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Wiley Interdisciplinary Reviews : Membrane Transport and Signaling    Follow    
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
     ISSN (Online) 2190-4618
     Published by John Wiley and Sons Homepage  [1594 journals]
  • Monitoring of intra‐ER free Ca2+
    • Abstract: The importance of calcium signaling in cell health and disease is the major driving force in current research of intracellular calcium homeostasis. Ca2+ release from the endoplasmic reticulum (ER) and other calcium stores seems to be the crucial factor in the activation of many cellular functions. Significant changes in ER Ca2+ content and dynamics have been implicated in the activation of the ER stress response, abnormal autophagy, and cell death which leads to a variety of pathological conditions. For example, in acute pancreatitis, an inflammatory disease of the exocrine pancreas caused primarily by bile stones or alcohol, excessive intracellular calcium overload due to Ca2+ release from internal stores followed by store operated Ca2+ entry (SOCE) leads to the premature activation of digestive proenzymes within pancreatic acinar cells. Recent data show that SOCE channel blockers are capable of substantially reducing the intracellular Ca2+ overload and subsequent cell necrosis without major alteration of ER Ca2+ content. We also demonstrate here that indirect ER measurements can be misleading and only direct intra‐ER Ca2+ monitoring offers reliable conclusions. In this respect, it is essential to summarize the methods available and provide examples of direct measurements of free Ca2+ concentration [Ca2+] in the ER lumen in pancreatic acinar cells. This article is aimed at highlighting the major techniques for monitoring ER Ca2+ with reference to their advantages, limitations, and views for future improvements. For further resources related to this article, please visit the WIREs website. Conflict of interest: The authors have declared no conflicts of interest for this article.
  • The challenge of determining the role of Rh glycoproteins in transport of
           NH3 and NH4+
    • Abstract: The mammalian Rh glycoproteins belong to the solute transporter family SLC42 and include the erythroid Rh‐associated glycoprotein (RhAG) and two epithelial membrane molecules Rhbg (human RhBG) and Rhcg (RhCG). Mammalian Rh glycoproteins are closely related to the ammonium transporters of the yeast (MEP proteins) and bacteria (Amt). Rhbg and Rhcg are expressed in several mammalian tissues including liver, kidney, skin, lung, and GI tract. In the kidney they are expressed in α‐intercalated cells and principal cells of the collecting duct. Whereas Rhbg is strictly present in the basolateral membrane; Rhcg is reported to be at both apical membrane and basolateral membranes. Recent functional studies strongly support a role of Rh glycoproteins in NH4+ transport. Other studies indicate that they mediate transport of CO2 and NH3. This review highlights the progress in determining the properties of Rh glycoproteins and the challenging questions that continue to hinder understanding their function and their physiological role. For further resources related to this article, please visit the WIREs website. Conflict of interest: The authors have declared no conflicts of interest for this article.
  • Issue information
  • Targeting endocannabinoid signaling in tumor‐associated macrophages
           as treatment for glioblastoma multiforme
    • Abstract: Glioblastoma multiforme (GBM) is the most common form of primary brain tumor and is diagnosed in approximately 15,000 people each year in the United States alone. No cure for this type of cancer exists, and the current standard of care treatments provide little benefit and are associated with debilitating side effects. Recent evidence shows that a large number of tumor‐associated macrophages (TAMs) invade the GBM tumor mass and secrete factors that directly and indirectly promote tumor growth. TAMs express a panel of unique receptors that could be targeted for therapeutic benefit. One such receptor, cannabinoid receptor 2 (CB2), is a member of the endocannabinoid (eCB) signaling system, and its activation has been shown to tightly control the migration and phenotype of both macrophages and microglia. Additional receptors, also engaged by eCBs and cannabinoid‐like compounds, are expressed by macrophages and microglia. These receptors also control cell migration and phenotype, but exhibit distinct pharmacological profiles and operate through a different mechanism of action. Strong evidence accumulated over the past decade indicates that membrane receptors expressed by TAMs represent novel targeting opportunities to treat GBM tumor progression. Here we review studies that significantly increased our understanding of the molecular mechanism of action of receptors engaged by eCBs and cannabinoid‐like compounds expressed by GBM tumor cells and TAMs. This evidence provides a strong rationale for developing new therapeutics that target the eCB signaling of TAMs for the treatment of GBM while minimizing the typical side effects associated with standard care. WIREs Membr Transp Signal 2014. doi: 10.1002/wmts.101 Conflict of interest: The authors have declared no conflicts of interest for this article. For further resources related to this article, please visit the WIREs website.
  • L‐type Ca2+ channels in heart and brain
    • Abstract: L‐type calcium channels (Cav1) represent one of the three major classes (Cav1–3) of voltage‐gated calcium channels. They were identified as the target of clinically used calcium channel blockers (CCBs; so‐called calcium antagonists) and were the first class accessible to biochemical characterization. Four of the 10 known α1 subunits (Cav1.1–Cav1.4) form the pore of L‐type calcium channels (LTCCs) and contain the high‐affinity drug‐binding sites for dihydropyridines and other chemical classes of organic CCBs. In essentially all electrically excitable cells one or more of these LTCC isoforms is expressed, and therefore it is not surprising that many body functions including muscle, brain, endocrine, and sensory function depend on proper LTCC activity. Gene knockouts and inherited human diseases have allowed detailed insight into the physiological and pathophysiological role of these channels. Genome‐wide association studies and analysis of human genomes are currently providing even more hints that even small changes of channel expression or activity may be associated with disease, such as psychiatric disease or cardiac arrhythmias. Therefore, it is important to understand the structure–function relationship of LTCC isoforms, their differential contribution to physiological function, as well as their fine‐tuning by modulatory cellular processes. WIREs Membr Transp Signal 2014. doi: 10.1002/wmts.102 Conflict of interest: The authors have declared no conflicts of interest for this article. For further resources related to this article, please visit the WIREs website.
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