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Physiology

  • Role of opioid signaling in kidney damage during the development of salt-induced hypertension
    Open Access
    Role of opioid signaling in kidney damage during the development of salt-induced hypertension

    Daria Golosova, Oleg Palygin, Ruslan Bohovyk, Christine A Klemens, Vladislav Levchenko, Denisha R Spires, Elena Isaeva, Ashraf El-Meanawy, Alexander Staruschenko

    Daria Golosova ... Alexander Staruschenko

    Published 12 October 2020

    Stimulation of kappa opioid receptors modulates calcium influx via TRPC6 channels in podocytes, which ultimately compromises the integrity of the glomerular filtration barrier and promotes a marked worsening of blood pressure control and renal damage.

  • Differential regulation of hepatic physiology and injury by the TAM receptors Axl and Mer
    Open Access
    Differential regulation of hepatic physiology and injury by the TAM receptors Axl and Mer

    Anna Zagórska, Paqui G Través, Lidia Jiménez-García, Jenna D Strickland, Joanne Oh, Francisco J Tapia, Rafael Mayoral, Patrick Burrola, Bryan L Copple, Greg Lemke

    Anna Zagórska ... Greg Lemke

    Published 22 June 2020

    The TAM receptor tyrosine kinases Mer and Axl play critical roles in liver homeostasis and in the response to both acute and chronic liver injury.

  • <em>Mylk3</em> null C57BL/6N mice develop cardiomyopathy, whereas <em>Nnt</em> null C57BL/6J mice do not
    Open Access
    Mylk3 null C57BL/6N mice develop cardiomyopathy, whereas Nnt null C57BL/6J mice do not

    Jack L Williams, Anju Paudyal, Sherine Awad, James Nicholson, Dominika Grzesik, Joaquin Botta, Eirini Meimaridou, Avinaash V Maharaj, Michelle Stewart, Andrew Tinker, Roger D Cox, Lou A Metherell

    Jack L Williams ... Lou A Metherell

    Published 25 March 2020

    Genetic differences between C57BL/6 substrains lead to different cardiovascular traits; a null mutation in Mylk3 likely causes cardiomyopathy in C57BL/6N mice, whereas C57BL/6J Nnt-null mice do not develop cardiomyopathy.

  • The health status alters the pituitary function and reproduction of mice in a <em>Cxcr2</em>-dependent manner
    Open Access
    The health status alters the pituitary function and reproduction of mice in a Cxcr2-dependent manner

    Colin Timaxian, Isabelle Raymond-Letron, Céline Bouclier, Linda Gulliver, Ludovic Le Corre, Karim Chébli, Anne Guillou, Patrice Mollard, Karl Balabanian, Gwendal Lazennec

    Colin Timaxian ... Gwendal Lazennec

    Published 10 February 2020

    This study explores the effects of microbiota on reproductive function of Cxcr2 knockout animals. Cxcr2 is involved in the control of pituitary action and the subsequent development of mammary gland, uterus and ovary.

  • Loss of autophagy impairs physiological steatosis by accumulation of NCoR1
    Open Access
    Loss of autophagy impairs physiological steatosis by accumulation of NCoR1

    Shun-saku Takahashi, Yu-Shin Sou, Tetsuya Saito, Akiko Kuma, Takayuki Yabe, Yuki Sugiura, Hyeon-Cheol Lee, Makoto Suematsu, Takehiko Yokomizo, Masato Koike, Shuji Terai, Noboru Mizushima, Satoshi Waguri, Masaaki Komatsu

    Shun-saku Takahashi ... Masaaki Komatsu

    Published 26 December 2019

    Autophagy regulates fatty acid and triglyceride synthesis at the transcriptional level by fine-tuning the levels of NCoR1, a negative regulator of nuclear receptors. Defective autophagy impairs physiological steatosis both under fasting conditions and after hepatectomy.

  • TMEM16A chloride channel does not drive mucus production
    Open Access
    TMEM16A chloride channel does not drive mucus production

    Filipa B Simões, Margarida C Quaresma, Luka A Clarke, Iris AL Silva, Ines Pankonien, Violeta Railean, Arthur Kmit, Margarida D Amaral

    Filipa B Simões ... Margarida D Amaral

    Published 15 November 2019

    Despite being essential for airway hydration, TMEM16A is not required for mucus (MUC5AC) production. Cell proliferation is the main driver for TMEM16A up-regulation during inflammation.

  • Expression of a constitutively active human <em>STING</em> mutant in hematopoietic cells produces an <em>Ifnar1</em>-dependent vasculopathy in mice
    Open Access
    Expression of a constitutively active human STING mutant in hematopoietic cells produces an Ifnar1-dependent vasculopathy in mice

    Gary R Martin, Kimiora Henare, Carolina Salazar, Teresa Scheidl-Yee, Laura J Eggen, Pankaj P Tailor, Jung Hwan Kim, John Podstawka, Marvin J Fritzler, Margaret M Kelly, Bryan G Yipp, Frank R Jirik

    Gary R Martin ... Frank R Jirik

    Published 20 June 2019

    Transgenic expression of a mutant hSTING cDNA under the control of the Vav1 gene promoter leads to a vasculopathy similar to that of the interferonopathy, STING-associated vasculopathy of infancy.

  • m<sup>6</sup>A-mRNA methylation regulates cardiac gene expression and cellular growth
    Open Access
    m6A-mRNA methylation regulates cardiac gene expression and cellular growth

    Vivien Kmietczyk, Eva Riechert, Laura Kalinski, Etienne Boileau, Ellen Malovrh, Brandon Malone, Agnieszka Gorska, Christoph Hofmann, Eshita Varma, Lonny Jürgensen, Verena Kamuf-Schenk, Janine Altmüller, Rewati Tappu, Martin Busch, Patrick Most, Hugo A Katus, Christoph Dieterich, Mirko Völkers

    Vivien Kmietczyk ... Mirko Völkers

    Published 9 April 2019

    This study provides evidence that m6A methylation is dynamically regulated during human and murine cardiac disease and highlights an important role of the m6A methylase Mettl3 in regulating cardiac growth by gene expression control.

  • Substrate fluxes in brown adipocytes upon adrenergic stimulation and uncoupling protein 1 ablation
    Open Access
    Substrate fluxes in brown adipocytes upon adrenergic stimulation and uncoupling protein 1 ablation

    Sabine Schweizer, Josef Oeckl, Martin Klingenspor, Tobias Fromme

    Sabine Schweizer ... Tobias Fromme

    Published 14 November 2018

    Quantification of substrate fluxes in brown adipocytes clarifies contributors to extracellular acidification, identifies a futile cycle of lipolysis and re-esterification, and suggests a role for glycogen during activation.

  • Secretory granule protein chromogranin B (CHGB) forms an anion channel in membranes
    Open Access
    Secretory granule protein chromogranin B (CHGB) forms an anion channel in membranes

    Gaya P Yadav, Hui Zheng, Qing Yang, Lauren G Douma, Linda B Bloom, Qiu-Xing Jiang

    Gaya P Yadav ... Qiu-Xing Jiang

    Published 24 September 2018

    The CHGB subfamily of secretory granule proteins forms a new family of anion-selective channels by interacting with membranes via two amphipathic α-helices. The channel exhibits higher anion selectivity, larger conductance, higher DIDS-binding affinity, and higher Cl− sensitivity than other known anion channels.

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