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  1. Article: A few kind words for the Devil.

    Schnaper, N / Schnaper, H W

    Journal of religion and health

    2014  Volume 8, Issue 2, Page(s) 107–122

    Language English
    Publishing date 2014-01-13
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2017250-3
    ISSN 1573-6571 ; 0022-4197
    ISSN (online) 1573-6571
    ISSN 0022-4197
    DOI 10.1007/BF01533140
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Antithrombin III, protein S, and coagulation in the nephrotic syndrome.

    Schnaper, H W

    Pediatric nephrology (Berlin, Germany)

    2001  Volume 16, Issue 1, Page(s) 98

    MeSH term(s) Antithrombin III/analysis ; Blood Coagulation ; Child ; Humans ; Nephrotic Syndrome/blood ; Protein S/analysis
    Chemical Substances Protein S ; Antithrombin III (9000-94-6)
    Language English
    Publishing date 2001-01
    Publishing country Germany
    Document type Comment ; Letter
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  3. Article: Signal transduction through protein kinase C.

    Schnaper, H W

    Pediatric nephrology (Berlin, Germany)

    2000  Volume 14, Issue 3, Page(s) 254–258

    MeSH term(s) Gene Expression Regulation, Developmental ; Glomerular Mesangium/cytology ; Glomerular Mesangium/enzymology ; Humans ; Kidney Glomerulus/blood supply ; Kidney Tubules/physiology ; Protein Kinase C/physiology ; Proteins/physiology ; Regional Blood Flow/physiology ; Signal Transduction ; TRPP Cation Channels
    Chemical Substances Proteins ; TRPP Cation Channels ; polycystic kidney disease 1 protein ; Protein Kinase C (EC 2.7.11.13)
    Language English
    Publishing date 2000-03
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s004670050050
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Cell signal transduction through the mitogen-activated protein kinase pathway.

    Schnaper, H W

    Pediatric nephrology (Berlin, Germany)

    1998  Volume 12, Issue 9, Page(s) 790–795

    MeSH term(s) Animals ; Calcium-Calmodulin-Dependent Protein Kinases/physiology ; Humans ; Kidney/cytology ; Kidney/enzymology ; MAP Kinase Kinase Kinases ; Mitogen-Activated Protein Kinase Kinases ; Protein Kinases/physiology ; Protein-Serine-Threonine Kinases/physiology ; Signal Transduction/physiology
    Chemical Substances Protein Kinases (EC 2.7.-) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Calcium-Calmodulin-Dependent Protein Kinases (EC 2.7.11.17) ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
    Language English
    Publishing date 1998-11
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s004670050550
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  5. Article: Estrogen: it's not just for reproduction any more.

    Schnaper, H W

    Kidney international

    1997  Volume 55, Issue 4, Page(s) 1577–1579

    MeSH term(s) Animals ; Calcium-Calmodulin-Dependent Protein Kinases/physiology ; Collagen/metabolism ; Estradiol/physiology ; Estrogens/physiology ; Female ; Glomerulosclerosis, Focal Segmental/metabolism ; Glomerulosclerosis, Focal Segmental/physiopathology ; Humans ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/physiology ; Mice ; Receptors, Estrogen/physiology ; Signal Transduction/physiology
    Chemical Substances Estrogens ; Receptors, Estrogen ; Estradiol (4TI98Z838E) ; Collagen (9007-34-5) ; Calcium-Calmodulin-Dependent Protein Kinases (EC 2.7.11.17)
    Language English
    Publishing date 1997-06-11
    Publishing country United States
    Document type Comment ; Editorial ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1046/j.1523-1755.1999.00451.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 797: Show issues Location:
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  6. Article ; Online: Serine-204 in the linker region of Smad3 mediates the collagen-I response to TGF-β in a cell phenotype-specific manner.

    Browne, J A / Liu, X / Schnaper, H W / Hayashida, T

    Experimental cell research

    2013  Volume 319, Issue 19, Page(s) 2928–2937

    Abstract: Regulation of TGF-β1/Smad3 signaling in fibrogenesis is complex. Previous work by our lab suggests that ERK MAP kinase phosphorylates the linker region (LR) of Smad3 to enhance TGF-β-induced collagen-I accumulation. However the roles of the individual ... ...

    Abstract Regulation of TGF-β1/Smad3 signaling in fibrogenesis is complex. Previous work by our lab suggests that ERK MAP kinase phosphorylates the linker region (LR) of Smad3 to enhance TGF-β-induced collagen-I accumulation. However the roles of the individual Smad3LR phosphorylation sites (T179, S204, S208 and S213) in the collagen-I response to TGF-β are not clear. To address this issue, we tested the ability of Smad3 constructs expressing wild-type Smad3 or Smad3 with mutated LR phosphorylation sites to reconstitute TGF-β-stimulated COL1A2 promoter activity in Smad3-null or -knockdown cells. Blocking ERK in fibroblasts and renal mesangial cells inhibited both S204 phosphorylation and Smad3-mediated COL1A2 promoter activity. Mutations replacing serine at S204 or S208 in the linker region decreased Smad3-mediated COL1A2 promoter activity, whereas mutating T179 enhanced basal COL1A2 promoter activity and did not prevent TGF-β stimulation. Interestingly, mutation of all four Smad3LR sites (T179, S204, S208 and S213) was not inhibitory, suggesting primacy of the two inhibitory sites. These results suggest that in these mesenchymal cells, phosphorylation of the T179 and possibly S213 sites may act as a brake on the signal, whereas S204 phosphorylation by ERK in some manner releases that brake. Renal epithelial cells (HKC) respond differently from MEF or mesangial cells; blocking ERK neither changed TGF-β-stimulated S204 phosphorylation nor prevented Smad3-mediated COL1A2 promoter activity in HKC. Furthermore, re-expression of wild type-Smad3 or the S204A-Smad3 mutant in Smad3-knockdown HKC reconstituted Smad3-mediated COL1A2 promoter activity. Collectively, these data suggest that Serine-204 phosphorylation in the Smad3LR is a critical event by which ERK enhances Smad3-mediated COL1A2 promoter activity in mesenchymal cells.
    MeSH term(s) Animals ; Cells, Cultured ; Collagen Type I/genetics ; Collagen Type I/metabolism ; Extracellular Signal-Regulated MAP Kinases/genetics ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Mice ; Mutation/genetics ; Phenotype ; Serine/metabolism ; Signal Transduction/physiology ; Smad3 Protein/metabolism ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transcriptional Activation/physiology ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism
    Chemical Substances Collagen Type I ; Smad3 Protein ; Smad3 protein, mouse ; Trans-Activators ; Transforming Growth Factor beta ; Serine (452VLY9402) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2013-09-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1493-x
    ISSN 1090-2422 ; 0014-4827
    ISSN (online) 1090-2422
    ISSN 0014-4827
    DOI 10.1016/j.yexcr.2013.07.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 563: Show issues Location:
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  7. Article: Integrin receptors, the cytoskeleton, and glomerular cell function.

    Schnaper, H W

    Pediatric nephrology (Berlin, Germany)

    1996  Volume 10, Issue 4, Page(s) 523–528

    MeSH term(s) Animals ; Cytoskeleton/physiology ; Cytoskeleton/ultrastructure ; Humans ; Integrins/physiology ; Kidney Glomerulus/cytology ; Kidney Glomerulus/physiology ; Kidney Glomerulus/ultrastructure ; Receptors, Cell Surface/physiology ; Signal Transduction/physiology
    Chemical Substances Integrins ; Receptors, Cell Surface
    Language English
    Publishing date 1996-08
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s004670050156
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  8. Article: Primary nephrotic syndrome of childhood.

    Schnaper, H W

    Current opinion in pediatrics

    1996  Volume 8, Issue 2, Page(s) 141–147

    Abstract: Primary nephrotic syndrome encompasses the spectrum of minimal change disease, focal segmental glomerulosclerosis, and related disorders. It is a common cause of morbidity and, more rarely, of mortality in children. Recent progress has permitted us to ... ...

    Abstract Primary nephrotic syndrome encompasses the spectrum of minimal change disease, focal segmental glomerulosclerosis, and related disorders. It is a common cause of morbidity and, more rarely, of mortality in children. Recent progress has permitted us to better understand the mechanism of proteinuria and how it causes the other findings of nephrosis. Developments related to the pathogenesis of nephrosis and why some patients develop focal segmental glomerulosclerosis are less striking, but recent studies have indicated useful directions for subsequent work in these areas. Finally, application of newer concepts to treatment has provided both a better prognosis for these diseases and decreased morbidity from treatment.
    MeSH term(s) Child ; Cyclosporine/therapeutic use ; Disease Progression ; Glomerulosclerosis, Focal Segmental/physiopathology ; Humans ; Immunosuppressive Agents/therapeutic use ; Kidney/physiopathology ; Nephrotic Syndrome/etiology ; Nephrotic Syndrome/physiopathology ; Nephrotic Syndrome/therapy ; Prognosis
    Chemical Substances Immunosuppressive Agents ; Cyclosporine (83HN0GTJ6D)
    Language English
    Publishing date 1996-04
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
    ZDB-ID 1049374-8
    ISSN 1531-698X ; 1040-8703
    ISSN (online) 1531-698X
    ISSN 1040-8703
    DOI 10.1097/00008480-199604000-00010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Balance between matrix synthesis and degradation: a determinant of glomerulosclerosis.

    Schnaper, H W

    Pediatric nephrology (Berlin, Germany)

    1995  Volume 9, Issue 1, Page(s) 104–111

    Abstract: In glomerular health and disease, the balance between extracellular matrix (ECM) protein synthesis and degradation determines the amount of matrix that accumulates locally. While cell and whole animal regulation of ECM synthesis has been the subject of ... ...

    Abstract In glomerular health and disease, the balance between extracellular matrix (ECM) protein synthesis and degradation determines the amount of matrix that accumulates locally. While cell and whole animal regulation of ECM synthesis has been the subject of ongoing study, attention has become focused on proteases that degrade matrix components only recently. Two major ECM protease systems have been defined. The plasminogen activators (PAs) are serine proteases that have matrix-degrading capability and also activate plasminogen to plasmin. Plasmin not only degrades ECM proteins, but also may activate members of the matrix metalloproteinase (MMP) family which comprise the second major matrix-degrading system. Specific biological antagonists of both the PAs and the MMPs tightly regulate proteolysis by these enzymes. All of these enzymes and inhibitors have been detected in the kidney, and their expression may be altered to facilitate ECM accumulation in conditions associated with matrix expansion, such as glomerulosclerosis. Work is in progress to determine how these systems are regulated in the kidney and to further define their contribution to the sclerotic process.
    MeSH term(s) Animals ; Extracellular Matrix/metabolism ; Extracellular Matrix/physiology ; Extracellular Matrix Proteins/biosynthesis ; Extracellular Matrix Proteins/metabolism ; Glomerulosclerosis, Focal Segmental/metabolism ; Glomerulosclerosis, Focal Segmental/pathology ; Humans ; Kidney/metabolism ; Kidney/pathology
    Chemical Substances Extracellular Matrix Proteins
    Language English
    Publishing date 1995-02
    Publishing country Germany
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/bf00858986
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  10. Article: Call for a registry of complications of immunization in nephrotic children!

    Schnaper, H W

    Pediatric nephrology (Berlin, Germany)

    1994  Volume 8, Issue 1, Page(s) 132

    MeSH term(s) Child, Preschool ; Humans ; Immunization/adverse effects ; Nephrotic Syndrome ; Registries
    Language English
    Publishing date 1994-02
    Publishing country Germany
    Document type Letter
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/bf00868296
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