Papers associated with skin (and gjb2)

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	The syndromic deafness mutation G12R impairs fast and slow gating in Cx26 hemichannels., García IE., J Gen Physiol. May 7, 2018; 150 (5): 697-711.
	Aberrant connexin26 hemichannels underlying keratitis-ichthyosis-deafness syndrome are potently inhibited by mefloquine., Levit NA., J Invest Dermatol. April 1, 2015; 135 (4): 1033-1042.
	The D50N mutation and syndromic deafness: altered Cx26 hemichannel properties caused by effects on the pore and intersubunit interactions., Sanchez HA., J Gen Physiol. July 1, 2013; 142 (1): 3-22.
	The human Cx26-D50A and Cx26-A88V mutations causing keratitis-ichthyosis-deafness syndrome display increased hemichannel activity., Mhaske PV., Am J Physiol Cell Physiol. June 15, 2013; 304 (12): C1150-8.
	Connexins in epidermal homeostasis and skin disease., Scott CA., Biochim Biophys Acta. August 1, 2012; 1818 (8): 1952-61.
	Zebrafish cx30.3: identification and characterization of a gap junction gene highly expressed in the skin., Tao L., Dev Dyn. October 1, 2010; 239 (10): 2627-36.
	Differentially altered Ca2+ regulation and Ca2+ permeability in Cx26 hemichannels formed by the A40V and G45E mutations that cause keratitis ichthyosis deafness syndrome., Sánchez HA., J Gen Physiol. July 1, 2010; 136 (1): 47-62.
	Connexin mutations causing skin disease and deafness increase hemichannel activity and cell death when expressed in Xenopus oocytes., Lee JR, Lee JR., J Invest Dermatol. April 1, 2009; 129 (4): 870-8.
	Aberrant hemichannel properties of Cx26 mutations causing skin disease and deafness., Gerido DA., Am J Physiol Cell Physiol. July 1, 2007; 293 (1): C337-45.
	Species specificity of mammalian connexin-26 to form open voltage-gated hemichannels., González D., FASEB J. November 1, 2006; 20 (13): 2329-38.
	An atlas of differential gene expression during early Xenopus embryogenesis., Pollet N., Mech Dev. March 1, 2005; 122 (3): 365-439.
	A novel connexin 26 gene mutation associated with features of the keratitis-ichthyosis-deafness syndrome and the follicular occlusion triad., Montgomery JR., J Am Acad Dermatol. September 1, 2004; 51 (3): 377-82.
	trans-dominant inhibition of connexin-43 by mutant connexin-26: implications for dominant connexin disorders affecting epidermal differentiation., Rouan F., J Cell Sci. June 1, 2001; 114 (Pt 11): 2105-13.
	Molecular cloning and functional expression of mouse connexin-30,a gap junction gene highly expressed in adult brain and skin., Dahl E., J Biol Chem. July 26, 1996; 271 (30): 17903-10.
	Molecular cloning and characterization of a new member of the gap junction gene family, connexin-31., Hoh JH., J Biol Chem. April 5, 1991; 266 (10): 6524-31.

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