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  • 1
    Keywords: CELLS ; Germany ; VENTILATION ; GENE ; GENES ; PROTEIN ; METABOLISM ; MICE ; FAMILY ; BINDING ; DOWN-REGULATION ; NK cells ; PHENOTYPE ; RAT-BRAIN ; THYROID-HORMONE ; LEVEL ; function ; ANTAGONISTS ; BROWN ADIPOSE-TISSUE ; CEREBRAL-CORTEX ; MODIFIED HOLE BOARD ; PRECHORDAL PLATE ; REDUCED EXPRESSION ; TYPE-2 IODOTHYRONINE DEIODINASE ; ZEBRAFISH DKK1
    Abstract: dickkopf (dkk) genes encode a small family of secreted Wnt antagonists, except for dkk3, which is divergent and whose function is poorly understood. Here, we describe the generation and characterization of dkk3 mutant mice. dkk3-deficient mice are viable and fertile. Phenotypic analysis shows no major alterations in organ morphology, physiology, and most clinical chemistry parameters. Since Dkk3 was proposed to function as thyroid hormone binding protein, we have analyzed deiodinase activities, as well as thyroid hormone levels. Mutant mice are euthyroid, and the data do not support a relationship of dkk3 with thyroid hormone metabolism. Altered phenotypes in dkk3 mutant mice were observed in the frequency of NK cells, immunoglobulin M, hemoglobin, and hematocrit levels, as well as lung ventilation. Furthermore, dkk3-deficient mice display hyperactivity
    Type of Publication: Journal article published
    PubMed ID: 16508007
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  • 2
    Keywords: CELLS ; EXPRESSION ; DOWN-REGULATION ; STEM-CELLS ; dkk1 ; HEAD INDUCTION ; Wnt signalling ; Lrp6 ; WNT/BETA-CATENIN ; Cre-loxP ; EPITHELIAL TRANSFORMATION ; Kidney papilla ; MAJOR URINARY PROTEINS ; METANEPHRIC MESENCHYME ; Pax3Cre ; Pax8Cre ; Wnt-4 ; Wnt-4Cre ; Wnt-7b
    Abstract: Wnt signalling regulates several aspects of kidney development such as nephrogenesis, ureteric bud branching and organisation of the collecting duct cells. We addressed the potential involvement of Dickkopf-1 (Dkk1), a secreted Wnt pathway antagonist. Dkk1 is expressed in the developing mouse kidney by pretubular cell aggregates and the nephrons derived from them. Besides the mesenchyme cells, the epithelial ureteric bud and more mature ureteric bud derivatives in the medulla and the papilla tip express the Dkk1 gene. To reveal the potential roles of Dkk1, we generated a floxed allele and used three Cre lines to inactivate Dkk1 function in the developing kidney. Interestingly. Dkk1 deficiency induced by Pax8Cre in the kidneys led in newborn mice to an overgrown papilla that was generated by stimulated proliferation of the collecting duct and loop of Henle cells, implying a role for Dkkl in the collecting duct and/or loop of Henle development. Since Pax8Cre-induced Dkkl deficiency reduced marker gene expression, Scnn1b in the collecting duct and Slc12a1 in the loop of Henle, these results together with the extended papilla phenotype are likely reasons for the decreased amount of ions and urine produced by Dkk1-deficient kidneys in the adult. Recombinant Dkk1 protein in cultured cells inhibited Wnt-7b-induced canonical Wnt signalling, which is critical for collecting duct and loop of Henle development. Moreover, Dkk1 deficiency led to an increase in the expression of canonical Wnt signalling of target Lef-1 gene expression in the stromal cells of the developing papilla. Based on the results, we propose that Dkk1 controls the degree of Wnt-7b signalling in the papilla to coordinate kidney organogenesis.
    Type of Publication: Journal article published
    PubMed ID: 21354128
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