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  1. Article ; Online: Renal denervation for resistant hypertension.

    Mircheva, Miryana / Neuhofer, Wolfgang / Popa, Ciprian / Krämer, Bernhard K / Heitzmann, Dirk

    Lancet (London, England)

    2015  Volume 386, Issue 10000, Page(s) 1239–1240

    MeSH term(s) Antihypertensive Agents/therapeutic use ; Catheter Ablation/methods ; Denervation/methods ; Female ; Humans ; Hypertension/therapy ; Male
    Chemical Substances Antihypertensive Agents
    Language English
    Publishing date 2015-09-26
    Publishing country England
    Document type Comment ; Letter
    ZDB-ID 3306-6
    ISSN 1474-547X ; 0023-7507 ; 0140-6736
    ISSN (online) 1474-547X
    ISSN 0023-7507 ; 0140-6736
    DOI 10.1016/S0140-6736(15)00258-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Physiology and pathophysiology of potassium channels in gastrointestinal epithelia.

    Heitzmann, Dirk / Warth, Richard

    Physiological reviews

    2008  Volume 88, Issue 3, Page(s) 1119–1182

    Abstract: Epithelial cells of the gastrointestinal tract are an important barrier between the "milieu interne" and the luminal content of the gut. They perform transport of nutrients, salts, and water, which is essential for the maintenance of body homeostasis. In ...

    Abstract Epithelial cells of the gastrointestinal tract are an important barrier between the "milieu interne" and the luminal content of the gut. They perform transport of nutrients, salts, and water, which is essential for the maintenance of body homeostasis. In these epithelia, a variety of K(+) channels are expressed, allowing adaptation to different needs. This review provides an overview of the current literature that has led to a better understanding of the multifaceted function of gastrointestinal K(+) channels, thereby shedding light on pathophysiological implications of impaired channel function. For instance, in gastric mucosa, K(+) channel function is a prerequisite for acid secretion of parietal cells. In epithelial cells of small intestine, K(+) channels provide the driving force for electrogenic transport processes across the plasma membrane, and they are involved in cell volume regulation. Fine tuning of salt and water transport and of K(+) homeostasis occurs in colonic epithelia cells, where K(+) channels are involved in secretory and reabsorptive processes. Furthermore, there is growing evidence for changes in epithelial K(+) channel expression during cell proliferation, differentiation, apoptosis, and, under pathological conditions, carcinogenesis. In the future, integrative approaches using functional and postgenomic/proteomic techniques will help us to gain comprehensive insights into the role of K(+) channels of the gastrointestinal tract.
    MeSH term(s) Animals ; Epithelial Cells/enzymology ; Epithelial Cells/metabolism ; Gastrointestinal Tract/enzymology ; Gastrointestinal Tract/metabolism ; Gastrointestinal Tract/physiopathology ; H(+)-K(+)-Exchanging ATPase/metabolism ; Humans ; Intestine, Large/metabolism ; Intestine, Small/metabolism ; Pancreas, Exocrine/metabolism ; Pancreas, Exocrine/secretion ; Parietal Cells, Gastric/enzymology ; Potassium Channels/classification ; Potassium Channels/metabolism ; Salivary Glands/metabolism ; Salivary Glands/secretion
    Chemical Substances Potassium Channels ; H(+)-K(+)-Exchanging ATPase (EC 3.6.3.10)
    Language English
    Publishing date 2008-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 209902-0
    ISSN 1522-1210 ; 0031-9333
    ISSN (online) 1522-1210
    ISSN 0031-9333
    DOI 10.1152/physrev.00020.2007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The in vivo respiratory phenotype of the adenosine A1 receptor knockout mouse.

    Heitzmann, Dirk / Buehler, Philipp / Schweda, Frank / Georgieff, Michael / Warth, Richard / Thomas, Joerg

    Respiratory physiology & neurobiology

    2016  Volume 222, Page(s) 16–28

    Abstract: The nucleoside adenosine has been implicated in the regulation of respiration, especially during hypoxia in the newborn. In this study the role of adenosine A1 receptors for the control of respiration was investigated in vivo. To this end, respiration of ...

    Abstract The nucleoside adenosine has been implicated in the regulation of respiration, especially during hypoxia in the newborn. In this study the role of adenosine A1 receptors for the control of respiration was investigated in vivo. To this end, respiration of unrestrained adult and neonatal adenosine A1 receptor knockout mice (A1R(-/-)) was measured in a plethysmographic device. Under control conditions (21% O2) and mild hypoxia (12-15% O2) no difference of respiratory parameters was observed between adult wildtype (A1R(+/+)) and A1R(-/-) mice. Under more severe hypoxia (6-10% O2) A1R(+/+) mice showed, after a transient increase of respiration, a decrease of respiration frequency (fR) and tidal volume (VT) leading to a decrease of minute volume (MV). This depression of respiration during severe hypoxia was absent in A1R(-/-) mice which displayed a stimulated respiration as indicated by the enhancement of MV by some 50-60%. During hypercapnia-hyperoxia (3-10% CO2/97-90 % O2), no obvious differences in respiration of A1R(-/-) and A1R(+/+) was observed. In neonatal mice, the respiratory response to hypoxia was surprisingly similar in both genotypes. However, neonatal A1R(-/-) mice appeared to have more frequently periods of apnea during hypoxia and in the post-hypoxic control period. In conclusion, these data indicate that the adenosine A1 receptor is an important molecular component mediating hypoxic depression in adult mice and it appears to stabilize respiration of neonatal mice.
    MeSH term(s) Aging/physiology ; Animals ; Animals, Newborn ; Apnea/physiopathology ; Blood Gas Analysis ; Disease Models, Animal ; Female ; Hypercapnia/physiopathology ; Hypoxia/physiopathology ; Male ; Mice, Knockout ; Phenotype ; Plethysmography, Whole Body ; Receptor, Adenosine A1/genetics ; Receptor, Adenosine A1/metabolism ; Respiration ; Tidal Volume/physiology
    Chemical Substances Receptor, Adenosine A1
    Language English
    Publishing date 2016-02-01
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2077867-3
    ISSN 1878-1519 ; 1569-9048
    ISSN (online) 1878-1519
    ISSN 1569-9048
    DOI 10.1016/j.resp.2015.11.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Abnormal respiration under hyperoxia in TASK-1/3 potassium channel double knockout mice.

    Buehler, Philipp K / Bleiler, Doris / Tegtmeier, Ines / Heitzmann, Dirk / Both, Christian / Georgieff, Michael / Lesage, Florian / Warth, Richard / Thomas, Jörg

    Respiratory physiology & neurobiology

    2017  Volume 244, Page(s) 17–25

    Abstract: Despite intensive research, the exact function of TASK potassium channels in central and peripheral chemoreception is still under debate. In this study, we investigated the respiration of unrestrained TASK-3 (TASK- ... ...

    Abstract Despite intensive research, the exact function of TASK potassium channels in central and peripheral chemoreception is still under debate. In this study, we investigated the respiration of unrestrained TASK-3 (TASK-3
    Language English
    Publishing date 2017-10
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2077867-3
    ISSN 1878-1519 ; 1569-9048
    ISSN (online) 1878-1519
    ISSN 1569-9048
    DOI 10.1016/j.resp.2017.06.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Book ; Online ; Thesis: Die Regulation des Na+2Cl-K+-Cotransporters in der basolateralen Membran der Rattenkolonkrypte

    Heitzmann, Dirk

    2000  

    Author's details vorgelegt von Dirk Heitzmann
    Language German
    Size Online-Ressource
    Edition [Elektronische Ressource]
    Document type Book ; Online ; Thesis
    Thesis / German Habilitation thesis Univ., Diss--Freiburg (Breisgau), 2001
    Database Former special subject collection: coastal and deep sea fishing

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  6. Article: No potassium, no acid: K+ channels and gastric acid secretion.

    Heitzmann, Dirk / Warth, Richard

    Physiology (Bethesda, Md.)

    2007  Volume 22, Page(s) 335–341

    Abstract: The gastric H+-K+-ATPase pumps H+ into the lumen and takes up K+ in parallel. In the acid-producing parietal cells, luminal KCNE2/KCNQ1 K+ channels play a pivotal role in replenishing K+ in the luminal fluid. Inactivation of KCNE2/KCNQ1 channels ... ...

    Abstract The gastric H+-K+-ATPase pumps H+ into the lumen and takes up K+ in parallel. In the acid-producing parietal cells, luminal KCNE2/KCNQ1 K+ channels play a pivotal role in replenishing K+ in the luminal fluid. Inactivation of KCNE2/KCNQ1 channels abrogates gastric acid secretion and dramatically modifies the architecture of gastric mucosa.
    MeSH term(s) Animals ; Gastric Acid/secretion ; H(+)-K(+)-Exchanging ATPase/metabolism ; Humans ; KCNQ1 Potassium Channel/metabolism ; Parietal Cells, Gastric/cytology ; Parietal Cells, Gastric/metabolism ; Parietal Cells, Gastric/pathology ; Potassium/metabolism ; Potassium Channels, Inwardly Rectifying/metabolism ; Potassium Channels, Voltage-Gated/antagonists & inhibitors ; Potassium Channels, Voltage-Gated/metabolism ; Signal Transduction/physiology
    Chemical Substances KCNQ1 Potassium Channel ; Potassium Channels, Inwardly Rectifying ; Potassium Channels, Voltage-Gated ; H(+)-K(+)-Exchanging ATPase (EC 3.6.3.10) ; Potassium (RWP5GA015D)
    Language English
    Publishing date 2007-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2158667-6
    ISSN 1548-9221 ; 1548-9213
    ISSN (online) 1548-9221
    ISSN 1548-9213
    DOI 10.1152/physiol.00016.2007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Book ; Online ; Thesis: Die Regulation des Na+2Cl-K+-Cotransporters in der basolateralen Membran der Rattenkolonkrypte

    Heitzmann, Dirk [Verfasser]

    2000  

    Author's details vorgelegt von Dirk Heitzmann
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  8. Article ; Online: Sex-dependent differences in the in vivo respiratory phenotype of the TASK-1 potassium channel knockout mouse.

    Jungbauer, Stefan / Buehler, Philipp Karl / Neubauer, Jacqueline / Haas, Cordula / Heitzmann, Dirk / Tegtmeier, Ines / Sterner, Christina / Barhanin, Jacques / Georgieff, Michael / Warth, Richard / Thomas, Jörg

    Respiratory physiology & neurobiology

    2017  Volume 245, Page(s) 13–28

    Abstract: TASK-1 potassium channels have been implicated in central and peripheral chemoreception; however, the precise contribution of TASK-1 for the control of respiration is still under debate. Here, we investigated the respiration of unrestrained adult and ... ...

    Abstract TASK-1 potassium channels have been implicated in central and peripheral chemoreception; however, the precise contribution of TASK-1 for the control of respiration is still under debate. Here, we investigated the respiration of unrestrained adult and neonatal TASK-1 knockout mice (TASK-1
    MeSH term(s) Aging/metabolism ; Anesthetics, Inhalation/pharmacology ; Animals ; Animals, Newborn ; Cohort Studies ; Female ; Humans ; Hypercapnia/physiopathology ; Infant ; Isoflurane/pharmacology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Tissue Proteins/deficiency ; Nerve Tissue Proteins/genetics ; Plethysmography, Whole Body ; Potassium Channels, Tandem Pore Domain/deficiency ; Potassium Channels, Tandem Pore Domain/genetics ; Respiration/drug effects ; Sex Characteristics ; Sudden Infant Death/genetics ; Tidal Volume/physiology
    Chemical Substances Anesthetics, Inhalation ; Nerve Tissue Proteins ; Potassium Channels, Tandem Pore Domain ; potassium channel subfamily K member 3 ; Isoflurane (CYS9AKD70P)
    Language English
    Publishing date 2017
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2077867-3
    ISSN 1878-1519 ; 1569-9048
    ISSN (online) 1878-1519
    ISSN 1569-9048
    DOI 10.1016/j.resp.2016.11.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Lasp1 regulates adherens junction dynamics and fibroblast transformation in destructive arthritis.

    Beckmann, Denise / Römer-Hillmann, Anja / Krause, Annika / Hansen, Uwe / Wehmeyer, Corinna / Intemann, Johanna / de Gorter, David J J / Dankbar, Berno / Hillen, Jan / Heitzmann, Marianne / Begemann, Isabell / Galic, Milos / Weinhage, Toni / Foell, Dirk / Ai, Rizi / Kremerskothen, Joachim / Kiener, Hans P / Müller, Sylvia / Kamradt, Thomas /
    Schröder, Christopher / Leitão, Elsa / Horsthemke, Bernhard / Rosenstiel, Philip / Nordström, Karl / Gasparoni, Gilles / Gasparoni, Nina / Walter, Jörn / Li, Na / Yang, Xinyi / Chung, Ho-Ryun / Pavenstädt, Hermann / Lindemann, Nico / Schnittler, Hans J / Wang, Wei / Firestein, Gary S / Pap, Thomas / Korb-Pap, Adelheid

    Nature communications

    2021  Volume 12, Issue 1, Page(s) 3624

    Abstract: The LIM and SH3 domain protein 1 (Lasp1) was originally cloned from metastatic breast cancer and characterised as an adaptor molecule associated with tumourigenesis and cancer cell invasion. However, the regulation of Lasp1 and its function in the ... ...

    Abstract The LIM and SH3 domain protein 1 (Lasp1) was originally cloned from metastatic breast cancer and characterised as an adaptor molecule associated with tumourigenesis and cancer cell invasion. However, the regulation of Lasp1 and its function in the aggressive transformation of cells is unclear. Here we use integrative epigenomic profiling of invasive fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthritis (RA) and from mouse models of the disease, to identify Lasp1 as an epigenomically co-modified region in chronic inflammatory arthritis and a functionally important binding partner of the Cadherin-11/β-Catenin complex in zipper-like cell-to-cell contacts. In vitro, loss or blocking of Lasp1 alters pathological tissue formation, migratory behaviour and platelet-derived growth factor response of arthritic FLS. In arthritic human TNF transgenic mice, deletion of Lasp1 reduces arthritic joint destruction. Therefore, we show a function of Lasp1 in cellular junction formation and inflammatory tissue remodelling and identify Lasp1 as a potential target for treating inflammatory joint disorders associated with aggressive cellular transformation.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Adherens Junctions/metabolism ; Animals ; Arthritis/metabolism ; Arthritis/pathology ; Arthritis, Rheumatoid/metabolism ; Arthritis, Rheumatoid/pathology ; Cadherins/metabolism ; Cell Transformation, Neoplastic/metabolism ; Cytoskeletal Proteins/genetics ; Cytoskeletal Proteins/metabolism ; Female ; Fibroblasts/metabolism ; Homeodomain Proteins ; LIM Domain Proteins/genetics ; LIM Domain Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Osteoblasts ; beta Catenin/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; CTNNB1 protein, human ; Cadherins ; Cytoskeletal Proteins ; Homeodomain Proteins ; LASP1 protein, human ; LIM Domain Proteins ; Lasp1 protein, mouse ; beta Catenin ; osteoblast cadherin (156621-71-5)
    Language English
    Publishing date 2021-06-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-021-23706-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: The TFIIH subunit p89 (XPB) localizes to the centrosome during mitosis.

    Weber, Achim / Chung, Hye-Jung / Springer, Erik / Heitzmann, Dirk / Warth, Richard

    Cellular oncology : the official journal of the International Society for Cellular Oncology

    2010  Volume 32, Issue 1-2, Page(s) 121–130

    Abstract: Background: The general transcription factor II H (TFIIH), comprised of a core complex and an associated CAK-complex, functions in transcription, DNA repair and cell cycle control. Mutations of the two largest subunits, p89 (XPB) and p80 (XPD), cause ... ...

    Abstract Background: The general transcription factor II H (TFIIH), comprised of a core complex and an associated CAK-complex, functions in transcription, DNA repair and cell cycle control. Mutations of the two largest subunits, p89 (XPB) and p80 (XPD), cause the hereditary cancer-prone syndrome xeroderma pigmentosum.
    Methods: The TFIIH subunit p89 was monitored during interphase and cell division by immunofluorescence staining, GFP-fusion constructs including deletions, live cell imaging and immuno-precipitations.
    Results: Here we demonstrate that during cell division, from prophase until telophase, the TFIIH core subunit p89, but not other subunits of TFIIH, associates with the centrosomes and the adjacent parts of the mitotic spindle. With overall constant levels throughout mitosis, p89 re-localizes to the newly formed nuclei by the end of mitosis. Furthermore, p89 interacts with the centrosomal protein gamma-tubulin. Truncations of p89 result in an abnormal subcellular distribution during interphase and abolished centrosomal association during mitosis.
    Conclusions: Our observations suggest a so far unappreciated role for p89 in cell cycle regulation, and may be the structural basis for a long known, but hitherto unexplained interaction between p89 and tubulin.
    MeSH term(s) Centrosome/metabolism ; DNA Helicases/genetics ; DNA Helicases/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; HeLa Cells ; Humans ; Mitosis ; Protein Transport ; Tubulin/metabolism
    Chemical Substances DNA-Binding Proteins ; Tubulin ; XPBC-ERCC-3 protein (146045-44-5) ; DNA Helicases (EC 3.6.4.-)
    Language English
    Publishing date 2010
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2157351-7
    ISSN 1875-8606 ; 1570-5870
    ISSN (online) 1875-8606
    ISSN 1570-5870
    DOI 10.3233/CLO-2009-0509
    Database MEDical Literature Analysis and Retrieval System OnLINE

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