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Article ; Online: Urinary Acidification Does Not Explain the Absence of Nephrocalcinosis in a Mouse Model of Familial Hypomagnesaemia with Hypercalciuria and Nephrocalcinosis (FHHNC).

Al-Shebel, Amr / Michel, Geert / Breiderhoff, Tilman / Müller, Dominik

International journal of molecular sciences

2024 Volume 25, Issue 3

Abstract: Patients with mutations ... ...

Abstract	Patients with mutations in
MeSH term(s)	Humans ; Animals ; Mice ; Hypercalciuria/genetics ; Nephrocalcinosis/genetics ; Calcium ; Salts ; Magnesium ; Hydrogen-Ion Concentration ; Claudins/genetics
Chemical Substances	Calcium (SY7Q814VUP) ; Salts ; Magnesium (I38ZP9992A) ; Claudins
Language	English
Publishing date	2024-02-01
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/ijms25031779
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Article ; Online: Modulation of intestinal IL-37 expression and its impact on the epithelial innate immune response and barrier integrity.

Kröhn, Laura / Azabdaftari, Aline / Heuberger, Julian / Hudert, Christian / Zilbauer, Matthias / Breiderhoff, Tilman / Bufler, Philip

Frontiers in immunology

2023 Volume 14, Page(s) 1261666

Abstract: Background and aims: Intestinal epithelial cells separate the luminal flora from lamina propria immune cells and regulate innate immune responses in the gut. An imbalance of the mucosal immune response and disrupted intestinal barrier integrity ... ...

Abstract	Background and aims: Intestinal epithelial cells separate the luminal flora from lamina propria immune cells and regulate innate immune responses in the gut. An imbalance of the mucosal immune response and disrupted intestinal barrier integrity contribute to the evolution of inflammatory bowel diseases. Interleukin (IL)-37 has broad anti- inflammatory activity and is expressed by the human intestinal epithelium. Mice ectopically expressing human IL-37 show reduced epithelial damage and inflammation after DSS-induced colitis. Here, we investigated the impact of IL-37 on the innate immune response and tight junction protein expression of mouse intestinal organoids and the modulation of Methods: Murine intestinal organoids were generated from IL-37tg and wildtype mice. Human ileal organoids were generated from healthy young donors. Results: Expression of transgene IL-37 or recombinant IL-37 protein did not significantly reduce overall proinflammatory cytokine mRNA expression in murine intestinal organoids. However, higher Conclusions: We speculate that the anti-inflammatory activity of IL-37 in the intestine is mainly mediated by lamina propria immune cells protecting intestinal epithelial integrity.
MeSH term(s)	Humans ; Mice ; Animals ; Tumor Necrosis Factor-alpha/metabolism ; Intestinal Mucosa ; Immunity, Innate ; Cytokines/metabolism ; RNA, Messenger/metabolism ; Interleukin-1/genetics ; Interleukin-1/metabolism
Chemical Substances	Tumor Necrosis Factor-alpha ; Cytokines ; RNA, Messenger ; IL37 protein, human ; Interleukin-1
Language	English
Publishing date	2023-09-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1261666
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Article ; Online: One gene, two paracellular ion channels-claudin-10 in the kidney.

Milatz, Susanne / Breiderhoff, Tilman

Pflugers Archiv : European journal of physiology

2017 Volume 469, Issue 1, Page(s) 115–121

Abstract: Claudins are tight junction membrane proteins and regulate the paracellular passage of ions and water. They can seal the paracellular cleft against solute passage but also form paracellular channels. They are tetraspan proteins with two extracellular ... ...

Abstract	Claudins are tight junction membrane proteins and regulate the paracellular passage of ions and water. They can seal the paracellular cleft against solute passage but also form paracellular channels. They are tetraspan proteins with two extracellular segments. Claudin-10 exists in at least two functional isoforms, claudin-10a and claudin-10b, that differ in their first transmembrane segment and first extracellular segment. Both isoforms act as selective paracellular ion channels, either for anions (claudin-10a) or for cations (claudin-10b). Their diverse functions are reflected in completely different expression patterns in the body, especially in the kidney. Their structural and functional similarities and differences make them ideal subjects to study determinants of claudin charge selectivity and pore formation. This review aims to summarise research on permeability properties of the claudin-10 channels and their role in physiology and pathophysiology of the kidney.
MeSH term(s)	Animals ; Claudins/genetics ; Claudins/metabolism ; Humans ; Ion Channels/genetics ; Ion Channels/metabolism ; Kidney/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Tight Junctions/metabolism
Chemical Substances	Claudins ; Ion Channels ; Membrane Proteins ; claudin 10
Language	English
Publishing date	2017
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-016-1921-7
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Article ; Online: Furosemide rescues hypercalciuria in familial hypomagnesaemia with hypercalciuria and nephrocalcinosis model.

Kriuchkova, Natalia / Breiderhoff, Tilman / Müller, Dominik / Yilmaz, Duygu Elif / Demirci, Hasan / Drewell, Hoora / Günzel, Dorothee / Himmerkus, Nina / Bleich, Markus / Persson, Pontus B / Mutig, Kerim

Acta physiologica (Oxford, England)

2023 Volume 237, Issue 3, Page(s) e13927

Abstract: Aim: Perturbed calcium homeostasis limits life expectancy in familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC). This rare disease occurs by loss-of-function mutations in CLDN16 or CLDN19 genes, causing impaired paracellular ... ...

Abstract	Aim: Perturbed calcium homeostasis limits life expectancy in familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC). This rare disease occurs by loss-of-function mutations in CLDN16 or CLDN19 genes, causing impaired paracellular reabsorption of divalent cations along the cortical thick ascending limb (cTAL). Only partial compensation takes place in the ensuing late distal convoluted tubule, connecting tubule, and collecting duct, where the luminal transient receptor potential channel V5 (TRPV5), as well as basolateral plasma membrane calcium ATPase (PMCA) and sodium-potassium exchanger (NCX1) mediate transcellular Ca Methods: Cldn16-deficient mice (Cldn16 Results: Cldn16 Conclusions: Furosemide significantly reduces hypercalciuria, likely via upregulation of luminal and basolateral Ca
MeSH term(s)	Animals ; Mice ; Calcium/metabolism ; Carrier Proteins ; Claudins/metabolism ; Furosemide/pharmacology ; Furosemide/therapeutic use ; Hypercalciuria/drug therapy ; Hypercalciuria/metabolism ; Magnesium/metabolism ; Nephrocalcinosis/drug therapy ; Nephrocalcinosis/metabolism
Chemical Substances	Calcium (SY7Q814VUP) ; Carrier Proteins ; Claudins ; Furosemide (7LXU5N7ZO5) ; Magnesium (I38ZP9992A)
Language	English
Publishing date	2023-01-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2218636-0
ISSN	1748-1716 ; 1748-1708
ISSN (online)	1748-1716
ISSN	1748-1708
DOI	10.1111/apha.13927
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Article ; Online: Strikingly conserved gene expression changes of polyamine regulating enzymes among various forms of acute and chronic kidney injury.

Sieckmann, Tobias / Schley, Gunnar / Ögel, Neslihan / Kelterborn, Simon / Boivin, Felix J / Fähling, Michael / Ashraf, Muhammad I / Reichel, Martin / Vigolo, Emilia / Hartner, Andrea / Lichtenberger, Falk-Bach / Breiderhoff, Tilman / Knauf, Felix / Rosenberger, Christian / Aigner, Felix / Schmidt-Ott, Kai / Scholz, Holger / Kirschner, Karin M

Kidney international

2023 Volume 104, Issue 1, Page(s) 90–107

Abstract: The polyamines spermidine and spermine and their common precursor molecule putrescine are involved in tissue injury and repair. Here, we test the hypothesis that impaired polyamine homeostasis contributes to various kidney pathologies in mice during ... ...

Abstract	The polyamines spermidine and spermine and their common precursor molecule putrescine are involved in tissue injury and repair. Here, we test the hypothesis that impaired polyamine homeostasis contributes to various kidney pathologies in mice during experimental models of ischemia-reperfusion, transplantation, rhabdomyolysis, cyclosporine treatment, arterial hypertension, diabetes, unilateral ureteral obstruction, high oxalate feeding, and adenine-induced injuries. We found a remarkably similar pattern in most kidney pathologies with reduced expression of enzymes involved in polyamine synthesis together with increased expression of polyamine degrading enzymes. Transcript levels of amine oxidase copper-containing 1 (Aoc1), an enzyme which catalyzes the breakdown of putrescine, were barely detectable by in situ mRNA hybridization in healthy kidneys. Aoc1 was highly expressed upon various experimental kidney injuries resulting in a significant reduction of kidney putrescine content. Kidney levels of spermine were also significantly reduced, whereas spermidine was increased in response to ischemia-reperfusion injury. Increased Aoc1 expression in injured kidneys was mainly accounted for by an Aoc1 isoform that harbors 22 additional amino acids at its N-terminus and shows increased secretion. Mice with germline deletion of Aoc1 and injured kidneys showed no decrease of kidney putrescine content; although they displayed no overt phenotype, they had fewer tubular casts upon ischemia-reperfusion injury. Hyperosmotic stress stimulated AOC1 expression at the transcriptional and post-transcription levels in metanephric explants and kidney cell lines. AOC1 expression was also significantly enhanced after kidney transplantation in humans. These data demonstrate that the kidneys respond to various forms of injury with down-regulation of polyamine synthesis and activation of the polyamine breakdown pathway. Thus, an imbalance in kidney polyamines may contribute to various etiologies of kidney injury.
MeSH term(s)	Humans ; Mice ; Animals ; Polyamines/metabolism ; Spermidine/metabolism ; Putrescine/metabolism ; Spermine/metabolism ; Spermine/pharmacology ; Acetyltransferases/genetics ; Acetyltransferases/metabolism ; Kidney/pathology ; Amine Oxidase (Copper-Containing)/metabolism ; Reperfusion Injury/pathology ; Gene Expression
Chemical Substances	Polyamines ; Spermidine (U87FK77H25) ; Putrescine (V10TVZ52E4) ; Spermine (2FZ7Y3VOQX) ; Acetyltransferases (EC 2.3.1.-) ; Amine Oxidase (Copper-Containing) (EC 1.4.3.21)
Language	English
Publishing date	2023-04-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2023.04.005
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Article ; Online: Pan-claudin family interactome analysis reveals shared and specific interactions.

Suarez-Artiles, Lorena / Breiderhoff, Tilman / Girardello, Rossana / Gonschior, Hannes / Rodius, Sophie / Lesur, Antoine / Reimer, Ulf / Ramberger, Evelyn / Perez-Hernandez, Daniel / Müller, Dominik / Mertins, Philipp / Dittmar, Gunnar

Cell reports

2022 Volume 41, Issue 6, Page(s) 111588

Abstract: Claudins are a family of transmembrane proteins expressed in epithelial tissues and are the major components of tight junctions (TJs), which define barrier properties in epithelia and maintain cell polarity. How claudins regulate the formation of TJs and ...

Abstract	Claudins are a family of transmembrane proteins expressed in epithelial tissues and are the major components of tight junctions (TJs), which define barrier properties in epithelia and maintain cell polarity. How claudins regulate the formation of TJs and which functions they exert outside of them is not entirely understood. Although the long and unstructured C-terminal tail is essential for regulation, it is unclear how it is involved in these functions beyond interacting with TJ-associated proteins such as TJ protein ZO-1 (TJP1). Here, we present an interactome study of the pan-claudin family in Madin-Darby canine kidney (MDCK)-C7 cells by combining two complementary mass spectrometry-based pull-down techniques creating an interaction landscape of the entire claudin family. The interaction partners of the claudins' C termini reveal their possible implications in localized biological processes in epithelial cells and their regulation by post-translational modifications (PTMs).
MeSH term(s)	Dogs ; Animals ; Claudins/metabolism ; Cell Line ; Tight Junctions/metabolism ; Madin Darby Canine Kidney Cells ; Cell Polarity
Chemical Substances	Claudins
Language	English
Publishing date	2022-10-14
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.2022.111588
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Article ; Online: Unrecognized role of claudin-10b in basolateral membrane infoldings of the thick ascending limb.

Quintanova, Catarina / Himmerkus, Nina / Svendsen, Samuel L / von Schwerdtner, Otto / Merkel, Cosima / Pinckert, Lennart / Mutig, Kerim / Breiderhoff, Tilman / Müller, Dominik / Günzel, Dorothee / Bleich, Markus

Annals of the New York Academy of Sciences

2022 Volume 1517, Issue 1, Page(s) 266–278

Abstract: Claudin-10b is an important component of the tight junction in the thick ascending limb (TAL) of Henle's loop and allows paracellular sodium transport. In immunofluorescence stainings, claudin-10b-positive cells exhibited extensive extra staining of ... ...

Abstract	Claudin-10b is an important component of the tight junction in the thick ascending limb (TAL) of Henle's loop and allows paracellular sodium transport. In immunofluorescence stainings, claudin-10b-positive cells exhibited extensive extra staining of basolateral, column-like structures. The precise localization and function have so far remained elusive. In isolated cortical TAL segments from C57BL/6J mice, kidney-specific claudin-10 knockout mice (cKO), and respective litter mates (WT), we investigated the localization and protein expression and function by fluorescence microscopy and electrophysiological measurements. Ultrastructural analysis of TAL in kidney sections was performed by electron microscopy. Claudin-10b colocalized with the basolateral Na
MeSH term(s)	Mice ; Animals ; Loop of Henle/metabolism ; Mice, Inbred C57BL ; Claudins/genetics ; Claudins/metabolism ; Tight Junctions/metabolism ; Sodium/metabolism ; Mice, Knockout
Chemical Substances	Claudins ; Sodium (9NEZ333N27)
Language	English
Publishing date	2022-08-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/nyas.14882
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Article ; Online: Cyclin M2 (CNNM2) knockout mice show mild hypomagnesaemia and developmental defects.

Franken, Gijs A C / Seker, Murat / Bos, Caro / Siemons, Laura A H / van der Eerden, Bram C J / Christ, Annabel / Hoenderop, Joost G J / Bindels, René J M / Müller, Dominik / Breiderhoff, Tilman / de Baaij, Jeroen H F

Scientific reports

2021 Volume 11, Issue 1, Page(s) 8217

Abstract: Patients with mutations in Cyclin M2 (CNNM2) suffer from hypomagnesaemia, seizures, and intellectual disability. Although the molecular function of CNNM2 is under debate, the protein is considered essential for renal ... ...

Abstract	Patients with mutations in Cyclin M2 (CNNM2) suffer from hypomagnesaemia, seizures, and intellectual disability. Although the molecular function of CNNM2 is under debate, the protein is considered essential for renal Mg
MeSH term(s)	Animals ; Animals, Newborn ; Cation Transport Proteins/genetics ; Embryo, Mammalian ; Female ; Intellectual Disability/blood ; Intellectual Disability/complications ; Intellectual Disability/genetics ; Intellectual Disability/pathology ; Magnesium/blood ; Magnesium Deficiency/blood ; Magnesium Deficiency/complications ; Magnesium Deficiency/genetics ; Magnesium Deficiency/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Pregnancy ; Seizures/blood ; Seizures/complications ; Seizures/genetics
Chemical Substances	Cation Transport Proteins ; Cnnm2 protein, mouse ; Magnesium (I38ZP9992A)
Language	English
Publishing date	2021-04-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-87548-6
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Article ; Online: Impact of claudin-10 deficiency on amelogenesis: Lesson from a HELIX tooth.

Obtel, Nicolas / Le Cabec, Adeline / Nguyen, Thè Nghia / Giabicani, Eloise / Van Malderen, Stijn J M / Garrevoet, Jan / Percot, Aline / Paris, Céline / Dean, Christopher / Hadj-Rabia, Smail / Houillier, Pascal / Breiderhoff, Tilman / Bardet, Claire / Coradin, Thibaud / Ramirez Rozzi, Fernando / Chaussain, Catherine

Annals of the New York Academy of Sciences

2022 Volume 1516, Issue 1, Page(s) 197–211

Abstract: In epithelia, claudin proteins are important components of the tight junctions as they determine the permeability and specificity to ions of the paracellular pathway. Mutations in CLDN10 cause the rare autosomal recessive HELIX syndrome (Hypohidrosis, ... ...

Abstract	In epithelia, claudin proteins are important components of the tight junctions as they determine the permeability and specificity to ions of the paracellular pathway. Mutations in CLDN10 cause the rare autosomal recessive HELIX syndrome (Hypohidrosis, Electrolyte imbalance, Lacrimal gland dysfunction, Ichthyosis, and Xerostomia), in which patients display severe enamel wear. Here, we assess whether this enamel wear is caused by an innate fragility directly related to claudin-10 deficiency in addition to xerostomia. A third molar collected from a female HELIX patient was analyzed by a combination of microanatomical and physicochemical approaches (i.e., electron microscopy, elemental mapping, Raman microspectroscopy, and synchrotron-based X-ray fluorescence). The enamel morphology, formation time, organization, and microstructure appeared to be within the natural variability. However, we identified accentuated strontium variations within the HELIX enamel, with alternating enrichments and depletions following the direction of the periodical striae of Retzius. These markings were also present in dentin. These data suggest that the enamel wear associated with HELIX may not be related to a disruption of enamel microstructure but rather to xerostomia. However, the occurrence of events of strontium variations within dental tissues might indicate repeated episodes of worsening of the renal dysfunction that may require further investigations.
MeSH term(s)	Amelogenesis ; Claudin-3 ; Claudin-4 ; Claudins/metabolism ; Electrolytes ; Female ; Humans ; Strontium ; Tight Junctions/metabolism ; Xerostomia
Chemical Substances	Claudin-3 ; Claudin-4 ; Claudins ; Electrolytes ; claudin 10 ; Strontium (YZS2RPE8LE)
Language	English
Publishing date	2022-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/nyas.14865
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Book ; Thesis: Funktionelle Analyse der Chloridkanäle CIC-3 und CIC-4 aus Säugetieren

Breiderhoff, Tilman

2001

Author's details	vorgelegt von Tilman Breiderhoff
Language	English
Size	Ill., graph. Darst
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Univ., FB Biologie, Diss.--Hamburg, 2001
Note	Enthält: 2 Zeitschriftenaufsätze
Database	Former special subject collection: coastal and deep sea fishing

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