Papers by Helmuth Sanchez
Journal of Biological Chemistry, Aug 1, 2014
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The Journal of General Physiology, Dec 26, 2011
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American Journal of Physiology-cell Physiology, Sep 1, 2009
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Cns & Neurological Disorders-drug Targets, May 1, 2011
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Brain Research Reviews, Dec 1, 2004
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Frontiers in Cellular Neuroscience, Oct 27, 2014
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The Journal of General Physiology, Jun 27, 2016
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Springer eBooks, 2012
The synchronization of numerous cellular events requires complex electric and metabolic cell-cell... more The synchronization of numerous cellular events requires complex electric and metabolic cell-cell interactions. Connexins are a family of membrane proteins that constitute the molecular basis of two kinds of channels: gap junction channels (GJCs), which allow direct cytoplasm-cytoplasm communication, and hemichannels (HCs) that provide a pathway for exchanges between the intra and extra-cellular milieu. Both kind of connexin-based channels support intercellular communication via intercellular propagation of calcium waves. Here, we review evidence supporting the role of Ca(2+) in the regulation of GJCs and HCs formed by connexins. Also it is speculated how these connexin-based channels could contribute to the propagation of intercellular Ca(2+) signals.
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The Journal of General Physiology, Jun 24, 2013
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American Journal of Physiology-cell Physiology, Dec 1, 2010
Although alkaline pH is known to trigger Ca2+ influx in diverse cells, no pH-sensitive Ca2+ chann... more Although alkaline pH is known to trigger Ca2+ influx in diverse cells, no pH-sensitive Ca2+ channel has been identified. Here, we report that extracellular alkalinization induces opening of connexin 43 hemichannels (Cx43 HCs). Increasing extracellular pH from 7.4 to 8.5, in the presence of physiological Ca2+/Mg2+ concentrations, rapidly increased the ethidium uptake rate and open probability of HCs in Cx43 and Cx43EGFP HeLa transfectants (HeLa-Cx3 and HeLa-Cx43EGFP, respectively) but not in parental HeLa cells (HeLa-parental) lacking Cx43 HCs. The increase in ethidium uptake induced by pH 8.5 was not affected by raising the extracellular Ca2+ concentration from 1.8 to 10 mM but was inhibited by a connexin HC inhibitor (La3+). Probenecid, a pannexin HC blocker, had no effect. Extracellular alkalinization increased the intracellular Ca2+ levels only in cells expressing HCs. The above changes induced by extracellular alkalinization did not change the cellular distribution of Cx43, suggesting that HC activation occurs through a gating mechanism. Experiments on cells expressing a COOH-terminal truncated Cx43 mutant indicated that the effects of alkalinization on intracellular Ca2+ and ethidium uptake did not depend on the Cx43 C terminus. Moreover, purified dephosphorylated Cx43 HCs reconstituted in liposomes were Ca2+ permeable, suggesting that Ca2+ influx through Cx43 HCs could account for the elevation in intracellular Ca2+ elicited by extracellular alkalinization. These studies identify a membrane pathway for Ca2+ influx and provide a potential explanation for the activation of cellular events induced by extracellular alkalinization.
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Frontiers in Neuroscience, Apr 27, 2022
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Acta Oto-laryngologica, Mar 1, 2023
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Cellular Immunology, Jun 1, 2007
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The Journal of General Physiology, Jun 28, 2010
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Frontiers in Cell and Developmental Biology, Jan 9, 2023
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Auditio, 2022
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International Journal of Molecular Sciences, 2021
Wound healing is a dynamic process required to maintain skin integrity and which relies on the pr... more Wound healing is a dynamic process required to maintain skin integrity and which relies on the precise migration of different cell types. A key molecule that regulates this process is ATP. However, the mechanisms involved in extracellular ATP management are poorly understood, particularly in the human dermis. Here, we explore the role, in human fibroblast migration during wound healing, of Pannexin 1 channels and their relationship with purinergic signals and in vivo cell surface filamentous actin dynamics. Using siRNA against Panx isoforms and different Panx1 channel inhibitors, we demonstrate in cultured human dermal fibroblasts that the absence or inhibition of Panx1 channels accelerates cell migration, increases single-cell motility, and promotes actin redistribution. These changes occur through a mechanism that involves the release of ATP to the extracellular space through a Panx1-dependent mechanism and the activation of the purinergic receptor P2X7. Together, these findings p...
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Journal of General Physiology, 2010
Mutations in GJB2, which encodes Cx26, are one of the most common causes of inherited deafness in... more Mutations in GJB2, which encodes Cx26, are one of the most common causes of inherited deafness in humans. More than 100 mutations have been identified scattered throughout the Cx26 protein, most of which cause nonsyndromic sensorineural deafness. In a subset of mutations, deafness is accompanied by hyperkeratotic skin disorders, which are typically severe and sometimes fatal. Many of these syndromic deafness mutations localize to the amino-terminal and first extracellular loop (E1) domains. Here, we examined two such mutations, A40V and G45E, which are positioned near the TM1/E1 boundary and are associated with keratitis ichthyosis deafness (KID) syndrome. Both of these mutants have been reported to form hemichannels that open aberrantly, leading to “leaky” cell membranes. Here, we quantified the Ca2+ sensitivities and examined the biophysical properties of these mutants at macroscopic and single-channel levels. We find that A40V hemichannels show significantly impaired regulation b...
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Frontiers in Neuroscience, Apr 27, 2022
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Papers by Helmuth Sanchez