Blood Pressure/drug effects ; Blood Pressure/physiology ; Cell Count ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Genotype ; Heterozygote ; Hypertension/chemically induced ; Hypertension/pathology ; Hypertension/prevention & control ; Male ; Mice ; Mice, Mutant Strains ; Nephrons/cytology ; Nephrons/drug effects ; Nephrons/physiology ; Phenotype ; Sodium Chloride/adverse effects ; Sodium Chloride/pharmacology ; Transforming Growth Factor beta2/genetics ; Transforming Growth Factor beta2/physiology
Chemical Substances	Tgfb2 protein, mouse ; Transforming Growth Factor beta2 ; Sodium Chloride (451W47IQ8X)
Language	English
Publishing date	2012-07-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00028.2012
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: 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: Regulation of renal fibrosis by Smad3 Thr388 phosphorylation.

Qu, Xinli / Li, Xueling / Zheng, Yaowu / Ren, Yi / Puelles, Victor G / Caruana, Georgina / Nikolic-Paterson, David J / Li, Jinhua

The American journal of pathology

2014 Volume 184, Issue 4, Page(s) 944–952

Abstract: Transforming growth factor-β (TGF-β) promotes tissue fibrosis via receptor-mediated phosphorylation of the receptor-activated Smad2/3, together with Smad4. Of these, Smad3 plays a major profibrotic role in mouse models of tissue fibrosis. Transcriptional ...

Abstract	Transforming growth factor-β (TGF-β) promotes tissue fibrosis via receptor-mediated phosphorylation of the receptor-activated Smad2/3, together with Smad4. Of these, Smad3 plays a major profibrotic role in mouse models of tissue fibrosis. Transcriptional activity of the Smad3 protein is regulated by phosphorylation of residues in the C-terminal domain and the linker region. Herein, we examined the role of a novel phosphorylation site within the MH2 domain (T388) in the regulation of Smad3 activity. Confocal microscopy using an Smad3 phosphorylated T388-specific antibody identified phosphorylation of Smad3 T388 in myofibroblasts and tubular epithelial cells in human focal and segmental glomerulosclerosis and mouse models of unilateral ureteric obstruction and diabetic nephropathy, whereas phosphorylated T388 was largely absent in normal kidney. In vitro, TGF-β1 induced phosphorylation of Smad3 T388 in a biphasic pattern. A point mutation of T388/V in an Smad3 construct demonstrated that phosphorylation of T388 promotes Smad3 binding to Smad4 and CDK8, but was not necessary for nuclear translocation. Furthermore, T388 phosphorylation was required for TGF-β-induced collagen I gene promoter activity and extracellular matrix production in cultured fibroblasts. In conclusion, our study identifies phosphorylation of T388 in the Smad3 MH2 domain as an important mechanism that regulates the profibrotic TGF-β/Smad3 signaling pathway, which has direct relevance to human and experimental fibrotic kidney disease.
MeSH term(s)	Animals ; Blotting, Western ; Fibrosis/metabolism ; Humans ; Immunoprecipitation ; Kidney Diseases/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microscopy, Confocal ; Phosphorylation ; Protein Structure, Tertiary ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/physiology ; Smad3 Protein/metabolism ; Transforming Growth Factor beta/metabolism
Chemical Substances	SMAD3 protein, human ; Smad3 Protein ; Smad3 protein, mouse ; Transforming Growth Factor beta
Language	English
Publishing date	2014-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2013.12.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Ud II Zs.76: 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 ▾

Article ; Online: Copy-number variation associated with congenital anomalies of the kidney and urinary tract.

Caruana, Georgina / Wong, Milagros N / Walker, Amanda / Heloury, Yves / Webb, Nathalie / Johnstone, Lilian / James, Paul A / Burgess, Trent / Bertram, John F

Pediatric nephrology (Berlin, Germany)

2014 Volume 30, Issue 3, Page(s) 487–495

Abstract: Background: The most common cause of end-stage renal disease in children can be attributed to congenital anomalies of the kidney and urinary tract (CAKUT). Despite this high incidence of disease, the genetic mutations responsible for the majority of ... ...

Abstract	Background: The most common cause of end-stage renal disease in children can be attributed to congenital anomalies of the kidney and urinary tract (CAKUT). Despite this high incidence of disease, the genetic mutations responsible for the majority of CAKUT cases remain unknown. Methods: To identify novel genomic regions associated with CAKUT, we screened 178 children presenting with the entire spectrum of structural anomalies associated with CAKUT for submicroscopic chromosomal imbalances (deletions or duplications) using single-nucleotide polymorphism (SNP) microarrays. Results: Copy-number variation (CNV) was detected in 10.1 % (18/178) of the patients; in 6.2 % of the total cohort, novel duplications or deletions of unknown significance were identified, and the remaining 3.9 % harboured CNV of known pathogenicity. CNVs were inherited in 90 % (9/10) of the families tested. In this cohort, patients diagnosed with multicystic dysplastic kidney (30 %) and posterior urethral valves (24 %) had a higher incidence of CNV. Conclusions: The genes contained in the altered genomic regions represent novel candidates for CAKUT. This study has demonstrated that a significant proportion of patients with CAKUT harbour submicroscopic chromosomal imbalances, warranting screening in clinics for CNV.
MeSH term(s)	Adolescent ; Child ; Child, Preschool ; DNA Copy Number Variations ; Female ; Humans ; Infant ; Infant, Newborn ; Male ; Polymorphism, Single Nucleotide ; Urogenital Abnormalities/genetics ; Vesico-Ureteral Reflux/genetics
Language	English
Publishing date	2014-10-01
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-014-2962-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2196: 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 ▾

Article ; Online: The Smad3/Smad4/CDK9 complex promotes renal fibrosis in mice with unilateral ureteral obstruction.

Qu, Xinli / Jiang, Mengjie / Sun, Yu Bo Yang / Jiang, Xiaoyun / Fu, Ping / Ren, Yi / Wang, Die / Dai, Lie / Caruana, Georgina / Bertram, John F / Nikolic-Paterson, David J / Li, Jinhua

Kidney international

2015 Volume 88, Issue 6, Page(s) 1323–1335

Abstract: Transforming growth factor-β1 (TGF-β1)/Smad signaling has a central role in the pathogenesis of renal fibrosis. Smad3 and Smad4 are pro-fibrotic, while Smad2 is anti-fibrotic. However, these Smads form heterogeneous complexes, the functions of which are ... ...

Abstract	Transforming growth factor-β1 (TGF-β1)/Smad signaling has a central role in the pathogenesis of renal fibrosis. Smad3 and Smad4 are pro-fibrotic, while Smad2 is anti-fibrotic. However, these Smads form heterogeneous complexes, the functions of which are poorly understood. Here we studied Smad complex function in renal fibrosis using the mouse model of unilateral ureteric obstruction. Mice heterozygous for Smad3/4 (Smad3/4
Language	English
Publishing date	2015-12
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	10.1038/ki.2015.235
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

To top

Full text online

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

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

Full text online

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

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

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