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    alomone labs trpc6
    Trpc6, supplied by alomone labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/trpc6/product/alomone labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    trpc6 - by Bioz Stars, 2022-08
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    86
    Cell Signaling Technology Inc trpc6
    Cell proliferation and SMC dedifferentiation are accentuated in canonical transient receptor potential 6 deficient ( <t>TRPC6</t> −/− ) mice after carotid wire injury. Wild-type (WT; n = 7 mice) and TRPC6 −/− (n = 6 mice) mice were analyzed at 28 days after carotid wire injury. A , Medial and intimal cell nuclei were counted in uninjured and injured WT and TRPC6 −/− CCA cross-sections. B and C , Active cell proliferation at 28 days after wire injury was assessed in uninjured and injured CCA cross-sections by Ki67 staining. B , Representative Ki67 staining. C , The percent of Ki67-positive cell nuclei was quantified and depicted in graphic form (n = 3 mice per genotype). D and E , Immunohistochemistry was performed for α-smooth muscle actin (α- SMA ) on cross sections from injured and uninjured CCA from WT and TRPC6 −/− mice. D , Representative α-SMA staining. E , Relative intensity of medial SMA staining was assessed semiquantitatively using Image J software on cross sections from uninjured and injured CCA from WT and TRPC6 −/− mice and depicted graphically (n = 3 mice per genotype). F , Representative immunostaining for Von-Willebrand factor in injured WT and TRPC6 −/− CCA at 100× objective. Scale bar ( black bar ) = 50 μm.
    Trpc6, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/trpc6/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    trpc6 - by Bioz Stars, 2022-08
    86/100 stars
      Buy from Supplier

    86
    Santa Cruz Biotechnology trpc6
    Biochemical interaction between TRPC3 and BK Ca channels. A, coimmunoprecipitation of TRPC3 and Slo1 channels in podocyte lysates. Slo1 channels can be detected in immunoprecipitates prepared using an antibody against <t>TRPC6</t> (left), and TRPC6 channels
    Trpc6, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/trpc6/product/Santa Cruz Biotechnology
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    trpc6 - by Bioz Stars, 2022-08
    86/100 stars
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    trpc6  (Abcam)
    86
    Abcam trpc6
    Sevoflurane preconditioning up-regulated <t>TRPC6,</t> HIF-1α, VEGF and CXCR4 in MSCs under H/R. Protein expressions of TRPC6, HIF-1α, VEGF and CXCR4 in MSCs under H/R ( a ). mRNA expression of TRPC6 in MSCs under H/R ( b ). VEGF level detected by ELISA assay in the supernatant of MSCs under H/R ( c ). Data are shown as Mean ± SEM, n = 3 per group ( a ), n = 5 per group (b and c). * P
    Trpc6, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/trpc6/product/Abcam
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    trpc6 - by Bioz Stars, 2022-08
    86/100 stars
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    Image Search Results


    Cell proliferation and SMC dedifferentiation are accentuated in canonical transient receptor potential 6 deficient ( TRPC6 −/− ) mice after carotid wire injury. Wild-type (WT; n = 7 mice) and TRPC6 −/− (n = 6 mice) mice were analyzed at 28 days after carotid wire injury. A , Medial and intimal cell nuclei were counted in uninjured and injured WT and TRPC6 −/− CCA cross-sections. B and C , Active cell proliferation at 28 days after wire injury was assessed in uninjured and injured CCA cross-sections by Ki67 staining. B , Representative Ki67 staining. C , The percent of Ki67-positive cell nuclei was quantified and depicted in graphic form (n = 3 mice per genotype). D and E , Immunohistochemistry was performed for α-smooth muscle actin (α- SMA ) on cross sections from injured and uninjured CCA from WT and TRPC6 −/− mice. D , Representative α-SMA staining. E , Relative intensity of medial SMA staining was assessed semiquantitatively using Image J software on cross sections from uninjured and injured CCA from WT and TRPC6 −/− mice and depicted graphically (n = 3 mice per genotype). F , Representative immunostaining for Von-Willebrand factor in injured WT and TRPC6 −/− CCA at 100× objective. Scale bar ( black bar ) = 50 μm.

    Journal: JVS-vascular science

    Article Title: Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury

    doi: 10.1016/j.jvssci.2020.07.002

    Figure Lengend Snippet: Cell proliferation and SMC dedifferentiation are accentuated in canonical transient receptor potential 6 deficient ( TRPC6 −/− ) mice after carotid wire injury. Wild-type (WT; n = 7 mice) and TRPC6 −/− (n = 6 mice) mice were analyzed at 28 days after carotid wire injury. A , Medial and intimal cell nuclei were counted in uninjured and injured WT and TRPC6 −/− CCA cross-sections. B and C , Active cell proliferation at 28 days after wire injury was assessed in uninjured and injured CCA cross-sections by Ki67 staining. B , Representative Ki67 staining. C , The percent of Ki67-positive cell nuclei was quantified and depicted in graphic form (n = 3 mice per genotype). D and E , Immunohistochemistry was performed for α-smooth muscle actin (α- SMA ) on cross sections from injured and uninjured CCA from WT and TRPC6 −/− mice. D , Representative α-SMA staining. E , Relative intensity of medial SMA staining was assessed semiquantitatively using Image J software on cross sections from uninjured and injured CCA from WT and TRPC6 −/− mice and depicted graphically (n = 3 mice per genotype). F , Representative immunostaining for Von-Willebrand factor in injured WT and TRPC6 −/− CCA at 100× objective. Scale bar ( black bar ) = 50 μm.

    Article Snippet: TRPC6 −/− VSMC show increased proliferation and migration as well as decreased contractile biomarker expression.

    Techniques: Mouse Assay, Staining, Immunohistochemistry, Software, Immunostaining

    Canonical transient receptor potential 6 deficient ( TRPC6 −/− ) SMC are phenotypically modulated in culture and in situ. A-C , Lysates were prepared from cultured wild-type (WT) and TRPC6 −/− VSMC (passages 6–8), resolved by sodium dodecyl sulfate polyacrylamide gel electrophoresis, and immunoblotted for SM22 and MYH11. Actin served as the loading control. A , Representative immunoblot. B and C , Relative MYH11 and SM22 protein expression quantified by densitometry (n = 3 immunoblots). D , Immunohistochemistry (IHC) performed on common carotid artery (CCA) cross-sections of 8- to 10-week-old male WT and TRPC6 −/− mice. (Top) IHC for SM22 and (Bottom) MYH11. E , SM22 protein levels were assessed at passages 1, 4, and 7 in WT and TRPC6 −/− VSMC by immunoblot analysis and quantified by densitometry. F and G , Lysates were prepared from cultured WT and TRPC6 −/− VSMC (passages 6–8) and immunoblotted for beta-actin and GAPDH. F , Representative western blot. G , The ratio of beta actin to GAPDH protein was quantified by densitometry (n = 3). H and I , Relative MYH11 and SM22 mRNA levels were assessed by quantitative real-time PCR in cultured WT and TRPC6 −/− VSMC (passages 6–8; n = 4).

    Journal: JVS-vascular science

    Article Title: Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury

    doi: 10.1016/j.jvssci.2020.07.002

    Figure Lengend Snippet: Canonical transient receptor potential 6 deficient ( TRPC6 −/− ) SMC are phenotypically modulated in culture and in situ. A-C , Lysates were prepared from cultured wild-type (WT) and TRPC6 −/− VSMC (passages 6–8), resolved by sodium dodecyl sulfate polyacrylamide gel electrophoresis, and immunoblotted for SM22 and MYH11. Actin served as the loading control. A , Representative immunoblot. B and C , Relative MYH11 and SM22 protein expression quantified by densitometry (n = 3 immunoblots). D , Immunohistochemistry (IHC) performed on common carotid artery (CCA) cross-sections of 8- to 10-week-old male WT and TRPC6 −/− mice. (Top) IHC for SM22 and (Bottom) MYH11. E , SM22 protein levels were assessed at passages 1, 4, and 7 in WT and TRPC6 −/− VSMC by immunoblot analysis and quantified by densitometry. F and G , Lysates were prepared from cultured WT and TRPC6 −/− VSMC (passages 6–8) and immunoblotted for beta-actin and GAPDH. F , Representative western blot. G , The ratio of beta actin to GAPDH protein was quantified by densitometry (n = 3). H and I , Relative MYH11 and SM22 mRNA levels were assessed by quantitative real-time PCR in cultured WT and TRPC6 −/− VSMC (passages 6–8; n = 4).

    Article Snippet: TRPC6 −/− VSMC show increased proliferation and migration as well as decreased contractile biomarker expression.

    Techniques: In Situ, Cell Culture, Polyacrylamide Gel Electrophoresis, Expressing, Western Blot, Immunohistochemistry, Mouse Assay, Real-time Polymerase Chain Reaction

    Luminal stenosis and negative remodeling are aggravated in canonical transient receptor potential 6 deficient ( TRPC6 −/− ) mice after carotid wire injury. A , Wild-type (WT) and TRPC6 −/− mice were subjected to carotid wire injury using either a 0.014-inch (n = 7 WT and n = 4 TRPC6 −/− mice) or 0.018-inch (n = 0 WT and n = 2 TRPC6 −/− mice) wire to produce cohorts with statistically similar percent CCA dilation. Filled circles designate mice injured with an 0.014-inch wire. Open circles designate mice injured with an 0.018-inch wire. B , Representative hematoxylin and eosin staining of WT and TRPC6 −/− uninjured and injured CCA 28 days after carotid wire injury. C-F , WT (n = 7 mice) and TRPC6 −/− (n = 6 mice) mice were analyzed at 28 days after injury. Filled and open circles correspond to mice injured with 0.014-inch and 0.018-inch wires, respectively. C , Luminal area in uninjured and injured WT and TRPC6 −/− mice at 28 days after carotid wire injury. D , Percent change in luminal area in injured WT and TRPC6 −/− CCA after carotid wire injury. E , The percent change in the area inside the external elastic lamina (EEL). F , The percent change in medial thickness.

    Journal: JVS-vascular science

    Article Title: Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury

    doi: 10.1016/j.jvssci.2020.07.002

    Figure Lengend Snippet: Luminal stenosis and negative remodeling are aggravated in canonical transient receptor potential 6 deficient ( TRPC6 −/− ) mice after carotid wire injury. A , Wild-type (WT) and TRPC6 −/− mice were subjected to carotid wire injury using either a 0.014-inch (n = 7 WT and n = 4 TRPC6 −/− mice) or 0.018-inch (n = 0 WT and n = 2 TRPC6 −/− mice) wire to produce cohorts with statistically similar percent CCA dilation. Filled circles designate mice injured with an 0.014-inch wire. Open circles designate mice injured with an 0.018-inch wire. B , Representative hematoxylin and eosin staining of WT and TRPC6 −/− uninjured and injured CCA 28 days after carotid wire injury. C-F , WT (n = 7 mice) and TRPC6 −/− (n = 6 mice) mice were analyzed at 28 days after injury. Filled and open circles correspond to mice injured with 0.014-inch and 0.018-inch wires, respectively. C , Luminal area in uninjured and injured WT and TRPC6 −/− mice at 28 days after carotid wire injury. D , Percent change in luminal area in injured WT and TRPC6 −/− CCA after carotid wire injury. E , The percent change in the area inside the external elastic lamina (EEL). F , The percent change in medial thickness.

    Article Snippet: TRPC6 −/− VSMC show increased proliferation and migration as well as decreased contractile biomarker expression.

    Techniques: Mouse Assay, Staining

    Canonical transient receptor potential 6 deficient ( TRPC6 −/− ) common carotid arteries (CCA) showed altered basal structure. A , Representative cross sections of wild-type (WT) and TRPC6 −/− CCA after hematoxylin and eosin staining. (Top) WT and TRPC6 −/− CCA, at 20 objective. (Bottom) WT and TRPC6 −/− CCA, at 40× objective. Scale bar height = 100 μm. B-F, Measurements of CCA from WT and TRPC6 −/− mice (n ≥ 10 mice per genotype, unless specified). B , Luminal diameter. C , Average medial thickness. D , Medial area. E , Medial and luminal fraction of total CCA area inside the external elastic lamina (EEL). F , Total number of cell nuclei in the media in CCA cross sections from WT and TRPC6 −/− mice (n = 6 WT mice, 7 TRPC6 −/− mice). G , Number of elastic lamellae in the media of CCA cross-sections from WT and TRPC6 −/− mice (n = 6 mice per genotype). H, Representative CCA cross sections from WT and TRPC6 −/− mice − stained with Weigert’s resorcin-fuchsin stain for elastin fibers. Scale bar height = 100 μm.

    Journal: JVS-vascular science

    Article Title: Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury

    doi: 10.1016/j.jvssci.2020.07.002

    Figure Lengend Snippet: Canonical transient receptor potential 6 deficient ( TRPC6 −/− ) common carotid arteries (CCA) showed altered basal structure. A , Representative cross sections of wild-type (WT) and TRPC6 −/− CCA after hematoxylin and eosin staining. (Top) WT and TRPC6 −/− CCA, at 20 objective. (Bottom) WT and TRPC6 −/− CCA, at 40× objective. Scale bar height = 100 μm. B-F, Measurements of CCA from WT and TRPC6 −/− mice (n ≥ 10 mice per genotype, unless specified). B , Luminal diameter. C , Average medial thickness. D , Medial area. E , Medial and luminal fraction of total CCA area inside the external elastic lamina (EEL). F , Total number of cell nuclei in the media in CCA cross sections from WT and TRPC6 −/− mice (n = 6 WT mice, 7 TRPC6 −/− mice). G , Number of elastic lamellae in the media of CCA cross-sections from WT and TRPC6 −/− mice (n = 6 mice per genotype). H, Representative CCA cross sections from WT and TRPC6 −/− mice − stained with Weigert’s resorcin-fuchsin stain for elastin fibers. Scale bar height = 100 μm.

    Article Snippet: TRPC6 −/− VSMC show increased proliferation and migration as well as decreased contractile biomarker expression.

    Techniques: Staining, Mouse Assay

    Acute, transient knockdown of canonical transient receptor potential 6 (TRPC6) promotes loss of the contractile phenotype in MOVAS cells. A , Wild-type (WT) and TRPC6 −/− CCA from 10-week-old male mice were explanted and homogenized in lysis buffer (n = 3 mice and 6 CCA per genotype). Lysates were resolved by SDS page and immunoblotted against TRPC3 and GAPDH. B-F , Immortalized mouse aortic smooth muscle cell line (MOVAS) cells were transiently transfected with 50 nmol/L control small interfering RNA (NsiRNA) or TRPC6 siRNA. Transfected cells were harvested at 48 hours and immunoblotted for TRPC6, TRPC3, and contractile biomarkers. B , Representative immunoblot of total TRPC6 and TRPC3 protein. C , Relative TRPC6 protein expression in NsiRNA and TRPC6 siRNA transfected cells was quantified by densitometry (n = 3). D , Representative immunoblot of contractile biomarkers. E and F , Relative protein expression of MYH11 and SM22 in NsiRNA and TRPC6 siRNA transfected cells quantified by densitometry (n = 3).

    Journal: JVS-vascular science

    Article Title: Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury

    doi: 10.1016/j.jvssci.2020.07.002

    Figure Lengend Snippet: Acute, transient knockdown of canonical transient receptor potential 6 (TRPC6) promotes loss of the contractile phenotype in MOVAS cells. A , Wild-type (WT) and TRPC6 −/− CCA from 10-week-old male mice were explanted and homogenized in lysis buffer (n = 3 mice and 6 CCA per genotype). Lysates were resolved by SDS page and immunoblotted against TRPC3 and GAPDH. B-F , Immortalized mouse aortic smooth muscle cell line (MOVAS) cells were transiently transfected with 50 nmol/L control small interfering RNA (NsiRNA) or TRPC6 siRNA. Transfected cells were harvested at 48 hours and immunoblotted for TRPC6, TRPC3, and contractile biomarkers. B , Representative immunoblot of total TRPC6 and TRPC3 protein. C , Relative TRPC6 protein expression in NsiRNA and TRPC6 siRNA transfected cells was quantified by densitometry (n = 3). D , Representative immunoblot of contractile biomarkers. E and F , Relative protein expression of MYH11 and SM22 in NsiRNA and TRPC6 siRNA transfected cells quantified by densitometry (n = 3).

    Article Snippet: TRPC6 −/− VSMC show increased proliferation and migration as well as decreased contractile biomarker expression.

    Techniques: Mouse Assay, Lysis, SDS Page, Transfection, Small Interfering RNA, Expressing

    Increased proliferation and migration of cultured canonical transient receptor potential 6 deficient ( TRPC6 −/− ) mouse aortic smooth muscle cells (VSMC). A , WT and TRPC6 −/− VSMC (passages 6–8) were incubated in culture media (DMEM + 20% fetal bovine serum [ FBS ]) for 24, 48, 72, and 96 hours. Cell number was determined at each time point. The increase in cell number relative to the number at 24 hours is depicted graphically. The increase in WT and TRPC6 −/− VSMC were compared by Student’s t test at 72 and 96 hours (n = 5) (B) WT and TRPC6 −/− VSMC were serum starved overnight and incubated with control medium (0.25% FBS), 5 ng/mL platelet-derived growth factor ( PDGF )-BB, 10 ng/mL PDGF-BB, or 10% FBS for 48 hours. The increase in cell number relative to control was determined at 48 hours (n = 4). C and D , WT and TRPC6 −/− VSMC (passages 6–8) were serum starved overnight and subjected to scrape assays. Scraped cells were immediately washed and incubated with control medium (0.25% FBS), 5 ng/mL PDGF-BB, 10 ng/mL PDGF-BB, or 10% FBS. The wound area was determined at 0 and 12 hours after scaping and percent wound closure at 12 hours was calculated. C , Representative scrape assay after 10% FBS stimulation; percent wound closure at 12 hours is listed in the lower panels. D , Graphic representation of percent wound closure (n = 4).

    Journal: JVS-vascular science

    Article Title: Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury

    doi: 10.1016/j.jvssci.2020.07.002

    Figure Lengend Snippet: Increased proliferation and migration of cultured canonical transient receptor potential 6 deficient ( TRPC6 −/− ) mouse aortic smooth muscle cells (VSMC). A , WT and TRPC6 −/− VSMC (passages 6–8) were incubated in culture media (DMEM + 20% fetal bovine serum [ FBS ]) for 24, 48, 72, and 96 hours. Cell number was determined at each time point. The increase in cell number relative to the number at 24 hours is depicted graphically. The increase in WT and TRPC6 −/− VSMC were compared by Student’s t test at 72 and 96 hours (n = 5) (B) WT and TRPC6 −/− VSMC were serum starved overnight and incubated with control medium (0.25% FBS), 5 ng/mL platelet-derived growth factor ( PDGF )-BB, 10 ng/mL PDGF-BB, or 10% FBS for 48 hours. The increase in cell number relative to control was determined at 48 hours (n = 4). C and D , WT and TRPC6 −/− VSMC (passages 6–8) were serum starved overnight and subjected to scrape assays. Scraped cells were immediately washed and incubated with control medium (0.25% FBS), 5 ng/mL PDGF-BB, 10 ng/mL PDGF-BB, or 10% FBS. The wound area was determined at 0 and 12 hours after scaping and percent wound closure at 12 hours was calculated. C , Representative scrape assay after 10% FBS stimulation; percent wound closure at 12 hours is listed in the lower panels. D , Graphic representation of percent wound closure (n = 4).

    Article Snippet: TRPC6 −/− VSMC show increased proliferation and migration as well as decreased contractile biomarker expression.

    Techniques: Migration, Cell Culture, Incubation, Derivative Assay

    Biochemical interaction between TRPC3 and BK Ca channels. A, coimmunoprecipitation of TRPC3 and Slo1 channels in podocyte lysates. Slo1 channels can be detected in immunoprecipitates prepared using an antibody against TRPC6 (left), and TRPC6 channels

    Journal:

    Article Title: Canonical Transient Receptor Potential Channel (TRPC) 3 and TRPC6 Associate with Large-Conductance Ca2+-Activated K+ (BKCa) Channels: Role in BKCa Trafficking to the Surface of Cultured Podocytes

    doi: 10.1124/mol.108.051912

    Figure Lengend Snippet: Biochemical interaction between TRPC3 and BK Ca channels. A, coimmunoprecipitation of TRPC3 and Slo1 channels in podocyte lysates. Slo1 channels can be detected in immunoprecipitates prepared using an antibody against TRPC6 (left), and TRPC6 channels

    Article Snippet: HEK293T cells were transfected with myc-tagged Slo1VEDEC with or without TRPC3 or TRPC6.

    Techniques:

    Coexpression of TRPC6 increases surface expression of myc-tagged Slo1 VEDEC channels in HEK293T cells. A, cell-surface biotinylation assays show increase in surface expression of myc-tagged Slo1 VEDEC in HEK293T cells coexpressing TRPC6 using an antibody

    Journal:

    Article Title: Canonical Transient Receptor Potential Channel (TRPC) 3 and TRPC6 Associate with Large-Conductance Ca2+-Activated K+ (BKCa) Channels: Role in BKCa Trafficking to the Surface of Cultured Podocytes

    doi: 10.1124/mol.108.051912

    Figure Lengend Snippet: Coexpression of TRPC6 increases surface expression of myc-tagged Slo1 VEDEC channels in HEK293T cells. A, cell-surface biotinylation assays show increase in surface expression of myc-tagged Slo1 VEDEC in HEK293T cells coexpressing TRPC6 using an antibody

    Article Snippet: HEK293T cells were transfected with myc-tagged Slo1VEDEC with or without TRPC3 or TRPC6.

    Techniques: Expressing

    Coexpression of TRPC6 increases the number of functional cell surface BK Ca channels in HEK293T cells expressing Slo1 VEDEC . A, typical families of voltage-evoked outward currents observed in whole-cell recordings using recording electrodes containing

    Journal:

    Article Title: Canonical Transient Receptor Potential Channel (TRPC) 3 and TRPC6 Associate with Large-Conductance Ca2+-Activated K+ (BKCa) Channels: Role in BKCa Trafficking to the Surface of Cultured Podocytes

    doi: 10.1124/mol.108.051912

    Figure Lengend Snippet: Coexpression of TRPC6 increases the number of functional cell surface BK Ca channels in HEK293T cells expressing Slo1 VEDEC . A, typical families of voltage-evoked outward currents observed in whole-cell recordings using recording electrodes containing

    Article Snippet: HEK293T cells were transfected with myc-tagged Slo1VEDEC with or without TRPC3 or TRPC6.

    Techniques: Functional Assay, Expressing

    Application of specific siRNAs cause knockdown of TRPC6 and TRPC3 channels in podocytes. Control cells were treated with a nonspecific siRNA. A, effectiveness of knockdown was demonstrated by immunoblot analysis and densitometric analysis using antibodies

    Journal:

    Article Title: Canonical Transient Receptor Potential Channel (TRPC) 3 and TRPC6 Associate with Large-Conductance Ca2+-Activated K+ (BKCa) Channels: Role in BKCa Trafficking to the Surface of Cultured Podocytes

    doi: 10.1124/mol.108.051912

    Figure Lengend Snippet: Application of specific siRNAs cause knockdown of TRPC6 and TRPC3 channels in podocytes. Control cells were treated with a nonspecific siRNA. A, effectiveness of knockdown was demonstrated by immunoblot analysis and densitometric analysis using antibodies

    Article Snippet: HEK293T cells were transfected with myc-tagged Slo1VEDEC with or without TRPC3 or TRPC6.

    Techniques:

    Colocalization of TRPC6 and Slo1 channels. Confocal analyses of native channels in podocytes (A) and of HEK293T cells transiently coexpressing Slo1 VEDEC and TRPC6 (B). Note extensive colocalization in both preparations.

    Journal:

    Article Title: Canonical Transient Receptor Potential Channel (TRPC) 3 and TRPC6 Associate with Large-Conductance Ca2+-Activated K+ (BKCa) Channels: Role in BKCa Trafficking to the Surface of Cultured Podocytes

    doi: 10.1124/mol.108.051912

    Figure Lengend Snippet: Colocalization of TRPC6 and Slo1 channels. Confocal analyses of native channels in podocytes (A) and of HEK293T cells transiently coexpressing Slo1 VEDEC and TRPC6 (B). Note extensive colocalization in both preparations.

    Article Snippet: HEK293T cells were transfected with myc-tagged Slo1VEDEC with or without TRPC3 or TRPC6.

    Techniques:

    Knockdown of TRPC6 reduces surface expression of endogenous Slo1 channels in podocytes. Cell-surface biotinylation assays show a reduction in surface expression of Slo1 48 h after siRNA knockdown of TRPC6 (A) but not after knockdown of TRPC3 (B). Bar

    Journal:

    Article Title: Canonical Transient Receptor Potential Channel (TRPC) 3 and TRPC6 Associate with Large-Conductance Ca2+-Activated K+ (BKCa) Channels: Role in BKCa Trafficking to the Surface of Cultured Podocytes

    doi: 10.1124/mol.108.051912

    Figure Lengend Snippet: Knockdown of TRPC6 reduces surface expression of endogenous Slo1 channels in podocytes. Cell-surface biotinylation assays show a reduction in surface expression of Slo1 48 h after siRNA knockdown of TRPC6 (A) but not after knockdown of TRPC3 (B). Bar

    Article Snippet: HEK293T cells were transfected with myc-tagged Slo1VEDEC with or without TRPC3 or TRPC6.

    Techniques: Expressing

    Biochemical interaction between TRPC6 and BK Ca channels. A, coimmunoprecipitation of TRPC6 and Slo1 channels in podocyte lysates. Slo1 channels can be detected in immunoprecipitates prepared using an antibody against TRPC6 (left), and TRPC6 channels

    Journal:

    Article Title: Canonical Transient Receptor Potential Channel (TRPC) 3 and TRPC6 Associate with Large-Conductance Ca2+-Activated K+ (BKCa) Channels: Role in BKCa Trafficking to the Surface of Cultured Podocytes

    doi: 10.1124/mol.108.051912

    Figure Lengend Snippet: Biochemical interaction between TRPC6 and BK Ca channels. A, coimmunoprecipitation of TRPC6 and Slo1 channels in podocyte lysates. Slo1 channels can be detected in immunoprecipitates prepared using an antibody against TRPC6 (left), and TRPC6 channels

    Article Snippet: HEK293T cells were transfected with myc-tagged Slo1VEDEC with or without TRPC3 or TRPC6.

    Techniques:

    Sevoflurane preconditioning up-regulated TRPC6, HIF-1α, VEGF and CXCR4 in MSCs under H/R. Protein expressions of TRPC6, HIF-1α, VEGF and CXCR4 in MSCs under H/R ( a ). mRNA expression of TRPC6 in MSCs under H/R ( b ). VEGF level detected by ELISA assay in the supernatant of MSCs under H/R ( c ). Data are shown as Mean ± SEM, n = 3 per group ( a ), n = 5 per group (b and c). * P

    Journal: Stem Cell Research & Therapy

    Article Title: Sevoflurane preconditioning promotes mesenchymal stem cells to relieve myocardial ischemia/reperfusion injury via TRPC6-induced angiogenesis

    doi: 10.1186/s13287-021-02649-3

    Figure Lengend Snippet: Sevoflurane preconditioning up-regulated TRPC6, HIF-1α, VEGF and CXCR4 in MSCs under H/R. Protein expressions of TRPC6, HIF-1α, VEGF and CXCR4 in MSCs under H/R ( a ). mRNA expression of TRPC6 in MSCs under H/R ( b ). VEGF level detected by ELISA assay in the supernatant of MSCs under H/R ( c ). Data are shown as Mean ± SEM, n = 3 per group ( a ), n = 5 per group (b and c). * P

    Article Snippet: After using TRPC6 siRNA, the down-regulation of TRPC6 was also accompanied by markedly decreased expressions of HIF-1α, CXCR4 and VEGF in sevoflurane preconditioned MSCs under H/R (Fig. a).

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay

    VEGF expression was decreased by TRPC6-knockdown in sevoflurane preconditioned MSCs under H/R. Representative images and quantification of Western Blotting to access protein expression of TRPC6, HIF-1α, VEGF and CXCR4 in all groups ( a ). VEGF level in the supernatant was measured by ELISA kits ( b ). Data are shown as Mean ± SEM, n = 3 per group. * P

    Journal: Stem Cell Research & Therapy

    Article Title: Sevoflurane preconditioning promotes mesenchymal stem cells to relieve myocardial ischemia/reperfusion injury via TRPC6-induced angiogenesis

    doi: 10.1186/s13287-021-02649-3

    Figure Lengend Snippet: VEGF expression was decreased by TRPC6-knockdown in sevoflurane preconditioned MSCs under H/R. Representative images and quantification of Western Blotting to access protein expression of TRPC6, HIF-1α, VEGF and CXCR4 in all groups ( a ). VEGF level in the supernatant was measured by ELISA kits ( b ). Data are shown as Mean ± SEM, n = 3 per group. * P

    Article Snippet: After using TRPC6 siRNA, the down-regulation of TRPC6 was also accompanied by markedly decreased expressions of HIF-1α, CXCR4 and VEGF in sevoflurane preconditioned MSCs under H/R (Fig. a).

    Techniques: Expressing, Western Blot, Enzyme-linked Immunosorbent Assay