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Bioss antibodies against unc80

Expression patterns of ADAR2-mediated RNA editing of <t>Unc80</t> in the brain and its structural implications. Total RNA was extracted from various tissues and brain regions from wild-type (WT) and Adar2-knockout (KO) mice. The samples were then analyzed using RT-PCR ( A ) and Sanger sequencing ( B ). The sequencing chromatograms highlight the absence of guanine (“G”) signals (indicated by arrows) in the KO samples, demonstrating the reliance of Unc80 editing on ADAR2’s enzymatic function. Differences in RNA editing levels across brain regions were also observed. The percentage represents the editing frequency, calculated by taking the peak area of G peak over the sum of A and G peaks. ( C ) Prediction of 3-dimensional protein structure models of Unc80 WT and Unc80 S2732G . The magnified view of the region of interest highlights the residue change from Ser to Gly due to editing. ( D ) Immunofluorescence analysis on olfactory bulb coronal sections, specifically localizing Unc80 (green) and NeuN (red) protein. The a and b correspond to magnified views of the white dashed boxes in left panel. The arrows indicate the positions of overlapping fluorescence (green and red). Scale bars = 200 µm in the left panel and 40 µm in the magnified images. (TA: Tibialis anterior muscle, GA: Gastrocnemius muscle, CT: cortex, CB: cerebellum, HP: hippocampus, OB: olfactory bulb).

Antibodies Against Unc80, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Imbalance in Unc80 RNA Editing Disrupts Dynamic Neuronal Activity and Olfactory Perception"

Article Title: Imbalance in Unc80 RNA Editing Disrupts Dynamic Neuronal Activity and Olfactory Perception

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms25115985

Expression patterns of ADAR2-mediated RNA editing of Unc80 in the brain and its structural implications. Total RNA was extracted from various tissues and brain regions from wild-type (WT) and Adar2-knockout (KO) mice. The samples were then analyzed using RT-PCR ( A ) and Sanger sequencing ( B ). The sequencing chromatograms highlight the absence of guanine (“G”) signals (indicated by arrows) in the KO samples, demonstrating the reliance of Unc80 editing on ADAR2’s enzymatic function. Differences in RNA editing levels across brain regions were also observed. The percentage represents the editing frequency, calculated by taking the peak area of G peak over the sum of A and G peaks. ( C ) Prediction of 3-dimensional protein structure models of Unc80 WT and Unc80 S2732G . The magnified view of the region of interest highlights the residue change from Ser to Gly due to editing. ( D ) Immunofluorescence analysis on olfactory bulb coronal sections, specifically localizing Unc80 (green) and NeuN (red) protein. The a and b correspond to magnified views of the white dashed boxes in left panel. The arrows indicate the positions of overlapping fluorescence (green and red). Scale bars = 200 µm in the left panel and 40 µm in the magnified images. (TA: Tibialis anterior muscle, GA: Gastrocnemius muscle, CT: cortex, CB: cerebellum, HP: hippocampus, OB: olfactory bulb).

Figure Legend Snippet: Expression patterns of ADAR2-mediated RNA editing of Unc80 in the brain and its structural implications. Total RNA was extracted from various tissues and brain regions from wild-type (WT) and Adar2-knockout (KO) mice. The samples were then analyzed using RT-PCR ( A ) and Sanger sequencing ( B ). The sequencing chromatograms highlight the absence of guanine (“G”) signals (indicated by arrows) in the KO samples, demonstrating the reliance of Unc80 editing on ADAR2’s enzymatic function. Differences in RNA editing levels across brain regions were also observed. The percentage represents the editing frequency, calculated by taking the peak area of G peak over the sum of A and G peaks. ( C ) Prediction of 3-dimensional protein structure models of Unc80 WT and Unc80 S2732G . The magnified view of the region of interest highlights the residue change from Ser to Gly due to editing. ( D ) Immunofluorescence analysis on olfactory bulb coronal sections, specifically localizing Unc80 (green) and NeuN (red) protein. The a and b correspond to magnified views of the white dashed boxes in left panel. The arrows indicate the positions of overlapping fluorescence (green and red). Scale bars = 200 µm in the left panel and 40 µm in the magnified images. (TA: Tibialis anterior muscle, GA: Gastrocnemius muscle, CT: cortex, CB: cerebellum, HP: hippocampus, OB: olfactory bulb).

Techniques Used: Expressing, Knock-Out, Reverse Transcription Polymerase Chain Reaction, Sequencing, Residue, Immunofluorescence, Fluorescence

Generation of Unc80 -deleted and site-specific RNA editing mouse models: ( A ) Experimental schematic of the CRISPR/Cas9-based genetic engineering to generate deficient and knock-in mouse models. gRNA (nucleotide with orange background) together with Cas9 created indels, thus establishing knockout mice. In parallel, the addition of synthesized homologous DNA templates corresponding to the Unc80 sequence region with a substitution for the “pre-edited” (G-form) allele (gain of editing) or the “unedited” version (loss of editing) resulted in the knock-in models. ( B ) Breeding schemes of mice with site-specific knock-ins at the Unc80 editing site. ( C ) Genomic DNA sequencing for genotyping demonstrates the WT sequence (top) and mutations in founder strains ( Unc80 +/− ). Deletions and point mutations are indicated by a red background and purple boxes, respectively, in heterozygous deletion (Unc80 +/− ) or knock-in mice ( Unc80 S/S , Unc80 G/G , and Unc80 S/G ). The green box denotes the targeted editing site. ( D ) Gross morphological comparison and body weights of newborn (P0) mice across genotypes. ( E ) Offspring genotyping from heterozygous Unc80 +/− crosses reveals a lower-than-expected birth rate for homozygous deletion offspring, whereas knock-in alleles followed an approximately Mendelian inheritance pattern. ( F,G ) Unc80 protein and mRNA levels in brain tissue lysates (cortex and olfactory bulb) from CRISPR-engineered Unc80 -deficient mice were assessed via immunoblotting ( F ) and qRT-PCR (OB, ( G )).

Figure Legend Snippet: Generation of Unc80 -deleted and site-specific RNA editing mouse models: ( A ) Experimental schematic of the CRISPR/Cas9-based genetic engineering to generate deficient and knock-in mouse models. gRNA (nucleotide with orange background) together with Cas9 created indels, thus establishing knockout mice. In parallel, the addition of synthesized homologous DNA templates corresponding to the Unc80 sequence region with a substitution for the “pre-edited” (G-form) allele (gain of editing) or the “unedited” version (loss of editing) resulted in the knock-in models. ( B ) Breeding schemes of mice with site-specific knock-ins at the Unc80 editing site. ( C ) Genomic DNA sequencing for genotyping demonstrates the WT sequence (top) and mutations in founder strains ( Unc80 +/− ). Deletions and point mutations are indicated by a red background and purple boxes, respectively, in heterozygous deletion (Unc80 +/− ) or knock-in mice ( Unc80 S/S , Unc80 G/G , and Unc80 S/G ). The green box denotes the targeted editing site. ( D ) Gross morphological comparison and body weights of newborn (P0) mice across genotypes. ( E ) Offspring genotyping from heterozygous Unc80 +/− crosses reveals a lower-than-expected birth rate for homozygous deletion offspring, whereas knock-in alleles followed an approximately Mendelian inheritance pattern. ( F,G ) Unc80 protein and mRNA levels in brain tissue lysates (cortex and olfactory bulb) from CRISPR-engineered Unc80 -deficient mice were assessed via immunoblotting ( F ) and qRT-PCR (OB, ( G )).

Techniques Used: CRISPR, Knock-In, Knock-Out, Synthesized, Sequencing, DNA Sequencing, Comparison, Western Blot, Quantitative RT-PCR

MEMRI-based neuronal activity assessment in the olfactory systems of Unc80 S/S and Unc80 G/G mice: ( A ) Anatomical MRI images and corresponding color mapping generated during odor stimulation. ( B ) Variation in MEMRI signal intensity in response to odor stimulation, with error bars representing the SD. ( C ) In vivo glutamate- and dopamine-sensitive CEST-MRI images showing anatomical and color mapping in various brain nuclei. ( D ) Quantitative changes in CEST-MRI signals across different brain nuclei for Unc80 S/S and Unc80 G/G mice, depicting both glutamate (left) and dopamine (right) contrasts. Brain regions assessed include the olfactory bulb (OB), anterior olfactory nucleus (AON), and anterior piriform cortex (APC). Error bars indicate SD. Statistical significance is denoted as follows: ns (not significant); p > 0.05; * p < 0.05; ** p < 0.01.

Figure Legend Snippet: MEMRI-based neuronal activity assessment in the olfactory systems of Unc80 S/S and Unc80 G/G mice: ( A ) Anatomical MRI images and corresponding color mapping generated during odor stimulation. ( B ) Variation in MEMRI signal intensity in response to odor stimulation, with error bars representing the SD. ( C ) In vivo glutamate- and dopamine-sensitive CEST-MRI images showing anatomical and color mapping in various brain nuclei. ( D ) Quantitative changes in CEST-MRI signals across different brain nuclei for Unc80 S/S and Unc80 G/G mice, depicting both glutamate (left) and dopamine (right) contrasts. Brain regions assessed include the olfactory bulb (OB), anterior olfactory nucleus (AON), and anterior piriform cortex (APC). Error bars indicate SD. Statistical significance is denoted as follows: ns (not significant); p > 0.05; * p < 0.05; ** p < 0.01.

Techniques Used: Activity Assay, Generated, In Vivo

Neurophysiological connection of Unc80 editing event to olfactory sensing and motor control: Habituation and dishabituation behaviors, in response to odors, were analyzed for Unc80 knockout and site-specific editing variants ( A , B ), along with odor-induced neuronal activity assays ( C , D ). Mice with different genotypes (wild-type vs. Unc80 +/− in ( A ), Unc80 S/S vs. Unc80 G/G in ( B )) were exposed to odors, and their explorative times near the odor source were recorded and presented as mean ± SD. The cohorts consisted of: WT (n = 13), Unc80 +/− (n = 5), Unc80 S/S (n = 9), Unc80 G/G (n = 8). For the neuronal activation assay, knock-in mice with site-specific edits were either not exposed or exposed to banana oil for up to 60 min and subsequently sacrificed for olfactory bulb isolation, from which total RNA and proteins were prepared for qRT-PCR ( C ) and Western blot ( D ) analyses, respectively. Changes in the expression of c-Fos were monitored as a readout for neuronal activation. The bar graph represents the relative mRNA expression levels of Fos. Statistical significance is indicated as follows: ns (not significant); p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001.

Figure Legend Snippet: Neurophysiological connection of Unc80 editing event to olfactory sensing and motor control: Habituation and dishabituation behaviors, in response to odors, were analyzed for Unc80 knockout and site-specific editing variants ( A , B ), along with odor-induced neuronal activity assays ( C , D ). Mice with different genotypes (wild-type vs. Unc80 +/− in ( A ), Unc80 S/S vs. Unc80 G/G in ( B )) were exposed to odors, and their explorative times near the odor source were recorded and presented as mean ± SD. The cohorts consisted of: WT (n = 13), Unc80 +/− (n = 5), Unc80 S/S (n = 9), Unc80 G/G (n = 8). For the neuronal activation assay, knock-in mice with site-specific edits were either not exposed or exposed to banana oil for up to 60 min and subsequently sacrificed for olfactory bulb isolation, from which total RNA and proteins were prepared for qRT-PCR ( C ) and Western blot ( D ) analyses, respectively. Changes in the expression of c-Fos were monitored as a readout for neuronal activation. The bar graph represents the relative mRNA expression levels of Fos. Statistical significance is indicated as follows: ns (not significant); p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001.

Techniques Used: Control, Knock-Out, Activity Assay, Activation Assay, Knock-In, Isolation, Quantitative RT-PCR, Western Blot, Expressing

Transcriptomic analysis of the olfactory bulb in Unc80 editing variant mice. Transcriptome-wide RNA-seq was conducted to identify changes in the olfactory bulb of Unc80 S/S and Unc80 G/G mice. ( A – C ) The overall transcriptome distribution is represented in a principal component analysis (PCA) plot ( A ) and a volcano plot ( B ), delineating genotype-specific gene expression profiles. A heatmap ( C ) displays genes with significant differential expression (|fold-change| > 1.5, p < 0.05; n = 6 per genotype, with samples pooled from three mice each) between the two strains. ( D ) Bubble chart of the enriched canonical pathway from IPA analysis. The x -axis represents the significance ( p -value), and the y -axis shows the top 17 significantly enriched pathways based on differentially expressed genes (DEGs). The size of the circles corresponds to the number of genes associated with each pathway. The colors of the bubbles denote the Z-score, indicating whether the pathway is activated (orange, positive Z-score) or inhibited (blue, negative Z-score). ( E ) Normalized read count plots highlight expression variations in gene sets linked to neuronal signaling between Unc80 S/S and Unc80 G/G mice. Statistical significance in this figure is indicated as follows: * p < 0.05; ** p < 0.01; *** p < 0.001.

Figure Legend Snippet: Transcriptomic analysis of the olfactory bulb in Unc80 editing variant mice. Transcriptome-wide RNA-seq was conducted to identify changes in the olfactory bulb of Unc80 S/S and Unc80 G/G mice. ( A – C ) The overall transcriptome distribution is represented in a principal component analysis (PCA) plot ( A ) and a volcano plot ( B ), delineating genotype-specific gene expression profiles. A heatmap ( C ) displays genes with significant differential expression (|fold-change| > 1.5, p < 0.05; n = 6 per genotype, with samples pooled from three mice each) between the two strains. ( D ) Bubble chart of the enriched canonical pathway from IPA analysis. The x -axis represents the significance ( p -value), and the y -axis shows the top 17 significantly enriched pathways based on differentially expressed genes (DEGs). The size of the circles corresponds to the number of genes associated with each pathway. The colors of the bubbles denote the Z-score, indicating whether the pathway is activated (orange, positive Z-score) or inhibited (blue, negative Z-score). ( E ) Normalized read count plots highlight expression variations in gene sets linked to neuronal signaling between Unc80 S/S and Unc80 G/G mice. Statistical significance in this figure is indicated as follows: * p < 0.05; ** p < 0.01; *** p < 0.001.

Techniques Used: Variant Assay, RNA Sequencing Assay, Expressing

Image Search Results

Journal: International Journal of Molecular Sciences

Article Title: Imbalance in Unc80 RNA Editing Disrupts Dynamic Neuronal Activity and Olfactory Perception

doi: 10.3390/ijms25115985

Figure Lengend Snippet: Expression patterns of ADAR2-mediated RNA editing of Unc80 in the brain and its structural implications. Total RNA was extracted from various tissues and brain regions from wild-type (WT) and Adar2-knockout (KO) mice. The samples were then analyzed using RT-PCR ( A ) and Sanger sequencing ( B ). The sequencing chromatograms highlight the absence of guanine (“G”) signals (indicated by arrows) in the KO samples, demonstrating the reliance of Unc80 editing on ADAR2’s enzymatic function. Differences in RNA editing levels across brain regions were also observed. The percentage represents the editing frequency, calculated by taking the peak area of G peak over the sum of A and G peaks. ( C ) Prediction of 3-dimensional protein structure models of Unc80 WT and Unc80 S2732G . The magnified view of the region of interest highlights the residue change from Ser to Gly due to editing. ( D ) Immunofluorescence analysis on olfactory bulb coronal sections, specifically localizing Unc80 (green) and NeuN (red) protein. The a and b correspond to magnified views of the white dashed boxes in left panel. The arrows indicate the positions of overlapping fluorescence (green and red). Scale bars = 200 µm in the left panel and 40 µm in the magnified images. (TA: Tibialis anterior muscle, GA: Gastrocnemius muscle, CT: cortex, CB: cerebellum, HP: hippocampus, OB: olfactory bulb).

Article Snippet: Sagittal frozen sections (30 μm) were cut with a cryostat (Leica Microsystems, Wetzlar, Germany, SM 2010R), permeabilized, and blocked with 10% BSA in 0.5% Triton X-100 for 2 h, then incubated overnight at 4 °C with primary antibodies against Unc80 (BS-12121R, BIOSS, Woburn, MA, USA) and NeuN (MAB377, Merck Millipore, Darmstadt, Germany).

Techniques: Expressing, Knock-Out, Reverse Transcription Polymerase Chain Reaction, Sequencing, Residue, Immunofluorescence, Fluorescence

Journal: International Journal of Molecular Sciences

Article Title: Imbalance in Unc80 RNA Editing Disrupts Dynamic Neuronal Activity and Olfactory Perception

doi: 10.3390/ijms25115985

Figure Lengend Snippet: Generation of Unc80 -deleted and site-specific RNA editing mouse models: ( A ) Experimental schematic of the CRISPR/Cas9-based genetic engineering to generate deficient and knock-in mouse models. gRNA (nucleotide with orange background) together with Cas9 created indels, thus establishing knockout mice. In parallel, the addition of synthesized homologous DNA templates corresponding to the Unc80 sequence region with a substitution for the “pre-edited” (G-form) allele (gain of editing) or the “unedited” version (loss of editing) resulted in the knock-in models. ( B ) Breeding schemes of mice with site-specific knock-ins at the Unc80 editing site. ( C ) Genomic DNA sequencing for genotyping demonstrates the WT sequence (top) and mutations in founder strains ( Unc80 +/− ). Deletions and point mutations are indicated by a red background and purple boxes, respectively, in heterozygous deletion (Unc80 +/− ) or knock-in mice ( Unc80 S/S , Unc80 G/G , and Unc80 S/G ). The green box denotes the targeted editing site. ( D ) Gross morphological comparison and body weights of newborn (P0) mice across genotypes. ( E ) Offspring genotyping from heterozygous Unc80 +/− crosses reveals a lower-than-expected birth rate for homozygous deletion offspring, whereas knock-in alleles followed an approximately Mendelian inheritance pattern. ( F,G ) Unc80 protein and mRNA levels in brain tissue lysates (cortex and olfactory bulb) from CRISPR-engineered Unc80 -deficient mice were assessed via immunoblotting ( F ) and qRT-PCR (OB, ( G )).

Techniques: CRISPR, Knock-In, Knock-Out, Synthesized, Sequencing, DNA Sequencing, Comparison, Western Blot, Quantitative RT-PCR

Journal: International Journal of Molecular Sciences

Article Title: Imbalance in Unc80 RNA Editing Disrupts Dynamic Neuronal Activity and Olfactory Perception

doi: 10.3390/ijms25115985

Figure Lengend Snippet: MEMRI-based neuronal activity assessment in the olfactory systems of Unc80 S/S and Unc80 G/G mice: ( A ) Anatomical MRI images and corresponding color mapping generated during odor stimulation. ( B ) Variation in MEMRI signal intensity in response to odor stimulation, with error bars representing the SD. ( C ) In vivo glutamate- and dopamine-sensitive CEST-MRI images showing anatomical and color mapping in various brain nuclei. ( D ) Quantitative changes in CEST-MRI signals across different brain nuclei for Unc80 S/S and Unc80 G/G mice, depicting both glutamate (left) and dopamine (right) contrasts. Brain regions assessed include the olfactory bulb (OB), anterior olfactory nucleus (AON), and anterior piriform cortex (APC). Error bars indicate SD. Statistical significance is denoted as follows: ns (not significant); p > 0.05; * p < 0.05; ** p < 0.01.

Techniques: Activity Assay, Generated, In Vivo

Journal: International Journal of Molecular Sciences

Article Title: Imbalance in Unc80 RNA Editing Disrupts Dynamic Neuronal Activity and Olfactory Perception

doi: 10.3390/ijms25115985

Figure Lengend Snippet: Neurophysiological connection of Unc80 editing event to olfactory sensing and motor control: Habituation and dishabituation behaviors, in response to odors, were analyzed for Unc80 knockout and site-specific editing variants ( A , B ), along with odor-induced neuronal activity assays ( C , D ). Mice with different genotypes (wild-type vs. Unc80 +/− in ( A ), Unc80 S/S vs. Unc80 G/G in ( B )) were exposed to odors, and their explorative times near the odor source were recorded and presented as mean ± SD. The cohorts consisted of: WT (n = 13), Unc80 +/− (n = 5), Unc80 S/S (n = 9), Unc80 G/G (n = 8). For the neuronal activation assay, knock-in mice with site-specific edits were either not exposed or exposed to banana oil for up to 60 min and subsequently sacrificed for olfactory bulb isolation, from which total RNA and proteins were prepared for qRT-PCR ( C ) and Western blot ( D ) analyses, respectively. Changes in the expression of c-Fos were monitored as a readout for neuronal activation. The bar graph represents the relative mRNA expression levels of Fos. Statistical significance is indicated as follows: ns (not significant); p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001.

Techniques: Control, Knock-Out, Activity Assay, Activation Assay, Knock-In, Isolation, Quantitative RT-PCR, Western Blot, Expressing

Journal: International Journal of Molecular Sciences

Article Title: Imbalance in Unc80 RNA Editing Disrupts Dynamic Neuronal Activity and Olfactory Perception

doi: 10.3390/ijms25115985

Figure Lengend Snippet: Transcriptomic analysis of the olfactory bulb in Unc80 editing variant mice. Transcriptome-wide RNA-seq was conducted to identify changes in the olfactory bulb of Unc80 S/S and Unc80 G/G mice. ( A – C ) The overall transcriptome distribution is represented in a principal component analysis (PCA) plot ( A ) and a volcano plot ( B ), delineating genotype-specific gene expression profiles. A heatmap ( C ) displays genes with significant differential expression (|fold-change| > 1.5, p < 0.05; n = 6 per genotype, with samples pooled from three mice each) between the two strains. ( D ) Bubble chart of the enriched canonical pathway from IPA analysis. The x -axis represents the significance ( p -value), and the y -axis shows the top 17 significantly enriched pathways based on differentially expressed genes (DEGs). The size of the circles corresponds to the number of genes associated with each pathway. The colors of the bubbles denote the Z-score, indicating whether the pathway is activated (orange, positive Z-score) or inhibited (blue, negative Z-score). ( E ) Normalized read count plots highlight expression variations in gene sets linked to neuronal signaling between Unc80 S/S and Unc80 G/G mice. Statistical significance in this figure is indicated as follows: * p < 0.05; ** p < 0.01; *** p < 0.001.

Techniques: Variant Assay, RNA Sequencing Assay, Expressing

a Illustrator and workflow for single-cell RNA sequencing (scRNA-seq) of SAN. b t -distributed stochastic neighbor embedding (t-SNE) analysis identified five clusters including four SAN cell clusters (Clusters 1, 2, 3, 4) and one atrial and ventricular (AV) cardiomyocytes cell cluster (Cluster 5) ( n = 771 biologically independent cells of 25 independent animals). c Heat map shows top differentially expressed genes (DEGs) of each cluster. Cluster 4 was highly expressed cell markers including Hcn4, Hcn1 , and Ednrb, Pde1a and identified as the core cell cluster. d Feature plot of DEGs shows Vsnl1, Unc80 , and Dlgap1 were expressed more specifically than Hcn4 and Hcn1 in Cluster 4. Location of each cluster was marked with the red circle. e Gene Ontology (GO) terms show the biological processes of SAN cell clusters and Cluster 4 was mainly associated with regulation of heart rate and ion transmembrane transport, while Cluster 1, 2, and 3 were all related to electrical activity but had certain difference.

Journal: Nature Communications

Article Title: Cellular and molecular landscape of mammalian sinoatrial node revealed by single-cell RNA sequencing

doi: 10.1038/s41467-020-20448-x

Figure Lengend Snippet: a Illustrator and workflow for single-cell RNA sequencing (scRNA-seq) of SAN. b t -distributed stochastic neighbor embedding (t-SNE) analysis identified five clusters including four SAN cell clusters (Clusters 1, 2, 3, 4) and one atrial and ventricular (AV) cardiomyocytes cell cluster (Cluster 5) ( n = 771 biologically independent cells of 25 independent animals). c Heat map shows top differentially expressed genes (DEGs) of each cluster. Cluster 4 was highly expressed cell markers including Hcn4, Hcn1 , and Ednrb, Pde1a and identified as the core cell cluster. d Feature plot of DEGs shows Vsnl1, Unc80 , and Dlgap1 were expressed more specifically than Hcn4 and Hcn1 in Cluster 4. Location of each cluster was marked with the red circle. e Gene Ontology (GO) terms show the biological processes of SAN cell clusters and Cluster 4 was mainly associated with regulation of heart rate and ion transmembrane transport, while Cluster 1, 2, and 3 were all related to electrical activity but had certain difference.

Article Snippet: Primary antibodies included HCN4 (Sigma, SAB5200035, 1:50), Connexin 43 (CST, 3512, 1:50), VSNL1 (Gene Tex, GTX115039, 1:50), Collagen I (Abcam, ab21286, 1:50), DLGAP1 (Affbiotech, AF0308, 1:50), UNC80 (BIOSS, BS-12121R, 1:50), APOLD1 (Novus Biologicals, NBP2-58460, 1:50), RYR3 (Novus Biologicals, NBP2-76962, 1:50), Connexin 40 (Invitrogen, 37-8900, 1:50), cTNT (Abcam, ab8295, 1:50).

Techniques: RNA Sequencing Assay, Activity Assay

a qPCR analysis shows the expression of Hcn4, Vsnl1, Dlgap1, and Unc80 in sinoatrial node (SAN), atrial, and ventricular tissue, respectively ( n = 4 biologically independent animals per group), Dunnett’s multiple comparisons test, data are represented as mean ± s.e.m., adjusted p value was labeled on the top. RA right atrium, LA left atrium, RV right ventricle, LV left ventricle. b – g Immunohistochemical analysis of VSNL1, DLGAP1, and UNC80 in SAN slices at low magnification. Representative images are shown from n = 3 biologically independent samples. b Immunofluorescence images of HCN4 (green), VSNL1 (red), and DAPI (blue). c Immunofluorescence images of HCN4 (green), DLGAP1 (red), and DAPI (blue). d Immunofluorescence images of HCN4 (green), UNC80 (red), and DAPI (blue). b – d The arrows indicate the tissues surrounding the SAN. Scale bar = 250 μm. e – g Localization of the VSNL1, DLGAP1, and UNC80 within SAN at high magnification. e Immunofluorescence images of HCN4 (green), VSNL1 (red), and DAPI (blue). f Immunofluorescence images of HCN4 (green), DLGAP1 (red), and DAPI (blue). g Immunofluorescence images of HCN4 (green), UNC80 (red), and DAPI (blue). Scale bar = 50 μm. e – g Zoom images (the red box regions in the merged image) show the higher magnification. Scale bar = 10 μm.

Journal: Nature Communications

Article Title: Cellular and molecular landscape of mammalian sinoatrial node revealed by single-cell RNA sequencing

doi: 10.1038/s41467-020-20448-x

Figure Lengend Snippet: a qPCR analysis shows the expression of Hcn4, Vsnl1, Dlgap1, and Unc80 in sinoatrial node (SAN), atrial, and ventricular tissue, respectively ( n = 4 biologically independent animals per group), Dunnett’s multiple comparisons test, data are represented as mean ± s.e.m., adjusted p value was labeled on the top. RA right atrium, LA left atrium, RV right ventricle, LV left ventricle. b – g Immunohistochemical analysis of VSNL1, DLGAP1, and UNC80 in SAN slices at low magnification. Representative images are shown from n = 3 biologically independent samples. b Immunofluorescence images of HCN4 (green), VSNL1 (red), and DAPI (blue). c Immunofluorescence images of HCN4 (green), DLGAP1 (red), and DAPI (blue). d Immunofluorescence images of HCN4 (green), UNC80 (red), and DAPI (blue). b – d The arrows indicate the tissues surrounding the SAN. Scale bar = 250 μm. e – g Localization of the VSNL1, DLGAP1, and UNC80 within SAN at high magnification. e Immunofluorescence images of HCN4 (green), VSNL1 (red), and DAPI (blue). f Immunofluorescence images of HCN4 (green), DLGAP1 (red), and DAPI (blue). g Immunofluorescence images of HCN4 (green), UNC80 (red), and DAPI (blue). Scale bar = 50 μm. e – g Zoom images (the red box regions in the merged image) show the higher magnification. Scale bar = 10 μm.

Techniques: Expressing, Labeling, Immunohistochemical staining, Immunofluorescence

Journal: Nature Communications

Article Title: Cellular and molecular landscape of mammalian sinoatrial node revealed by single-cell RNA sequencing

doi: 10.1038/s41467-020-20448-x

Techniques: RNA Sequencing Assay, Activity Assay

Journal: Nature Communications

Article Title: Cellular and molecular landscape of mammalian sinoatrial node revealed by single-cell RNA sequencing

doi: 10.1038/s41467-020-20448-x

Techniques: Expressing, Labeling, Immunohistochemical staining, Immunofluorescence

Journal: eLife

Article Title: Unified single-cell analysis of testis gene regulation and pathology in five mouse strains

doi: 10.7554/eLife.43966

Figure Lengend Snippet:

Article Snippet: Antibody , Goat polyclonal anti-UNC80 (L-16) , Santa Cruz Biotechnology , Cat# sc-165859 , (1:100) dilution.

Techniques: Sequencing, Software

Representative currents elicited by voltage ramps (−80 mV to +20 mV over 1000 ms) from (A) untransfected cells, (B) eGFP cells (C) M3R cells, and (D) M3R + NALCN/Unc80/Src cells before application of muscarinic receptor agonist (100 μM muscarine iodide or Oxo-M). Control, response and recovery indicated by arrows.

Journal: Biochimie Open

Article Title: Lack of current observed in HEK293 cells expressing NALCN channels

doi: 10.1016/j.biopen.2018.01.001

Figure Lengend Snippet: Representative currents elicited by voltage ramps (−80 mV to +20 mV over 1000 ms) from (A) untransfected cells, (B) eGFP cells (C) M3R cells, and (D) M3R + NALCN/Unc80/Src cells before application of muscarinic receptor agonist (100 μM muscarine iodide or Oxo-M). Control, response and recovery indicated by arrows.

Article Snippet: Plasmids encoding NALCN/eGFP (in a bicistronic pTracer expression vector, CVM promoter, Invitrogen), UNC80 and Src (in a pcDNA3 vector, Invitrogen) were kindly provided by D. Ren (University of Pennsylvania, Philadelphia).

Techniques:

Currents observed in M3R and M3R + NALCN/Unc80/Src cells exhibited similar properties to currents observed in untransfected cells and eGFP transfected cells. (A) The amplitude of the current at +20 mV before and after application of muscarinic receptor agonist (muscarine iodide or Oxo-M) at 100 μM for all cells tested. There was a significant main effect between the current amplitude before and after agonist (within-subject effect in a two-way mixed-design ANOVA, DF = 1, p = 7.0 × 10 −7 , followed by Bonferroni post hoc tests; where * indicates p < 0.05). There were no significant differences between the current amplitudes of untransfected, eGFP, M3R or M3R + NALCN/Unc80/Src cells (between subject effects; DF = 3, p = 0.53). (B) The amplitude of the current at +20 mV before and after application of muscarinic receptor agonist (muscarine iodide or Oxo-M) at 100 μM for only responsive cells. There was a significant main effect between the current amplitude before and after agonist (within-subject effect in a two-way mixed-design ANOVA, DF = 1, p = 9.1 × 10 −6 , followed by Bonferroni post hoc tests; where * indicates p < 0.05). There were no significant differences between the current amplitudes of untransfected, eGFP, M3R or M3R + NALCN/Unc80/Src cells (between subject effects; DF = 3, p = 0.55). (C) Percentage of untransfected, eGFP, M3R and M3R + NALCN/Unc80/Src cells considered responsive to muscarinic receptor agonist application were not significantly different (p = 0.51, Chi-square test). (D) Mean reversal potentials for currents elicited from responsive untransfected, eGFP, M3R and M3R + NALCN/Unc80/Src cells were not significantly different (p = 0.49, one way ANOVA). All error bars represent ±SEM.

Journal: Biochimie Open

Article Title: Lack of current observed in HEK293 cells expressing NALCN channels

doi: 10.1016/j.biopen.2018.01.001

Figure Lengend Snippet: Currents observed in M3R and M3R + NALCN/Unc80/Src cells exhibited similar properties to currents observed in untransfected cells and eGFP transfected cells. (A) The amplitude of the current at +20 mV before and after application of muscarinic receptor agonist (muscarine iodide or Oxo-M) at 100 μM for all cells tested. There was a significant main effect between the current amplitude before and after agonist (within-subject effect in a two-way mixed-design ANOVA, DF = 1, p = 7.0 × 10 −7 , followed by Bonferroni post hoc tests; where * indicates p < 0.05). There were no significant differences between the current amplitudes of untransfected, eGFP, M3R or M3R + NALCN/Unc80/Src cells (between subject effects; DF = 3, p = 0.53). (B) The amplitude of the current at +20 mV before and after application of muscarinic receptor agonist (muscarine iodide or Oxo-M) at 100 μM for only responsive cells. There was a significant main effect between the current amplitude before and after agonist (within-subject effect in a two-way mixed-design ANOVA, DF = 1, p = 9.1 × 10 −6 , followed by Bonferroni post hoc tests; where * indicates p < 0.05). There were no significant differences between the current amplitudes of untransfected, eGFP, M3R or M3R + NALCN/Unc80/Src cells (between subject effects; DF = 3, p = 0.55). (C) Percentage of untransfected, eGFP, M3R and M3R + NALCN/Unc80/Src cells considered responsive to muscarinic receptor agonist application were not significantly different (p = 0.51, Chi-square test). (D) Mean reversal potentials for currents elicited from responsive untransfected, eGFP, M3R and M3R + NALCN/Unc80/Src cells were not significantly different (p = 0.49, one way ANOVA). All error bars represent ±SEM.

Techniques: Transfection

Identification and characterization of biallelic UNC80 mutations. (A) IGV views of aligned exome sequencing short reads showing paternally inherited NM_032504.1:c.3983-3_3994delinsA. (B) IGV views of aligned exome sequencing short reads showing maternally inherited NM_032504.1:c.2431C>T. Neither mutation has been previously published. (C) Sanger traces for PCR amplification products of NM_032504.1:c.3983-3_3994delinsA. (D) Sanger traces for PCR amplification products of NM_032504.1:c.2431C>T. (E) UNC80 qRT-PCR amplification showing the absence of detectable UNC80 mRNA in cultured skin fibroblasts derived from patient II-3. Target amplification was normalized to that of GAPDH and shown as expression relative to control.

Journal: American journal of medical genetics. Part A

Article Title: Phenotypic Evolution of UNC80 Loss of Function

doi: 10.1002/ajmg.a.37929

Figure Lengend Snippet: Identification and characterization of biallelic UNC80 mutations. (A) IGV views of aligned exome sequencing short reads showing paternally inherited NM_032504.1:c.3983-3_3994delinsA. (B) IGV views of aligned exome sequencing short reads showing maternally inherited NM_032504.1:c.2431C>T. Neither mutation has been previously published. (C) Sanger traces for PCR amplification products of NM_032504.1:c.3983-3_3994delinsA. (D) Sanger traces for PCR amplification products of NM_032504.1:c.2431C>T. (E) UNC80 qRT-PCR amplification showing the absence of detectable UNC80 mRNA in cultured skin fibroblasts derived from patient II-3. Target amplification was normalized to that of GAPDH and shown as expression relative to control.

Article Snippet: Quantitative real-time PCR was performed on 100ng of cDNA and UNC80 TaqMan Assay Hs00699496_m1, GAPDH TaqMan Assay Hs03929097_g1, and TaqMan Gene Expression Mastermix (Life Technologies, Carlsbad, CA).

Techniques: Sequencing, Mutagenesis, Amplification, Quantitative RT-PCR, Cell Culture, Derivative Assay, Expressing, Control

STRING diagram referenced by Exomiser and showing the proximity of UNC80 in the interactome to NALCN. The edges of this diagram indicate predicted functional links and are colored to indicate supporting evidence for that link (green indicates proteins in the same neighborhood; pink indicates a connection made through experimentation; yellow connections established via text mining for co-occurrence of gene or protein names in abstracts; and light blue indicates relationships supported in databases Biocarta, BioCyc, GO, KEGG, and Reactome). Applying Exomiser to each variant that passed the frequency and segregation filters, we were able to compare the patient’s HPO terms to all human diseases associated with the gene containing the variant in OMIM or Orphanet, to phenotypes associated with orthologs mutated in mice or zebrafish, and lastly to phenotypes associated with nearby genes in the protein-protein association network. For the propositae, Exomiser calculated the phenotype score by considering the similarity of their phenotype to mutation of NACLN (Table I) and the proximity of NACLN to UNC80. The Exomiser variant score is a measure of the predicted pathogenicity and allele frequency of a variant. Exomiser also generated a general score that was calculated from the phenotype and variant scores.

Journal: American journal of medical genetics. Part A

Article Title: Phenotypic Evolution of UNC80 Loss of Function

doi: 10.1002/ajmg.a.37929

Figure Lengend Snippet: STRING diagram referenced by Exomiser and showing the proximity of UNC80 in the interactome to NALCN. The edges of this diagram indicate predicted functional links and are colored to indicate supporting evidence for that link (green indicates proteins in the same neighborhood; pink indicates a connection made through experimentation; yellow connections established via text mining for co-occurrence of gene or protein names in abstracts; and light blue indicates relationships supported in databases Biocarta, BioCyc, GO, KEGG, and Reactome). Applying Exomiser to each variant that passed the frequency and segregation filters, we were able to compare the patient’s HPO terms to all human diseases associated with the gene containing the variant in OMIM or Orphanet, to phenotypes associated with orthologs mutated in mice or zebrafish, and lastly to phenotypes associated with nearby genes in the protein-protein association network. For the propositae, Exomiser calculated the phenotype score by considering the similarity of their phenotype to mutation of NACLN (Table I) and the proximity of NACLN to UNC80. The Exomiser variant score is a measure of the predicted pathogenicity and allele frequency of a variant. Exomiser also generated a general score that was calculated from the phenotype and variant scores.

Techniques: Functional Assay, Variant Assay, Mutagenesis, Generated

Comparison of features among individuals with UNC80 mutations (table adapted from Perez et al., Shamseldin et al., and Stray-Pedersen et al.)

Journal: American journal of medical genetics. Part A

Article Title: Phenotypic Evolution of UNC80 Loss of Function

doi: 10.1002/ajmg.a.37929

Figure Lengend Snippet: Comparison of features among individuals with UNC80 mutations (table adapted from Perez et al., Shamseldin et al., and Stray-Pedersen et al.)

Techniques: Comparison

Review

Structured Review

Images

1) Product Images from "Imbalance in Unc80 RNA Editing Disrupts Dynamic Neuronal Activity and Olfactory Perception"

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