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Wild type human cx26 hcx26 cdna

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The wild-type human Cx26 (hCx26) cDNA is a genetic sequence that encodes the connexin 26 protein, which is a component of gap junctions in human cells. Gap junctions facilitate intercellular communication by allowing the passage of small molecules and ions between neighboring cells.

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Lab products found in correlation

Mmessage machine t7 ultra kit, by Thermo Fisher Scientific (2 mentions) Pgem ha vector, by Promega (2 mentions) Quickchange 2 site directed mutagenesis kit, by Agilent Technologies (2 mentions)

2 protocols using wild type human cx26 hcx26 cdna

1

In vitro Characterization of Connexin 26 Mutations

Cited 1 time
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Wild-type human Cx26 (hCx26) cDNA was purchased from OriGene and was subcloned in the pGEM-HA vector (Promega) for in vitro translation. Mutations of hCx26 were produced with Quick-Change II Site-Directed Mutagenesis kits (Agilent Technologies). DNA sequencing performed at the New Jersey Medical School Molecular Resource Facility confirmed the amino acid substitutions. Nhe1-linearized hCx26 wild type, Cx43 and mutant DNAs were transcribed in vitro to cRNAs using the T7 Ultra mMessage Machine kit (Ambion). Electrophysiological data were collected using the two-electrode voltage-clamp technique as in our previous studies (Lopez et al., 2013a (link)).
García I.E., Maripillán J., Jara O., Ceriani R., Palacios-Muñoz A., Ramachandran J., Olivero P., Pérez-Acle T., González C., Sáez J.C., Contreras J.E, & Martínez A.D. (2015). Keratitis-Ichthyosis-Deafness syndrome-associated Cx26 mutants produce nonfunctional gap junctions but hyperactive hemichannels when co-expressed with wild type Cx43. The Journal of investigative dermatology, 135(5), 1338-1347.
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2

In vitro Characterization of Connexin 26 Mutations

Cited 1 time
Check if the same lab product or an alternative is used in the 5 most similar protocols
Wild-type human Cx26 (hCx26) cDNA was purchased from OriGene and was subcloned in the pGEM-HA vector (Promega) for in vitro translation. Mutations of hCx26 were produced with Quick-Change II Site-Directed Mutagenesis kits (Agilent Technologies). DNA sequencing performed at the New Jersey Medical School Molecular Resource Facility confirmed the amino acid substitutions. Nhe1-linearized hCx26 wild type, Cx43 and mutant DNAs were transcribed in vitro to cRNAs using the T7 Ultra mMessage Machine kit (Ambion). Electrophysiological data were collected using the two-electrode voltage-clamp technique as in our previous studies (Lopez et al., 2013a (link)).
García I.E., Maripillán J., Jara O., Ceriani R., Palacios-Muñoz A., Ramachandran J., Olivero P., Pérez-Acle T., González C., Sáez J.C., Contreras J.E, & Martínez A.D. (2015). Keratitis-Ichthyosis-Deafness syndrome-associated Cx26 mutants produce nonfunctional gap junctions but hyperactive hemichannels when co-expressed with wild type Cx43. The Journal of investigative dermatology, 135(5), 1338-1347.
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