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  1. Book ; Online ; Thesis: The regulation of VPS34 and WNK1 kinase in the proximal tubule of the kidney in health and disease

    Zanon Rodriguez, Luis Verfasser] / [Theilig, Franziska [Akademischer Betreuer] / Roeder, Thomas [Gutachter]

    2023  

    Author's details Luis Zanon Rodriguez ; Gutachter: Thomas Roeder ; Betreuer: Franziska Theilig
    Keywords Naturwissenschaften ; Science
    Subject code sg500
    Language English
    Publisher Universitätsbibliothek Kiel
    Publishing place Kiel
    Document type Book ; Online ; Thesis
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  2. Book ; Online ; Thesis: Untersuchungen des Einflusses von Phosphorylierungen des Endozytose-Rezeptors Megalin sowie von Diabetes und Hypoxie auf die Funktion des proximalen Tubulus

    Kunke, Madlen Verfasser] / [Theilig, Franziska [Akademischer Betreuer] / Roeder, Thomas [Gutachter]

    2022  

    Author's details Madlen Kunke ; Gutachter: Thomas Roeder ; Betreuer: Franziska Theilig
    Keywords Biowissenschaften, Biologie ; Life Science, Biology
    Subject code sg570
    Language German
    Publisher Universitätsbibliothek Kiel
    Publishing place Kiel
    Document type Book ; Online ; Thesis
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  3. Article ; Online: Tubular

    Dahlke, Eileen / Engmann, Toni / Anan, Yaman / Häsler, Robert / Solinas, Giovanni / Theilig, Franziska

    International journal of molecular sciences

    2022  Volume 23, Issue 17

    Abstract: Acute kidney injury (AKI) is a common renal injury leading to relevant morbidity and mortality worldwide. Most of the clinical cases of AKI are caused by ischemia reperfusion (I/R) injury with renal ischemia injury followed by reperfusion injury and ... ...

    Abstract Acute kidney injury (AKI) is a common renal injury leading to relevant morbidity and mortality worldwide. Most of the clinical cases of AKI are caused by ischemia reperfusion (I/R) injury with renal ischemia injury followed by reperfusion injury and activation of the innate immune response converging to NF-ĸB pathway induction. Despite the clear role of NF-ĸB in inflammation, it has recently been acknowledged that NF-ĸB may impact other cell functions. To identify NF-ĸB function with respect to metabolism, vascular function and oxidative stress after I/R injury and to decipher in detail the underlying mechanism, we generated a transgenic mouse model with targeted deletion of IKKβ along the tubule and applied I/R injury followed by its analysis after 2 and 14 days after I/R injury. Tubular IKKβ deletion ameliorated renal function and reduced tissue damage. RNAseq data together with immunohistochemical, biochemical and morphometric analysis demonstrated an ameliorated vascular organization and mRNA expression profile for increased angiogenesis in mice with tubular IKKβ deletion at 2 days after I/R injury. RNAseq and protein analysis indicate an ameliorated metabolism, oxidative species handling and timely-adapted cell proliferation and apoptosis as well as reduced fibrosis in mice with tubular IKKβ deletion at 14 days after I/R injury. In conclusion, mice with tubular IKKβ deletion upon I/R injury display improved renal function and reduced tissue damage and fibrosis in association with improved vascularization, metabolism, reactive species disposal and fine-tuned cell proliferation.
    MeSH term(s) Acute Kidney Injury/genetics ; Acute Kidney Injury/metabolism ; Animals ; Apoptosis/genetics ; Fibrosis ; I-kappa B Kinase/genetics ; Ischemia ; Kidney/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; NF-kappa B/metabolism ; Reperfusion Injury/genetics
    Chemical Substances NF-kappa B ; I-kappa B Kinase (EC 2.7.11.10)
    Language English
    Publishing date 2022-09-05
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms231710199
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  4. Article ; Online: Megalin Orchestrates FcRn Endocytosis and Trafficking.

    Dahlke, Eileen / Anan, Yaman / Klie, Lea Maximiliane / Hartkopf, Ariane Elisabeth / Theilig, Franziska

    Cells

    2022  Volume 12, Issue 1

    Abstract: The neonatal Fc receptor (FcRn) is highly expressed in the renal proximal tubule and is important for the reclamation of albumin by cellular transcytosis to prevent its loss in the urine. The initial event of this transcellular transport mechanism is the ...

    Abstract The neonatal Fc receptor (FcRn) is highly expressed in the renal proximal tubule and is important for the reclamation of albumin by cellular transcytosis to prevent its loss in the urine. The initial event of this transcellular transport mechanism is the endocytosis of albumin by the apical scavenger receptors megalin and cubilin. An interaction of megalin and FcRn was postulated, however, evidence is still missing. Similarly, the intracellular trafficking of FcRn remains unknown and shall be identified in our study. Using a Venus-based bimolecular fluorescence complementation system, we detected an interaction between megalin and FcRn in the endosomal compartment, which significantly increased with the induction of endocytosis using albumin or lactoglobulin as a ligand. The interaction between megalin and FcRn occurred at a neutral and acidic pH between the extracellular domains of both proteins. Amnionless, another transmembrane acceptor of cubilin, revealed no interaction with FcRn. With the induction of endocytosis by albumin or lactoglobulin, super resolution microscopy demonstrated a redistribution of megalin and FcRn into clathrin vesicles and early endosomes. This trafficking into clathrin vesicles was impaired in megalin-deficient cells upon albumin-induced endocytosis, supporting the role of megalin in FcRn redistribution. Our results indicate that megalin and FcRn specifically bind and interact within their extracellular domains. The availability of megalin is necessary for the redistribution of FcRn. Megalin, therefore, orchestrates FcRn endocytosis and intracellular trafficking as an early event intranscytosis.
    MeSH term(s) Albumins/metabolism ; Clathrin ; Endocytosis ; Ligands ; Low Density Lipoprotein Receptor-Related Protein-2/metabolism ; Protein Transport
    Chemical Substances Albumins ; Clathrin ; Ligands ; Low Density Lipoprotein Receptor-Related Protein-2
    Language English
    Publishing date 2022-12-22
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12010053
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  5. Article ; Online: Spread of glomerular to tubulointerstitial disease with a focus on proteinuria.

    Theilig, Franziska

    Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft

    2010  Volume 192, Issue 3, Page(s) 125–132

    Abstract: Chronic kidney disease is characterized by the decline in renal excretory, homeostatic and endocrine functions. In most instances, the primary event is glomerular injury. With ongoing progression and glomerular extracapillary proliferation, ... ...

    Abstract Chronic kidney disease is characterized by the decline in renal excretory, homeostatic and endocrine functions. In most instances, the primary event is glomerular injury. With ongoing progression and glomerular extracapillary proliferation, tubulointerstitial damage occurs with consequent nephron loss and development of fibrotic lesions, finally resulting in terminal renal failure. Renal tubulointerstitial damage is the final common pathway in all forms of renal disease leading to CKD. Recent research has focused on how glomerular injury spreads to the tubulointerstitium. Presently, four possible mechanisms are being discussed: (1) obstruction of the urinary pole; (2) proteinuria-induced overload of the proximal tubule; (3) chronic hypoxia and (4) inflammation induced by a glomerulotubular feedback loop. Fibrosis is hypothesized to account for further deterioration of renal functions. As to the role of fibrosis, conflicting results have been published and new data question the damaging character of fibrosis.
    MeSH term(s) Chronic Disease ; Disease Progression ; Epithelial Cells/pathology ; Fibrosis/pathology ; Humans ; Hypoxia/pathology ; Kidney/pathology ; Kidney Failure, Chronic/etiology ; Kidney Failure, Chronic/pathology ; Kidney Glomerulus/pathology ; Kidney Tubules, Proximal/pathology ; Nephritis, Interstitial/pathology ; Nephrons/pathology ; Proteinuria/etiology ; Proteinuria/pathology
    Language English
    Publishing date 2010-05-20
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1106738-x
    ISSN 1618-0402 ; 0940-9602
    ISSN (online) 1618-0402
    ISSN 0940-9602
    DOI 10.1016/j.aanat.2010.03.003
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  6. Book ; Online ; Thesis: Interaktion der Metalloprotease Meprin β mit dem Zelloberflächenprotein CD99 und den CD99-Varianten D92H und D92Y

    Bedau, Tillmann [Verfasser] / Becker-Pauly, Christoph [Akademischer Betreuer] / Theilig, Franziska [Gutachter]

    2021  

    Author's details Tillmann Bedau ; Gutachter: Franziska Theilig ; Betreuer: Christoph Becker-Pauly
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Publisher Universitätsbibliothek Kiel
    Publishing place Kiel
    Document type Book ; Online ; Thesis
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  7. Book ; Online ; Thesis: Regulation von K2P-Kanälen durch Membranspannung, Pharmaka und Membranlipide

    Jürs, Björn Christian [Verfasser] / Baukrowitz, Thomas [Akademischer Betreuer] / Theilig, Franziska [Gutachter]

    2021  

    Author's details Björn Christian Jürs ; Gutachter: Franziska Theilig ; Betreuer: Thomas Baukrowitz
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Publisher Universitätsbibliothek Kiel
    Publishing place Kiel
    Document type Book ; Online ; Thesis
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  8. Article ; Online: ANP-induced signaling cascade and its implications in renal pathophysiology.

    Theilig, Franziska / Wu, Qingyu

    American journal of physiology. Renal physiology

    2015  Volume 308, Issue 10, Page(s) F1047–55

    Abstract: The balance between vasoconstrictor/sodium-retaining and vasodilator/natriuretic systems is essential for maintaining body fluid and electrolyte homeostasis. Natriuretic peptides, such as atrial natriuretic peptide (ANP), belong to the vasodilator/ ... ...

    Abstract The balance between vasoconstrictor/sodium-retaining and vasodilator/natriuretic systems is essential for maintaining body fluid and electrolyte homeostasis. Natriuretic peptides, such as atrial natriuretic peptide (ANP), belong to the vasodilator/natriuretic system. ANP is produced by the conversion of pro-ANP into ANP, which is achieved by a proteolytical cleavage executed by corin. In the kidney, ANP binds to the natriuretic peptide receptor-A (NPR-A) and enhances its guanylyl cyclase activity, thereby increasing intracellular cyclic guanosine monophosphate production to promote natriuretic and renoprotective responses. In the glomerulus, ANP increases glomerular permeability and filtration rate and antagonizes the deleterious effects of the renin-angiotensin-aldosterone system activation. Along the nephron, natriuretic and diuretic actions of ANP are mediated by inhibiting the basolaterally expressed Na(+)-K(+)-ATPase, reducing apical sodium, potassium, and protein organic cation transporter in the proximal tubule, and decreasing Na(+)-K(+)-2Cl(-) cotransporter activity and renal concentration efficiency in the thick ascending limb. In the medullary collecting duct, ANP reduces sodium reabsorption by inhibiting the cyclic nucleotide-gated cation channels, the epithelial sodium channel, and the heteromeric channel transient receptor potential-vanilloid 4 and -polycystin 2 and diminishes vasopressin-induced water reabsorption. Long-term ANP treatment may lead to NPR-A desensitization and ANP resistance, resulting in augmented sodium and water reabsorption. In mice, corin deficiency impairs sodium excretion and causes salt-sensitive hypertension. Characteristics of ANP resistance and corin deficiency are also encountered in patients with edema-associated diseases, highlighting the importance of ANP signaling in salt-water balance and renal pathophysiology.
    MeSH term(s) Animals ; Atrial Natriuretic Factor/physiology ; Glomerular Filtration Rate/physiology ; Humans ; Kidney/physiopathology ; Mice ; Models, Animal ; Serine Endopeptidases/physiology ; Signal Transduction/physiology ; Water-Electrolyte Balance/physiology
    Chemical Substances Atrial Natriuretic Factor (85637-73-6) ; CORIN protein, human (EC 3.4.21.-) ; Corin protein, mouse (EC 3.4.21.-) ; Serine Endopeptidases (EC 3.4.21.-)
    Language English
    Publishing date 2015-05-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00164.2014
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    Uc I Zs.89: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  9. Book ; Online ; Thesis: Parakrine Signalwege der Niere

    Theilig, Franziska

    zelluläre Verteilung und Interaktion von NO- und Protaglandinsynthese

    2005  

    Author's details gvon Franziska Theilig
    Language German
    Size Online-Ressource
    Document type Book ; Online ; Thesis
    Thesis / German Habilitation thesis Humboldt-Univ., Diss--Berlin, 2005
    Database Former special subject collection: coastal and deep sea fishing

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  10. Article ; Online: JNK1 ablation improves pancreatic β-cell mass and function in db/db diabetic mice without affecting insulin sensitivity and adipose tissue inflammation.

    Mazzoli, Arianna / Sardi, Claudia / Breasson, Ludovic / Theilig, Franziska / Becattini, Barbara / Solinas, Giovanni

    FASEB bioAdvances

    2020  Volume 3, Issue 2, Page(s) 94–107

    Abstract: The cJun N-terminal Kinases (JNK) emerged as a major link between obesity and insulin resistance, but their role in the loss of pancreatic β-cell mass and function driving the progression from insulin resistance to type-2 diabetes and in the ... ...

    Abstract The cJun N-terminal Kinases (JNK) emerged as a major link between obesity and insulin resistance, but their role in the loss of pancreatic β-cell mass and function driving the progression from insulin resistance to type-2 diabetes and in the complications of diabetes was not investigated to the same extent. Furthermore, it was shown that pan-JNK inhibition exacerbates kidney damage in the db/db model of obesity-driven diabetes. Here we investigate the role of JNK1 in the db/db model of obesity-driven type-2 diabetes. Mice with systemic ablation of JNK1 (JNK1
    Language English
    Publishing date 2020-12-30
    Publishing country United States
    Document type Journal Article
    ISSN 2573-9832
    ISSN (online) 2573-9832
    DOI 10.1096/fba.2020-00081
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