004-700 Search Results


sally sue  (Bio-Techne corporation)
94
Bio-Techne corporation sally sue
Sally Sue, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sally sue  (Protein Simple Inc)
94
Protein Simple Inc sally sue
Sally Sue, supplied by Protein Simple Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human kcnq4  (OriGene)
91
OriGene human kcnq4
Fig. 1 Autosomal dominant non-syndromic hearing loss (DFNA2)-associated <t>KCNQ4</t> variants. a Exon structure of human KCNQ4 cDNA and domain structure of KCNQ4 are shown. Only variants identified in individuals with DFNA2 are shown. KCNQ4 contains 14 exons; the positions of the start (ATG) and stop (TGA) codons are indicated. Loss-of-function mutations, such as nonsense and frameshift mutations, are indicated. b Missense and in-frame deletion mutations are indicated. Note that mutations are clustered in exons 5 and 6, which encode part of the transmembrane (TM) 5, pore region, and TM6. The pathogenic variants identified by our group are shown in blue
Human Kcnq4, supplied by OriGene, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nm 004700  (Biotechnology Information)
86
Biotechnology Information nm 004700
Fig. 1 Autosomal dominant non-syndromic hearing loss (DFNA2)-associated <t>KCNQ4</t> variants. a Exon structure of human KCNQ4 cDNA and domain structure of KCNQ4 are shown. Only variants identified in individuals with DFNA2 are shown. KCNQ4 contains 14 exons; the positions of the start (ATG) and stop (TGA) codons are indicated. Loss-of-function mutations, such as nonsense and frameshift mutations, are indicated. b Missense and in-frame deletion mutations are indicated. Note that mutations are clustered in exons 5 and 6, which encode part of the transmembrane (TM) 5, pore region, and TM6. The pathogenic variants identified by our group are shown in blue
Nm 004700, supplied by Biotechnology Information, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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kcnq4 nm 004700 human tagged orf clone  (OriGene)
N/A
Lenti ORF clone of Human potassium voltage gated channel KQT like subfamily member 4 KCNQ4 transcript variant 1 mGFP tagged
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kcnq4 nm 004700 human tagged orf clone lentiviral particle  (OriGene)
N/A
Lenti ORF particles KCNQ4 Myc DDK tagged Human potassium voltage gated channel KQT like subfamily member 4 KCNQ4 transcript variant 1 200ul 10 7 TU mL
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kcnq4 nm 004700 human untagged clone  (OriGene)
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KCNQ4 untagged Human potassium voltage gated channel KQT like subfamily member 4 KCNQ4 transcript variant 1
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Image Search Results


Fig. 1 Autosomal dominant non-syndromic hearing loss (DFNA2)-associated KCNQ4 variants. a Exon structure of human KCNQ4 cDNA and domain structure of KCNQ4 are shown. Only variants identified in individuals with DFNA2 are shown. KCNQ4 contains 14 exons; the positions of the start (ATG) and stop (TGA) codons are indicated. Loss-of-function mutations, such as nonsense and frameshift mutations, are indicated. b Missense and in-frame deletion mutations are indicated. Note that mutations are clustered in exons 5 and 6, which encode part of the transmembrane (TM) 5, pore region, and TM6. The pathogenic variants identified by our group are shown in blue

Journal: Experimental & molecular medicine

Article Title: Rare KCNQ4 variants found in public databases underlie impaired channel activity that may contribute to hearing impairment.

doi: 10.1038/s12276-019-0300-9

Figure Lengend Snippet: Fig. 1 Autosomal dominant non-syndromic hearing loss (DFNA2)-associated KCNQ4 variants. a Exon structure of human KCNQ4 cDNA and domain structure of KCNQ4 are shown. Only variants identified in individuals with DFNA2 are shown. KCNQ4 contains 14 exons; the positions of the start (ATG) and stop (TGA) codons are indicated. Loss-of-function mutations, such as nonsense and frameshift mutations, are indicated. b Missense and in-frame deletion mutations are indicated. Note that mutations are clustered in exons 5 and 6, which encode part of the transmembrane (TM) 5, pore region, and TM6. The pathogenic variants identified by our group are shown in blue

Article Snippet: Plasmid construction and site-directed mutagenesis Complementary DNAs (cDNAs) of human KCNQ4 were purchased from OriGene Technologies (Rockville, MD, USA) and subcloned into the pENTR-D-TOPO vector (Invitrogen, Carlsbad, CA, USA).

Techniques:

Fig. 4 Effect of retigabine on current produced by KCNQ4 mutants. a Enhancement of voltage-gated potassium channel activity of wild-type (WT) KCNQ4 by retigabine. b Summary bar graph of current produced by KCNQ4 mutants and rescued by retigabine versus that of WT, obtained from steady-state currents elicited at 40 mV shown in Supplementary Fig. 2. Current values were 131.4 ± 37.6 pA/pF (n = 11), 194 ± 28.3 pA/pF (n = 9), 229.2 ± 62.2 pA/pF (n = 6), 129.7 ± 23.2 pA/pF (n = 8), 126.4 ± 17.8 pA/pF (n = 10), 58.8 ± 21.5 pA/pF (n = 6), 24.4 ± 3.3 pA/pF (n = 4), 37.4 ± 8.6 pA/pF (n = 4), and 30.4 ± 5.8 pA/pF (n = 5) for p.T278A, p.S273A, p.L281M, p.L295P, p.R433W, p.N264S, p.S269F, p.W276S, and green fluorescent protein, respectively. c Effect of retigabine on thallium influx in cells expressing WT and mutant KCNQ4. Data represent the mean ± SEM. **P < 0.01, ***P < 0.001 compared to WT (a, b) or mock (c). Statistical analysis was performed using one-way ANOVA with Bonferroni’s multiple comparison

Journal: Experimental & molecular medicine

Article Title: Rare KCNQ4 variants found in public databases underlie impaired channel activity that may contribute to hearing impairment.

doi: 10.1038/s12276-019-0300-9

Figure Lengend Snippet: Fig. 4 Effect of retigabine on current produced by KCNQ4 mutants. a Enhancement of voltage-gated potassium channel activity of wild-type (WT) KCNQ4 by retigabine. b Summary bar graph of current produced by KCNQ4 mutants and rescued by retigabine versus that of WT, obtained from steady-state currents elicited at 40 mV shown in Supplementary Fig. 2. Current values were 131.4 ± 37.6 pA/pF (n = 11), 194 ± 28.3 pA/pF (n = 9), 229.2 ± 62.2 pA/pF (n = 6), 129.7 ± 23.2 pA/pF (n = 8), 126.4 ± 17.8 pA/pF (n = 10), 58.8 ± 21.5 pA/pF (n = 6), 24.4 ± 3.3 pA/pF (n = 4), 37.4 ± 8.6 pA/pF (n = 4), and 30.4 ± 5.8 pA/pF (n = 5) for p.T278A, p.S273A, p.L281M, p.L295P, p.R433W, p.N264S, p.S269F, p.W276S, and green fluorescent protein, respectively. c Effect of retigabine on thallium influx in cells expressing WT and mutant KCNQ4. Data represent the mean ± SEM. **P < 0.01, ***P < 0.001 compared to WT (a, b) or mock (c). Statistical analysis was performed using one-way ANOVA with Bonferroni’s multiple comparison

Article Snippet: Plasmid construction and site-directed mutagenesis Complementary DNAs (cDNAs) of human KCNQ4 were purchased from OriGene Technologies (Rockville, MD, USA) and subcloned into the pENTR-D-TOPO vector (Invitrogen, Carlsbad, CA, USA).

Techniques: Produced, Activity Assay, Expressing, Mutagenesis, Comparison