α enac  (Alomone Labs)


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    Structured Review

    Alomone Labs α enac
    Potential mechanism for PDE-exo-miR-432-5p involved in DSR. The level of PDE-exo-miR-432-5p increases in the PDE of H/HA patients, which can bind to the 3'UTR of <t>α-</t> ENaC and decrease its expression in peritoneal mesothelial cells, affecting the sodium ion transport in PD. Red rectangle, toxin; green triangle, ion; blue ellipse, water; bilayer vesicle, exosome. PDE, peritoneal dialysis effluent; DSR, dialytic sodium removal; H/HA, high/high average group of patients; 3'UTR, 3'untranslated region; PD, peritoneal dialysis.
    α Enac, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/α enac/product/Alomone Labs
    Average 93 stars, based on 11 article reviews
    Price from $9.99 to $1999.99
    α enac - by Bioz Stars, 2022-08
    93/100 stars

    Images

    1) Product Images from "Peritoneal dialysis effluent-derived exosomal miR-432-5p: an assessment tool for peritoneal dialysis efficacy"

    Article Title: Peritoneal dialysis effluent-derived exosomal miR-432-5p: an assessment tool for peritoneal dialysis efficacy

    Journal: Annals of Translational Medicine

    doi: 10.21037/atm-21-3957

    Potential mechanism for PDE-exo-miR-432-5p involved in DSR. The level of PDE-exo-miR-432-5p increases in the PDE of H/HA patients, which can bind to the 3'UTR of α- ENaC and decrease its expression in peritoneal mesothelial cells, affecting the sodium ion transport in PD. Red rectangle, toxin; green triangle, ion; blue ellipse, water; bilayer vesicle, exosome. PDE, peritoneal dialysis effluent; DSR, dialytic sodium removal; H/HA, high/high average group of patients; 3'UTR, 3'untranslated region; PD, peritoneal dialysis.
    Figure Legend Snippet: Potential mechanism for PDE-exo-miR-432-5p involved in DSR. The level of PDE-exo-miR-432-5p increases in the PDE of H/HA patients, which can bind to the 3'UTR of α- ENaC and decrease its expression in peritoneal mesothelial cells, affecting the sodium ion transport in PD. Red rectangle, toxin; green triangle, ion; blue ellipse, water; bilayer vesicle, exosome. PDE, peritoneal dialysis effluent; DSR, dialytic sodium removal; H/HA, high/high average group of patients; 3'UTR, 3'untranslated region; PD, peritoneal dialysis.

    Techniques Used: Expressing

    Expression of α- ENaC in peritoneum and mesothelial cells. (A) Expression of α- ENaC in human peritoneum determined by IHC. Staining method: IHC. Scale bar: 20 µm. (B) α- ENaC gene expression in mesothelial cells detected by AGE. (C) Detection of α- ENaC protein expression in mesothelial cells by western blot. PBS, phosphate-buffered saline; IHC, immunohistochemistry; AGE, agarose gel electrophoresis.
    Figure Legend Snippet: Expression of α- ENaC in peritoneum and mesothelial cells. (A) Expression of α- ENaC in human peritoneum determined by IHC. Staining method: IHC. Scale bar: 20 µm. (B) α- ENaC gene expression in mesothelial cells detected by AGE. (C) Detection of α- ENaC protein expression in mesothelial cells by western blot. PBS, phosphate-buffered saline; IHC, immunohistochemistry; AGE, agarose gel electrophoresis.

    Techniques Used: Expressing, Immunohistochemistry, Staining, Western Blot, Agarose Gel Electrophoresis

    Verification of SCNN1A as a target gene of miR-432-5p. (A) Predicted alignment of miR-432-5p with the 3'UTR of SCNN1A mRNA. (B,D) The relative expression of miR-432-5p and α- ENaC mRNA measured by qRT-PCR. (C,E) Western blot analysis of α- ENaC protein expression level. (F) Cell viability of Met-5A after transfection detected by CCK-8. (G) Determination of the interaction between miR-432-5p and SCNN1A by the dual luciferase reporter assay. **, P
    Figure Legend Snippet: Verification of SCNN1A as a target gene of miR-432-5p. (A) Predicted alignment of miR-432-5p with the 3'UTR of SCNN1A mRNA. (B,D) The relative expression of miR-432-5p and α- ENaC mRNA measured by qRT-PCR. (C,E) Western blot analysis of α- ENaC protein expression level. (F) Cell viability of Met-5A after transfection detected by CCK-8. (G) Determination of the interaction between miR-432-5p and SCNN1A by the dual luciferase reporter assay. **, P

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot, Transfection, CCK-8 Assay, Luciferase, Reporter Assay

    2) Product Images from "(Pro)renin receptor contributes to regulation of renal epithelial sodium channel"

    Article Title: (Pro)renin receptor contributes to regulation of renal epithelial sodium channel

    Journal: Journal of hypertension

    doi: 10.1097/HJH.0000000000000825

    Expression of (Pro)renin receptor (PRR) in the kidney. PRR mRNA (a) and protein expression (b) in response to different doses of PRR shRNA. PRR mRNA and protein expression in total kidney tissue (c and d), renal medulla (e and f), and renal medulla α-ENaC
    Figure Legend Snippet: Expression of (Pro)renin receptor (PRR) in the kidney. PRR mRNA (a) and protein expression (b) in response to different doses of PRR shRNA. PRR mRNA and protein expression in total kidney tissue (c and d), renal medulla (e and f), and renal medulla α-ENaC

    Techniques Used: Expressing, shRNA

    3) Product Images from "(Pro)Renin receptor mediates obesity-induced antinatriuresis and elevated blood pressure via upregulation of the renal epithelial sodium channel"

    Article Title: (Pro)Renin receptor mediates obesity-induced antinatriuresis and elevated blood pressure via upregulation of the renal epithelial sodium channel

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0202419

    Renal medullary expression of PRR, SGK-1, and α-ENaC. Renal medullary mRNA (A) and protein (B) expressions of (Pro)renin receptor (PRR), phosphorylation of SGK-1 (C) and total expression of SGK-1 (D), mRNA (E) and protein (F) expressions of α-ENaC in mice fed with regular diet (RD) and high fed diet (HFD) with or without PRR KO. mRNA normalized to β-actin, representative blots (top), quantitative results normalized to β-actin. Data presented as mean ± SEM, NS no significant difference, *p
    Figure Legend Snippet: Renal medullary expression of PRR, SGK-1, and α-ENaC. Renal medullary mRNA (A) and protein (B) expressions of (Pro)renin receptor (PRR), phosphorylation of SGK-1 (C) and total expression of SGK-1 (D), mRNA (E) and protein (F) expressions of α-ENaC in mice fed with regular diet (RD) and high fed diet (HFD) with or without PRR KO. mRNA normalized to β-actin, representative blots (top), quantitative results normalized to β-actin. Data presented as mean ± SEM, NS no significant difference, *p

    Techniques Used: Expressing, Mouse Assay

    4) Product Images from "Salt-deficient diet exacerbates cystogenesis in ARPKD via epithelial sodium channel (ENaC)"

    Article Title: Salt-deficient diet exacerbates cystogenesis in ARPKD via epithelial sodium channel (ENaC)

    Journal: EBioMedicine

    doi: 10.1016/j.ebiom.2019.01.006

    ENaC protein and mRNA expression in PCK rats fed diets with varying sodium content. (a) Western blotting showing expression levels of α-ENaC in the renal cortex of the PCK rats fed a SD, NS and HS diets, and a summary graph with densitometry values (normalized to β-actin expression for the same samples). Each lane on the blot is one animal. (b) mRNA expression for α-, β-, and γ-ENaC in the renal cortex of the PCK rats fed a SD, NS and HS diets. (c) Western blotting showing expression levels of AQP2 in the renal cortex of the PCK rats fed a SD, NS and HS diets, and a summary graph with densitometry values (normalized to β-actin expression for the same samples). (d) miRNAs found to be differentially expressed ( p
    Figure Legend Snippet: ENaC protein and mRNA expression in PCK rats fed diets with varying sodium content. (a) Western blotting showing expression levels of α-ENaC in the renal cortex of the PCK rats fed a SD, NS and HS diets, and a summary graph with densitometry values (normalized to β-actin expression for the same samples). Each lane on the blot is one animal. (b) mRNA expression for α-, β-, and γ-ENaC in the renal cortex of the PCK rats fed a SD, NS and HS diets. (c) Western blotting showing expression levels of AQP2 in the renal cortex of the PCK rats fed a SD, NS and HS diets, and a summary graph with densitometry values (normalized to β-actin expression for the same samples). (d) miRNAs found to be differentially expressed ( p

    Techniques Used: Expressing, Western Blot

    5) Product Images from "(Pro)renin receptor contributes to regulation of renal epithelial sodium channel"

    Article Title: (Pro)renin receptor contributes to regulation of renal epithelial sodium channel

    Journal: Journal of hypertension

    doi: 10.1097/HJH.0000000000000825

    Expression of (Pro)renin receptor (PRR) in the kidney. PRR mRNA (a) and protein expression (b) in response to different doses of PRR shRNA. PRR mRNA and protein expression in total kidney tissue (c and d), renal medulla (e and f), and renal medulla α-ENaC
    Figure Legend Snippet: Expression of (Pro)renin receptor (PRR) in the kidney. PRR mRNA (a) and protein expression (b) in response to different doses of PRR shRNA. PRR mRNA and protein expression in total kidney tissue (c and d), renal medulla (e and f), and renal medulla α-ENaC

    Techniques Used: Expressing, shRNA

    6) Product Images from "Regulation of mechanosensitive biliary epithelial transport by the Epithelial Na+ Channel, ENaC"

    Article Title: Regulation of mechanosensitive biliary epithelial transport by the Epithelial Na+ Channel, ENaC

    Journal: Hepatology (Baltimore, Md.)

    doi: 10.1002/hep.28301

    Role of ENaCα subunit in flow-stimulated Na + currents A. Representative Western blot (left panel), and cumulative data (middle) demonstrating ENaCα protein levels in cells transfected with non-targeting siRNA (scramble), and cells transfected with ENaCα siRNA. β-actin used as loading control (* p
    Figure Legend Snippet: Role of ENaCα subunit in flow-stimulated Na + currents A. Representative Western blot (left panel), and cumulative data (middle) demonstrating ENaCα protein levels in cells transfected with non-targeting siRNA (scramble), and cells transfected with ENaCα siRNA. β-actin used as loading control (* p

    Techniques Used: Flow Cytometry, Western Blot, Transfection

    Functional effects of overexpression of ENaC subunits on flow-stimulated Na + currents A. Representative Western blot (left panel) and cumulative data (right panel) demonstrating relative change in ENaCα protein level in control Mz-Cha-1 cells, cells transfected with non-targeting siRNA (mock), ENaCα siRNA, ENaC α subunit (overexpression), and GFP alone. β-actin used as loading control. *p
    Figure Legend Snippet: Functional effects of overexpression of ENaC subunits on flow-stimulated Na + currents A. Representative Western blot (left panel) and cumulative data (right panel) demonstrating relative change in ENaCα protein level in control Mz-Cha-1 cells, cells transfected with non-targeting siRNA (mock), ENaCα siRNA, ENaC α subunit (overexpression), and GFP alone. β-actin used as loading control. *p

    Techniques Used: Functional Assay, Over Expression, Flow Cytometry, Western Blot, Transfection

    Expression and localization of ENaC in biliary epithelium A. RT-PCR. Species specific ENaC subunit primers were used to detect ENaC subunits in all models. In human biliary Mz-Cha-1 cells, ENaC α, β, and γ were detected (band sizes of 349, 349, and 288 respectively). In mouse large cholangiocytes (MLC, left panel) and mouse small cholangiocytes (MSC, right panel) ENaCα and γ (band sizes of 424 and 427, respectively) were detected. B. Membrane localization of ENaCα protein in polarized MLC monolayers. Staining with Alexa Fluor 555 phalloidin (red), to label the cell membrane, anti-ENaCα antibody (green), and DAPI (blue), demonstrates ENaCα protein in the apical plasma membrane, right panel (x-z plane shown below each image, arrow head indicates apical membrane). Control preparations (without primary antibody), right panel. Scale bar =10μm. C. Localization of ENaCα in mouse whole liver sections. Left panel, ENaCα was expressed on the apical membrane of intrahepatic bile ducts (arrow) and hepatic artery (arrow head). Middle panel, ENaCα is also detected in hepatic sinusoids lined by endothelial cells, while the portal vein (pv) and central vein (cv), have weaker expression. Right panel, the gallbladder shows strong staining in both the apical surface of the epithelial cells as well as macrophages in the lamina propria (arrow). All images at 400x magnification.
    Figure Legend Snippet: Expression and localization of ENaC in biliary epithelium A. RT-PCR. Species specific ENaC subunit primers were used to detect ENaC subunits in all models. In human biliary Mz-Cha-1 cells, ENaC α, β, and γ were detected (band sizes of 349, 349, and 288 respectively). In mouse large cholangiocytes (MLC, left panel) and mouse small cholangiocytes (MSC, right panel) ENaCα and γ (band sizes of 424 and 427, respectively) were detected. B. Membrane localization of ENaCα protein in polarized MLC monolayers. Staining with Alexa Fluor 555 phalloidin (red), to label the cell membrane, anti-ENaCα antibody (green), and DAPI (blue), demonstrates ENaCα protein in the apical plasma membrane, right panel (x-z plane shown below each image, arrow head indicates apical membrane). Control preparations (without primary antibody), right panel. Scale bar =10μm. C. Localization of ENaCα in mouse whole liver sections. Left panel, ENaCα was expressed on the apical membrane of intrahepatic bile ducts (arrow) and hepatic artery (arrow head). Middle panel, ENaCα is also detected in hepatic sinusoids lined by endothelial cells, while the portal vein (pv) and central vein (cv), have weaker expression. Right panel, the gallbladder shows strong staining in both the apical surface of the epithelial cells as well as macrophages in the lamina propria (arrow). All images at 400x magnification.

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Staining

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    Alomone Labs α enac
    Potential mechanism for PDE-exo-miR-432-5p involved in DSR. The level of PDE-exo-miR-432-5p increases in the PDE of H/HA patients, which can bind to the 3'UTR of <t>α-</t> ENaC and decrease its expression in peritoneal mesothelial cells, affecting the sodium ion transport in PD. Red rectangle, toxin; green triangle, ion; blue ellipse, water; bilayer vesicle, exosome. PDE, peritoneal dialysis effluent; DSR, dialytic sodium removal; H/HA, high/high average group of patients; 3'UTR, 3'untranslated region; PD, peritoneal dialysis.
    α Enac, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/α enac/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    α enac - by Bioz Stars, 2022-08
    93/100 stars
      Buy from Supplier

    93
    Alomone Labs guinea pig anti nav1 9 polyclonal antibody
    <t>Nav1.9</t> knockout affects ribbon synapse density and survival of spiral ganglion neurons. Representative images of ribbon synapse immunostained with Ctbp2 (green) from WT ( a ) and Nav1.9 −/− mice ( b ). c Quantitative analysis of ribbon synapse counts per IHC from five randomly selected visual fields for each mouse. n = 7 for WT group, n = 5 for Nav1.9 −/− group. * p = 0.034 by Mann–Whitney test. Representative images of spiral ganglion neurons in Rosenthal’s canal from WT ( d ) and Nav1.9 −/− mice ( e ). f Spiral ganglion neuron counts in the basal turn, the middle turn and apical turn together in 3 midmodiolar sections for each animal. n = 5 for WT group, n = 4 for Nav1.9 −/− group. * p = 0.014 by Mann–Whitney test. Data are expressed as mean ± s.d
    Guinea Pig Anti Nav1 9 Polyclonal Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/guinea pig anti nav1 9 polyclonal antibody/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    guinea pig anti nav1 9 polyclonal antibody - by Bioz Stars, 2022-08
    93/100 stars
      Buy from Supplier

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    Potential mechanism for PDE-exo-miR-432-5p involved in DSR. The level of PDE-exo-miR-432-5p increases in the PDE of H/HA patients, which can bind to the 3'UTR of α- ENaC and decrease its expression in peritoneal mesothelial cells, affecting the sodium ion transport in PD. Red rectangle, toxin; green triangle, ion; blue ellipse, water; bilayer vesicle, exosome. PDE, peritoneal dialysis effluent; DSR, dialytic sodium removal; H/HA, high/high average group of patients; 3'UTR, 3'untranslated region; PD, peritoneal dialysis.

    Journal: Annals of Translational Medicine

    Article Title: Peritoneal dialysis effluent-derived exosomal miR-432-5p: an assessment tool for peritoneal dialysis efficacy

    doi: 10.21037/atm-21-3957

    Figure Lengend Snippet: Potential mechanism for PDE-exo-miR-432-5p involved in DSR. The level of PDE-exo-miR-432-5p increases in the PDE of H/HA patients, which can bind to the 3'UTR of α- ENaC and decrease its expression in peritoneal mesothelial cells, affecting the sodium ion transport in PD. Red rectangle, toxin; green triangle, ion; blue ellipse, water; bilayer vesicle, exosome. PDE, peritoneal dialysis effluent; DSR, dialytic sodium removal; H/HA, high/high average group of patients; 3'UTR, 3'untranslated region; PD, peritoneal dialysis.

    Article Snippet: Blots were blocked with 5% nonfat milk and then incubated overnight at 4 ℃ with the primary antibodies CD9, CD63, CD81, Hsp70 (1:1,000; SBI Medical, Fort Lauderdale, FL, USA), α- ENaC (1:500; Alomone Labs, Jerusalem, Israel), or GAPDH (1:5,000; Proteintech Group Inc., Rosemont, IL, USA).

    Techniques: Expressing

    Expression of α- ENaC in peritoneum and mesothelial cells. (A) Expression of α- ENaC in human peritoneum determined by IHC. Staining method: IHC. Scale bar: 20 µm. (B) α- ENaC gene expression in mesothelial cells detected by AGE. (C) Detection of α- ENaC protein expression in mesothelial cells by western blot. PBS, phosphate-buffered saline; IHC, immunohistochemistry; AGE, agarose gel electrophoresis.

    Journal: Annals of Translational Medicine

    Article Title: Peritoneal dialysis effluent-derived exosomal miR-432-5p: an assessment tool for peritoneal dialysis efficacy

    doi: 10.21037/atm-21-3957

    Figure Lengend Snippet: Expression of α- ENaC in peritoneum and mesothelial cells. (A) Expression of α- ENaC in human peritoneum determined by IHC. Staining method: IHC. Scale bar: 20 µm. (B) α- ENaC gene expression in mesothelial cells detected by AGE. (C) Detection of α- ENaC protein expression in mesothelial cells by western blot. PBS, phosphate-buffered saline; IHC, immunohistochemistry; AGE, agarose gel electrophoresis.

    Article Snippet: Blots were blocked with 5% nonfat milk and then incubated overnight at 4 ℃ with the primary antibodies CD9, CD63, CD81, Hsp70 (1:1,000; SBI Medical, Fort Lauderdale, FL, USA), α- ENaC (1:500; Alomone Labs, Jerusalem, Israel), or GAPDH (1:5,000; Proteintech Group Inc., Rosemont, IL, USA).

    Techniques: Expressing, Immunohistochemistry, Staining, Western Blot, Agarose Gel Electrophoresis

    Verification of SCNN1A as a target gene of miR-432-5p. (A) Predicted alignment of miR-432-5p with the 3'UTR of SCNN1A mRNA. (B,D) The relative expression of miR-432-5p and α- ENaC mRNA measured by qRT-PCR. (C,E) Western blot analysis of α- ENaC protein expression level. (F) Cell viability of Met-5A after transfection detected by CCK-8. (G) Determination of the interaction between miR-432-5p and SCNN1A by the dual luciferase reporter assay. **, P

    Journal: Annals of Translational Medicine

    Article Title: Peritoneal dialysis effluent-derived exosomal miR-432-5p: an assessment tool for peritoneal dialysis efficacy

    doi: 10.21037/atm-21-3957

    Figure Lengend Snippet: Verification of SCNN1A as a target gene of miR-432-5p. (A) Predicted alignment of miR-432-5p with the 3'UTR of SCNN1A mRNA. (B,D) The relative expression of miR-432-5p and α- ENaC mRNA measured by qRT-PCR. (C,E) Western blot analysis of α- ENaC protein expression level. (F) Cell viability of Met-5A after transfection detected by CCK-8. (G) Determination of the interaction between miR-432-5p and SCNN1A by the dual luciferase reporter assay. **, P

    Article Snippet: Blots were blocked with 5% nonfat milk and then incubated overnight at 4 ℃ with the primary antibodies CD9, CD63, CD81, Hsp70 (1:1,000; SBI Medical, Fort Lauderdale, FL, USA), α- ENaC (1:500; Alomone Labs, Jerusalem, Israel), or GAPDH (1:5,000; Proteintech Group Inc., Rosemont, IL, USA).

    Techniques: Expressing, Quantitative RT-PCR, Western Blot, Transfection, CCK-8 Assay, Luciferase, Reporter Assay

    Expression of (Pro)renin receptor (PRR) in the kidney. PRR mRNA (a) and protein expression (b) in response to different doses of PRR shRNA. PRR mRNA and protein expression in total kidney tissue (c and d), renal medulla (e and f), and renal medulla α-ENaC

    Journal: Journal of hypertension

    Article Title: (Pro)renin receptor contributes to regulation of renal epithelial sodium channel

    doi: 10.1097/HJH.0000000000000825

    Figure Lengend Snippet: Expression of (Pro)renin receptor (PRR) in the kidney. PRR mRNA (a) and protein expression (b) in response to different doses of PRR shRNA. PRR mRNA and protein expression in total kidney tissue (c and d), renal medulla (e and f), and renal medulla α-ENaC

    Article Snippet: Antibodies to PRR (1 : 1000 dilutions, Abcam, Cambridge, Massachusetts, USA), prorenin/renin (1 : 200 dilutions; Santa Cruz biotechnology, Inc., Santa Cruz, California, USA), SGK-1 (1 : 1000 dilutions, Cell Signaling, USA), p-Nedd4–2 (1 : 1000 dilutions, Abcam, Cambridge, Massachusetts, USA), α-ENaC (1 : 500 dilutions; ASC-030, Alomone Labs, Israel) were used in the Western blot as previously described [ , ].

    Techniques: Expressing, shRNA

    Renal medullary expression of PRR, SGK-1, and α-ENaC. Renal medullary mRNA (A) and protein (B) expressions of (Pro)renin receptor (PRR), phosphorylation of SGK-1 (C) and total expression of SGK-1 (D), mRNA (E) and protein (F) expressions of α-ENaC in mice fed with regular diet (RD) and high fed diet (HFD) with or without PRR KO. mRNA normalized to β-actin, representative blots (top), quantitative results normalized to β-actin. Data presented as mean ± SEM, NS no significant difference, *p

    Journal: PLoS ONE

    Article Title: (Pro)Renin receptor mediates obesity-induced antinatriuresis and elevated blood pressure via upregulation of the renal epithelial sodium channel

    doi: 10.1371/journal.pone.0202419

    Figure Lengend Snippet: Renal medullary expression of PRR, SGK-1, and α-ENaC. Renal medullary mRNA (A) and protein (B) expressions of (Pro)renin receptor (PRR), phosphorylation of SGK-1 (C) and total expression of SGK-1 (D), mRNA (E) and protein (F) expressions of α-ENaC in mice fed with regular diet (RD) and high fed diet (HFD) with or without PRR KO. mRNA normalized to β-actin, representative blots (top), quantitative results normalized to β-actin. Data presented as mean ± SEM, NS no significant difference, *p

    Article Snippet: Western blotAntibodies to PRR (1:1000 dilutions, Abcam, Cambridge, MA, USA), p-SGK-1 (1:1000 dilutions, Cell signaling, USA), SGK-1 (1:1000 dilutions, Cell signaling, USA), α-ENaC (1:500 dilutions; ASC-030, Alamone labs, Israel) were used in the Western blot of renal medullary protein as previously described.

    Techniques: Expressing, Mouse Assay

    Nav1.9 knockout affects ribbon synapse density and survival of spiral ganglion neurons. Representative images of ribbon synapse immunostained with Ctbp2 (green) from WT ( a ) and Nav1.9 −/− mice ( b ). c Quantitative analysis of ribbon synapse counts per IHC from five randomly selected visual fields for each mouse. n = 7 for WT group, n = 5 for Nav1.9 −/− group. * p = 0.034 by Mann–Whitney test. Representative images of spiral ganglion neurons in Rosenthal’s canal from WT ( d ) and Nav1.9 −/− mice ( e ). f Spiral ganglion neuron counts in the basal turn, the middle turn and apical turn together in 3 midmodiolar sections for each animal. n = 5 for WT group, n = 4 for Nav1.9 −/− group. * p = 0.014 by Mann–Whitney test. Data are expressed as mean ± s.d

    Journal: BMC Neuroscience

    Article Title: SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves

    doi: 10.1186/s12868-021-00613-8

    Figure Lengend Snippet: Nav1.9 knockout affects ribbon synapse density and survival of spiral ganglion neurons. Representative images of ribbon synapse immunostained with Ctbp2 (green) from WT ( a ) and Nav1.9 −/− mice ( b ). c Quantitative analysis of ribbon synapse counts per IHC from five randomly selected visual fields for each mouse. n = 7 for WT group, n = 5 for Nav1.9 −/− group. * p = 0.034 by Mann–Whitney test. Representative images of spiral ganglion neurons in Rosenthal’s canal from WT ( d ) and Nav1.9 −/− mice ( e ). f Spiral ganglion neuron counts in the basal turn, the middle turn and apical turn together in 3 midmodiolar sections for each animal. n = 5 for WT group, n = 4 for Nav1.9 −/− group. * p = 0.014 by Mann–Whitney test. Data are expressed as mean ± s.d

    Article Snippet: Immunohistochemistry and synaptic counts After washes with 0.1% Triton X-100 in PBS, sections on adhesion microscope slides were blocked with 10% normal goat serum (ZLI-9021, ZSGB-BIO) and incubated with rabbit anti-SCN11A polyclonal antibody (AT322395, 1:200, OriGene, Rockville, MD), guinea pig anti-Nav1.9 polyclonal antibody (AGP-030, 1:200, alomone labs, Israel), mouse anti-CtBP2 (612044, 1:100, BD Biosciences), in 10% goat serum diluted in 0.1 M PBS at 4 ℃ overnight and then incubated with secondary antibodies containing anti-mouse Alexa Fluo™ 488 (lot 1810918, 1:400, goat, Thermo Fisher), anti-rabbit Alexa Fluor™ 568 (lot 1494753, 1:400, goat, Thermo Fisher), or anti-guinea pig Alexa FluroTM647 (A-21450, 1:400, goat, Thermo Fisher).

    Techniques: Knock-Out, Mouse Assay, Immunohistochemistry, MANN-WHITNEY

    Nav1.9 knockout does not affect the morphology of hair cells. a The digital image of a dissected cochlea including the hook region (left) from a 4 months old mouse. Schematic drawing of the same cochlea with percent distance from the apex plotted (right). b Scale is showing frequency, percent distance from the apex, and distance (mm), according to Müller et al. [ 22 ]: x = 100 − (156.53 − 82.46 * log(F)). The full basilar membrane length is 6.3 mm for this particular cochlea. C, Images of organ of Cortis from 4 months old mice stained by DAPI (blue), with the apical turn (0–25% distance from the apex), the middle turn (30–55% distance from the apex) and the basal turn (60–85% distance from the apex). d Images of the organ of Corti of Nav1.9 −/− mice at postnatal ages of 2 months by SEM, containing the apical turn ( b1 – b3 ), the middle turn ( b4 – b6 ), and the basal turn ( b7 – b9 )

    Journal: BMC Neuroscience

    Article Title: SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves

    doi: 10.1186/s12868-021-00613-8

    Figure Lengend Snippet: Nav1.9 knockout does not affect the morphology of hair cells. a The digital image of a dissected cochlea including the hook region (left) from a 4 months old mouse. Schematic drawing of the same cochlea with percent distance from the apex plotted (right). b Scale is showing frequency, percent distance from the apex, and distance (mm), according to Müller et al. [ 22 ]: x = 100 − (156.53 − 82.46 * log(F)). The full basilar membrane length is 6.3 mm for this particular cochlea. C, Images of organ of Cortis from 4 months old mice stained by DAPI (blue), with the apical turn (0–25% distance from the apex), the middle turn (30–55% distance from the apex) and the basal turn (60–85% distance from the apex). d Images of the organ of Corti of Nav1.9 −/− mice at postnatal ages of 2 months by SEM, containing the apical turn ( b1 – b3 ), the middle turn ( b4 – b6 ), and the basal turn ( b7 – b9 )

    Article Snippet: Immunohistochemistry and synaptic counts After washes with 0.1% Triton X-100 in PBS, sections on adhesion microscope slides were blocked with 10% normal goat serum (ZLI-9021, ZSGB-BIO) and incubated with rabbit anti-SCN11A polyclonal antibody (AT322395, 1:200, OriGene, Rockville, MD), guinea pig anti-Nav1.9 polyclonal antibody (AGP-030, 1:200, alomone labs, Israel), mouse anti-CtBP2 (612044, 1:100, BD Biosciences), in 10% goat serum diluted in 0.1 M PBS at 4 ℃ overnight and then incubated with secondary antibodies containing anti-mouse Alexa Fluo™ 488 (lot 1810918, 1:400, goat, Thermo Fisher), anti-rabbit Alexa Fluor™ 568 (lot 1494753, 1:400, goat, Thermo Fisher), or anti-guinea pig Alexa FluroTM647 (A-21450, 1:400, goat, Thermo Fisher).

    Techniques: Knock-Out, Mouse Assay, Staining

    CRISPR/Cas 9-mediated generation of a Nav1.9 −/− mouse model. a A representative illustration of the CRISPR/Cas9 targeting strategy for generating Nav1.9 knockout (KO) mice. The Cas9 mRNA and two single guide RNAs targeting a region from SCN11A exon 3 to 5, were microinjected into mouse zygotes. b Schematic diagram of primer pair design for PCR genotyping, a representative PCR genotyping result for Nav1.9 wild-type (WT), homozygous (Nav1.9 −/− ) and heterozygous (Nav1.9 +/− ), the region of junction of DSB is absent in the WT mice. Primer 2: primer pairs containing forward primer and KO specific reverse primer; Primer 1: primer pairs containing forward primer and WT specific reverse primer. c This successfully eliminated all of exon 3, 4 and 5, as confirmed by Sanger sequencing, induces reading frame shift and thus a premature translational- termination codon during the truncated protein expression. d The protein expression of Nav1.9 in the cochleas of Nav1.9 −/− mice (n = 3) or WT mice (n = 4) was measured by western blot

    Journal: BMC Neuroscience

    Article Title: SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves

    doi: 10.1186/s12868-021-00613-8

    Figure Lengend Snippet: CRISPR/Cas 9-mediated generation of a Nav1.9 −/− mouse model. a A representative illustration of the CRISPR/Cas9 targeting strategy for generating Nav1.9 knockout (KO) mice. The Cas9 mRNA and two single guide RNAs targeting a region from SCN11A exon 3 to 5, were microinjected into mouse zygotes. b Schematic diagram of primer pair design for PCR genotyping, a representative PCR genotyping result for Nav1.9 wild-type (WT), homozygous (Nav1.9 −/− ) and heterozygous (Nav1.9 +/− ), the region of junction of DSB is absent in the WT mice. Primer 2: primer pairs containing forward primer and KO specific reverse primer; Primer 1: primer pairs containing forward primer and WT specific reverse primer. c This successfully eliminated all of exon 3, 4 and 5, as confirmed by Sanger sequencing, induces reading frame shift and thus a premature translational- termination codon during the truncated protein expression. d The protein expression of Nav1.9 in the cochleas of Nav1.9 −/− mice (n = 3) or WT mice (n = 4) was measured by western blot

    Article Snippet: Immunohistochemistry and synaptic counts After washes with 0.1% Triton X-100 in PBS, sections on adhesion microscope slides were blocked with 10% normal goat serum (ZLI-9021, ZSGB-BIO) and incubated with rabbit anti-SCN11A polyclonal antibody (AT322395, 1:200, OriGene, Rockville, MD), guinea pig anti-Nav1.9 polyclonal antibody (AGP-030, 1:200, alomone labs, Israel), mouse anti-CtBP2 (612044, 1:100, BD Biosciences), in 10% goat serum diluted in 0.1 M PBS at 4 ℃ overnight and then incubated with secondary antibodies containing anti-mouse Alexa Fluo™ 488 (lot 1810918, 1:400, goat, Thermo Fisher), anti-rabbit Alexa Fluor™ 568 (lot 1494753, 1:400, goat, Thermo Fisher), or anti-guinea pig Alexa FluroTM647 (A-21450, 1:400, goat, Thermo Fisher).

    Techniques: CRISPR, Knock-Out, Mouse Assay, Polymerase Chain Reaction, Sequencing, Expressing, Western Blot

    Distribution of Nav1.9 in primary auditory afferents. a The voltage-gated sodium channel Nav1.9 and Nav1.1 mRNA levels in modiolus of WT ICR mice at the postnatal 0, 7th, 14th, 21th, 28th and 60th day. Each time point contains 5 mice. * p = 0.028, ** p = 0.004. b A schematic representing the localization of Nav1.9 channels at primary afferent peripheral nerve endings on hair cells in cochlea, in SGN somata, in the auditory nerve located within the modiolus, and in the cochlear nuclei. c Nav1.9 is present in cochlea basilar membrane by surface preparation technique and immunofluorescence staining in cryo-section. c1 Horizontal section showing three rows of OHCs and one row of IHCs. In a linear distribution below the IHCs, Nav1.9 (purple) is in the afferent endings beneath the IHC bases. Also stained are the afferent radial fibers leading through the tunnel of Corti to their first hemi-nodes beneath the foramina nervosa. Scales = 75 μm. c2 The diagram of the cochlea’s afferent innervations pattern. c3 Nav1.9 is in the nerve endings of internal spiral fibers or radial fibers beneath IHC (red), the cilia of which exhibit phalloidin labeling (green). Scales = 50 μm. c4 The high magnification image of c3. Scale = 10 μm. d The expression of Nav1.9 in the SGNs of P60 WT mouse was measured by immunofluorescence. Nav1.9, MBP, and cell nucleus are stained as red, green and blue, respectively. e Some neurons from the dorsal cochlear nucleus are labeled by Nav1.9 (red)

    Journal: BMC Neuroscience

    Article Title: SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves

    doi: 10.1186/s12868-021-00613-8

    Figure Lengend Snippet: Distribution of Nav1.9 in primary auditory afferents. a The voltage-gated sodium channel Nav1.9 and Nav1.1 mRNA levels in modiolus of WT ICR mice at the postnatal 0, 7th, 14th, 21th, 28th and 60th day. Each time point contains 5 mice. * p = 0.028, ** p = 0.004. b A schematic representing the localization of Nav1.9 channels at primary afferent peripheral nerve endings on hair cells in cochlea, in SGN somata, in the auditory nerve located within the modiolus, and in the cochlear nuclei. c Nav1.9 is present in cochlea basilar membrane by surface preparation technique and immunofluorescence staining in cryo-section. c1 Horizontal section showing three rows of OHCs and one row of IHCs. In a linear distribution below the IHCs, Nav1.9 (purple) is in the afferent endings beneath the IHC bases. Also stained are the afferent radial fibers leading through the tunnel of Corti to their first hemi-nodes beneath the foramina nervosa. Scales = 75 μm. c2 The diagram of the cochlea’s afferent innervations pattern. c3 Nav1.9 is in the nerve endings of internal spiral fibers or radial fibers beneath IHC (red), the cilia of which exhibit phalloidin labeling (green). Scales = 50 μm. c4 The high magnification image of c3. Scale = 10 μm. d The expression of Nav1.9 in the SGNs of P60 WT mouse was measured by immunofluorescence. Nav1.9, MBP, and cell nucleus are stained as red, green and blue, respectively. e Some neurons from the dorsal cochlear nucleus are labeled by Nav1.9 (red)

    Article Snippet: Immunohistochemistry and synaptic counts After washes with 0.1% Triton X-100 in PBS, sections on adhesion microscope slides were blocked with 10% normal goat serum (ZLI-9021, ZSGB-BIO) and incubated with rabbit anti-SCN11A polyclonal antibody (AT322395, 1:200, OriGene, Rockville, MD), guinea pig anti-Nav1.9 polyclonal antibody (AGP-030, 1:200, alomone labs, Israel), mouse anti-CtBP2 (612044, 1:100, BD Biosciences), in 10% goat serum diluted in 0.1 M PBS at 4 ℃ overnight and then incubated with secondary antibodies containing anti-mouse Alexa Fluo™ 488 (lot 1810918, 1:400, goat, Thermo Fisher), anti-rabbit Alexa Fluor™ 568 (lot 1494753, 1:400, goat, Thermo Fisher), or anti-guinea pig Alexa FluroTM647 (A-21450, 1:400, goat, Thermo Fisher).

    Techniques: Mouse Assay, Immunofluorescence, Staining, Immunohistochemistry, Labeling, Expressing

    Auditory compound action potentials are affected by Nav1.9 knockout. Nav1.9 knockout induces higher CAP P1 threshold, * p = 0.013 with Mann–Whitney test ( a ), lower CAP P1 amplitude, * p = 0.041 with independent samples t test ( b ), compared with WT group; c the CAP P1 latency is not affected at the time point of postnatal day 60, p = 0.242 with independent samples t test. d Representative CAP waveforms from a WT mouse. e Representative CAP waveforms from a Nav1.9 −/− mice. Data are expressed as mean ± s.d

    Journal: BMC Neuroscience

    Article Title: SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves

    doi: 10.1186/s12868-021-00613-8

    Figure Lengend Snippet: Auditory compound action potentials are affected by Nav1.9 knockout. Nav1.9 knockout induces higher CAP P1 threshold, * p = 0.013 with Mann–Whitney test ( a ), lower CAP P1 amplitude, * p = 0.041 with independent samples t test ( b ), compared with WT group; c the CAP P1 latency is not affected at the time point of postnatal day 60, p = 0.242 with independent samples t test. d Representative CAP waveforms from a WT mouse. e Representative CAP waveforms from a Nav1.9 −/− mice. Data are expressed as mean ± s.d

    Article Snippet: Immunohistochemistry and synaptic counts After washes with 0.1% Triton X-100 in PBS, sections on adhesion microscope slides were blocked with 10% normal goat serum (ZLI-9021, ZSGB-BIO) and incubated with rabbit anti-SCN11A polyclonal antibody (AT322395, 1:200, OriGene, Rockville, MD), guinea pig anti-Nav1.9 polyclonal antibody (AGP-030, 1:200, alomone labs, Israel), mouse anti-CtBP2 (612044, 1:100, BD Biosciences), in 10% goat serum diluted in 0.1 M PBS at 4 ℃ overnight and then incubated with secondary antibodies containing anti-mouse Alexa Fluo™ 488 (lot 1810918, 1:400, goat, Thermo Fisher), anti-rabbit Alexa Fluor™ 568 (lot 1494753, 1:400, goat, Thermo Fisher), or anti-guinea pig Alexa FluroTM647 (A-21450, 1:400, goat, Thermo Fisher).

    Techniques: Knock-Out, MANN-WHITNEY, Mouse Assay

    Audiological characterization of Nav1.9 −/− mice. a Mean ABR thresholds of six wild-type, four heterozygous and seven homozygous versus sound frequency, ** p = 0.002, ** p = 0.001 at 12 kHz compared with homozygous, * p = 0.01, *** p = 0.000 at 16 kHz compared with homozygous by one-way ANOVA with Bonferroni’s post-hoc test. b Example of ABR waveforms at 16 kHz in one ear of a wild-type superimposed on an example of ABR waveforms in one ear of Nav1.9 −/− mice. c ABR thresholds of WT and homozygous mice of postnatal day 21 to 60 at 8 kHz. p = 0.807 at P21; p = 0.932 at P30; p = 0.504 with independent samples t test; n.s.: not significant. d ABR threshold of WT and homozygous mice of postnatal day 21 to 60 at 16 kHz. * p = 0.016, ** p = 0.006, *** p = 0.000 with Mann–Whitney test. Data are expressed as mean ± s.d

    Journal: BMC Neuroscience

    Article Title: SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves

    doi: 10.1186/s12868-021-00613-8

    Figure Lengend Snippet: Audiological characterization of Nav1.9 −/− mice. a Mean ABR thresholds of six wild-type, four heterozygous and seven homozygous versus sound frequency, ** p = 0.002, ** p = 0.001 at 12 kHz compared with homozygous, * p = 0.01, *** p = 0.000 at 16 kHz compared with homozygous by one-way ANOVA with Bonferroni’s post-hoc test. b Example of ABR waveforms at 16 kHz in one ear of a wild-type superimposed on an example of ABR waveforms in one ear of Nav1.9 −/− mice. c ABR thresholds of WT and homozygous mice of postnatal day 21 to 60 at 8 kHz. p = 0.807 at P21; p = 0.932 at P30; p = 0.504 with independent samples t test; n.s.: not significant. d ABR threshold of WT and homozygous mice of postnatal day 21 to 60 at 16 kHz. * p = 0.016, ** p = 0.006, *** p = 0.000 with Mann–Whitney test. Data are expressed as mean ± s.d

    Article Snippet: Immunohistochemistry and synaptic counts After washes with 0.1% Triton X-100 in PBS, sections on adhesion microscope slides were blocked with 10% normal goat serum (ZLI-9021, ZSGB-BIO) and incubated with rabbit anti-SCN11A polyclonal antibody (AT322395, 1:200, OriGene, Rockville, MD), guinea pig anti-Nav1.9 polyclonal antibody (AGP-030, 1:200, alomone labs, Israel), mouse anti-CtBP2 (612044, 1:100, BD Biosciences), in 10% goat serum diluted in 0.1 M PBS at 4 ℃ overnight and then incubated with secondary antibodies containing anti-mouse Alexa Fluo™ 488 (lot 1810918, 1:400, goat, Thermo Fisher), anti-rabbit Alexa Fluor™ 568 (lot 1494753, 1:400, goat, Thermo Fisher), or anti-guinea pig Alexa FluroTM647 (A-21450, 1:400, goat, Thermo Fisher).

    Techniques: Mouse Assay, MANN-WHITNEY