Bernhard Gess

Salt‐losing nephropathy in mice with a null mutation of the Clcnk2 gene

Alexandra Grill, Ina Maria Schießl, Bernhard Gess, Katharina Fremter et autres

Abstract Aim The basolateral chloride channel ClC‐Kb facilitates Cl reabsorption in the distal nephron of the human kidney. Functional mutations in CLCNKB are associated with Bartter's syndrome type 3, a hereditary salt‐losing nephropathy. To address the function of ClC‐K2 in vivo , …

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The angiotensin receptor-associated protein Atrap is a stimulator of the cardiac Ca2+-ATPase SERCA2a

Katharina Mederle, Bernhard Gess, Florentina Pluteanu, Jelena Plačkić et autres

AIMS: The angiotensin II type 1 receptor-associated protein (Atrap) is highly expressed in the heart, but its function in the heart is unknown. We hypothesized that cardiac Atrap may interact with proteins other than the AT1 receptor. METHODS AND RESULTS: To identify …

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Intravital Imaging Reveals Angiotensin II–Induced Transcytosis of Albumin by Podocytes

Ina Maria Schießl, Anna Hammer, Veronika Kattler, Bernhard Gess et autres

Albuminuria is a hallmark of kidney disease of various etiologies and usually caused by deterioration of glomerular filtration barrier integrity. We recently showed that angiotensin II (Ang II) acutely increases albumin filtration in the healthy kidney. Here, we used intravital microscopy to …

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Atrap interacts with the cardiac Ca 2+ ‐ATPase SERCA2A and facilitates ventricular relaxation (1150.7)

Katharina Mederle, Bernhard Gess, Hayo Castrop

The angiotensin II type 1 receptor‐associated protein (Atrap) is highly expressed in the heart. We hypothesized that cardiac Atrap may interact with proteins other than the AT1 receptor. To identify novel interacting partners of Atrap, we performed pull‐down assays. In 3 independent …

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Atrap Deficiency Increases Arterial Blood Pressure and Plasma Volume

Mona Oppermann, Bernhard Gess, Frank Schweda, Hayo Castrop

The angiotensin receptor-associated protein (Atrap) interacts with angiotensin II (AngII) type 1 (AT1) receptors and facilitates their internalization in vitro, but little is known about the function of Atrap in vivo. Here, we detected Atrap expression in several organs of wild-type mice; …

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Hypoxia up-regulates triosephosphate isomerase expression via a HIF-dependent pathway

Bernhard Gess, Karl‐Heinz Hofbauer, Rainer Deutzmann, Armin Kurtz

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Oxygen tension regulates the expression of a group of procollagen hydroxylases

Karl‐Heinz Hofbauer, Bernhard Gess, Christiane Lohaus, Helmut E. Meyer et autres

In this study, we have characterized the influence of hypoxia on the expression of hydroxylases crucially involved in collagen fiber formation, such as prolyl-4-hydroxylases (Ph4) and procollagen lysyl-hydroxylases (PLOD). Using the rat vascular smooth muscle cell line A7r5, we found that an …

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The cellular oxygen tension regulates expression of the endoplasmic oxidoreductase ERO1‐Lα

Bernhard Gess, Karl‐Heinz Hofbauer, Roland H. Wenger, Christiane Lohaus et autres

The formation of disulfide bonds in the endoplasmic reticulum requires protein disulfide isomerase (PDI) and endoplasmic reticulum oxidoreductin 1 (ERO1) that reoxidizes PDI. We report here that the expression of the rat, mouse and human homologues of ERO1-Like protein alpha but not …

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Endogenous nitric oxide attenuates erythropoietin gene expression in vivo

Vladimir Todorov, Bernhard Gess, Axel Gödecke, Charlotte Wagner et autres

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Endogenous nitric oxide attenuates erythropoietin gene expression in vivo

Vladimir Todorov, Bernhard Gess, A. Gödecke, Charlotte Wagner et autres

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Acute hypoxia upregulates NOS gene expression in rats

Bernhard Gess, K. Th. Schricker, Roman Pfeifer, Armin Kurtz

This study aimed to investigate the influence of acute tissue hypoxygenation on the expression of NO synthase (NOS) genes in vivo. To this end, male Sprague-Dawley rats were exposed either to 9% oxygen or to 0.1% carbon monoxide for 6 h, and …

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In vivo carbon monoxide exposure and hypoxic hypoxia stimulate immediate early gene expression

Bernhard Gess, Konrad Wolf, G x FC nter A. J. Riegger, Armin Kurtz

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