a889425  (Alomone Labs)


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    Alomone Labs a889425
    The increase in rubidium ion (Rb + ) uptake in wild-type (WT) cells exposed to capsaicin (1 µM) was prevented by <t>A889425</t> (1 µM), a TRPV1 antagonist ( A ), and bumetanide, a sodium-potassium/two-chloride cotransporter (NKCC1) inhibitor ( B ). Added alone, bumetanide reduced Rb + uptake. The increase in Rb + uptake in capsaicin-treated cells was prevented by 10 nM bumetanide as well as 10 μM bumetanide. Data are the mean ± SE of results from 6 to 12 independent experiments. * P
    A889425, 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/a889425/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    a889425 - by Bioz Stars, 2021-12
    93/100 stars

    Images

    1) Product Images from "TRPV1 activation stimulates NKCC1 and increases hydrostatic pressure in the mouse lens"

    Article Title: TRPV1 activation stimulates NKCC1 and increases hydrostatic pressure in the mouse lens

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00391.2019

    The increase in rubidium ion (Rb + ) uptake in wild-type (WT) cells exposed to capsaicin (1 µM) was prevented by A889425 (1 µM), a TRPV1 antagonist ( A ), and bumetanide, a sodium-potassium/two-chloride cotransporter (NKCC1) inhibitor ( B ). Added alone, bumetanide reduced Rb + uptake. The increase in Rb + uptake in capsaicin-treated cells was prevented by 10 nM bumetanide as well as 10 μM bumetanide. Data are the mean ± SE of results from 6 to 12 independent experiments. * P
    Figure Legend Snippet: The increase in rubidium ion (Rb + ) uptake in wild-type (WT) cells exposed to capsaicin (1 µM) was prevented by A889425 (1 µM), a TRPV1 antagonist ( A ), and bumetanide, a sodium-potassium/two-chloride cotransporter (NKCC1) inhibitor ( B ). Added alone, bumetanide reduced Rb + uptake. The increase in Rb + uptake in capsaicin-treated cells was prevented by 10 nM bumetanide as well as 10 μM bumetanide. Data are the mean ± SE of results from 6 to 12 independent experiments. * P

    Techniques Used:

    2) Product Images from "Activation of TRPV1 channels leads to stimulation of NKCC1 cotransport in the lens"

    Article Title: Activation of TRPV1 channels leads to stimulation of NKCC1 cotransport in the lens

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00252.2018

    Effect of Na-K-2Cl cotransporter (NKCC) inhibitor bumetanide (Bum; A ) and transient receptor potential vanilloid 1 (TRPV1) antagonist A889425 (A88; B ) on the Rb uptake response to capsaicin (Cap, 100nM). Intact lenses were preincubated 20 min with or without bumetanide (10 µM) or A889425 (1.0 µM) in isosmotic Krebs solution and then transferred to RbCl-containing Krebs solution with or without (Control, Con) capsaicin for 10 min in the continued presence or absence of bumetanide or A889425. Each value is the mean ± SE of results from 5–6 lenses. *** P
    Figure Legend Snippet: Effect of Na-K-2Cl cotransporter (NKCC) inhibitor bumetanide (Bum; A ) and transient receptor potential vanilloid 1 (TRPV1) antagonist A889425 (A88; B ) on the Rb uptake response to capsaicin (Cap, 100nM). Intact lenses were preincubated 20 min with or without bumetanide (10 µM) or A889425 (1.0 µM) in isosmotic Krebs solution and then transferred to RbCl-containing Krebs solution with or without (Control, Con) capsaicin for 10 min in the continued presence or absence of bumetanide or A889425. Each value is the mean ± SE of results from 5–6 lenses. *** P

    Techniques Used:

    Effect of transient receptor potential vanilloid 1 (TRPV1) antagonist A889425 (A88) on the Na-K-2Cl cotransporter 1 (NKCC1) phosphorylation response to hyperosmotic solution (Hyper; A ) and capsaicin (Cap; B ). Intact lenses were preincubated in Krebs solution (300 mosM) with or without A889425 (1 µM) for 20 min and then exposed to capsaicin (100 nM) or hyperosmotic solution (350 mosM) for 10 min in the continued presence or absence of A889425. The capsule epithelium was then removed for Western blot analysis. Figures show bands for phospho-(p)NKCC1 detected using a rabbit polyclonal anti-phospho-NKCC1 (Thr 212/217 ) antibody; figures also show bands for β-actin. Band density of active (phosphorylated) NKCC1 was normalized to β-actin band density. In each panel a representative blot is presented along with a bar graph that shows densitometric analysis (means ± SE) of results from 3 independent experiments. *Significant difference ( P
    Figure Legend Snippet: Effect of transient receptor potential vanilloid 1 (TRPV1) antagonist A889425 (A88) on the Na-K-2Cl cotransporter 1 (NKCC1) phosphorylation response to hyperosmotic solution (Hyper; A ) and capsaicin (Cap; B ). Intact lenses were preincubated in Krebs solution (300 mosM) with or without A889425 (1 µM) for 20 min and then exposed to capsaicin (100 nM) or hyperosmotic solution (350 mosM) for 10 min in the continued presence or absence of A889425. The capsule epithelium was then removed for Western blot analysis. Figures show bands for phospho-(p)NKCC1 detected using a rabbit polyclonal anti-phospho-NKCC1 (Thr 212/217 ) antibody; figures also show bands for β-actin. Band density of active (phosphorylated) NKCC1 was normalized to β-actin band density. In each panel a representative blot is presented along with a bar graph that shows densitometric analysis (means ± SE) of results from 3 independent experiments. *Significant difference ( P

    Techniques Used: Western Blot

    Effect of Na-K-2Cl cotransporter (NKCC) inhibitor bumetanide (Bum; A ) and transient receptor potential vanilloid 1 (TRPV1) antagonist A889425 (A88; B ) on the Rb uptake response to hyperosmotic solution. Intact lenses were preincubated 20 min with or without bumetanide (10 µM) or A889425 (1.0 µM) in isosmotic Krebs solution and then transferred to RbCl-containing control (300 mosM) or hyperosmotic (350 mosM) Krebs solution for 10 min in the continued presence or absence (Control, Con, of bumetanide or A889425. Each value is the mean ± SE of results from 5–6 lenses. ***Significant difference ( P
    Figure Legend Snippet: Effect of Na-K-2Cl cotransporter (NKCC) inhibitor bumetanide (Bum; A ) and transient receptor potential vanilloid 1 (TRPV1) antagonist A889425 (A88; B ) on the Rb uptake response to hyperosmotic solution. Intact lenses were preincubated 20 min with or without bumetanide (10 µM) or A889425 (1.0 µM) in isosmotic Krebs solution and then transferred to RbCl-containing control (300 mosM) or hyperosmotic (350 mosM) Krebs solution for 10 min in the continued presence or absence (Control, Con, of bumetanide or A889425. Each value is the mean ± SE of results from 5–6 lenses. ***Significant difference ( P

    Techniques Used:

    3) Product Images from "TRPV1-dependent ERK1/2 activation in porcine lens epithelium"

    Article Title: TRPV1-dependent ERK1/2 activation in porcine lens epithelium

    Journal: Experimental eye research

    doi: 10.1016/j.exer.2018.04.006

    The inhibitory influence of a TRPV1 antagonist A889425 on the ERK activation response to hyperosmotic solution and also the response to capsaicin. Intact lenses were pre-incubated for 20 min in the presence of absence of A889425 (1 μM) and then treated for 5 min with either hyperosmotic Krebs solution (350 mOsm) (Panel A) or capsaicin (100 nM) (Panel B) in the continued presence/absence of A889425. The epithelium was then removed for analysis of ERK1/2 phosphorylation. The bar graph in each panel shows mean ± SEM of 3 independent experiments. * (p
    Figure Legend Snippet: The inhibitory influence of a TRPV1 antagonist A889425 on the ERK activation response to hyperosmotic solution and also the response to capsaicin. Intact lenses were pre-incubated for 20 min in the presence of absence of A889425 (1 μM) and then treated for 5 min with either hyperosmotic Krebs solution (350 mOsm) (Panel A) or capsaicin (100 nM) (Panel B) in the continued presence/absence of A889425. The epithelium was then removed for analysis of ERK1/2 phosphorylation. The bar graph in each panel shows mean ± SEM of 3 independent experiments. * (p

    Techniques Used: Activation Assay, Incubation

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    • a889425  (Alomone Labs)
    93
    Alomone Labs a889425
    The increase in rubidium ion (Rb + ) uptake in wild-type (WT) cells exposed to capsaicin (1 µM) was prevented by <t>A889425</t> (1 µM), a TRPV1 antagonist ( A ), and bumetanide, a sodium-potassium/two-chloride cotransporter (NKCC1) inhibitor ( B ). Added alone, bumetanide reduced Rb + uptake. The increase in Rb + uptake in capsaicin-treated cells was prevented by 10 nM bumetanide as well as 10 μM bumetanide. Data are the mean ± SE of results from 6 to 12 independent experiments. * P
    A889425, 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/a889425/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    a889425 - by Bioz Stars, 2021-12
    93/100 stars
    		  Buy from Supplier
    kir2 1  (Alomone Labs)
    80
    Alomone Labs kir2 1
    Direct interaction between miR‐195 and Cavβ1, <t>Kir2.1</t> and Kv4.3. (A) Direct interaction between miR‐195 and Cavβ1. A fragment of miR‐195 that binds to CACNB1. miR‐195 is complementary to the CACNB1 gene 943‐949, which encodes Cavβ1, and the corresponding mutant sequence is designed based on the binding site. (B) Luciferase reporter with a CACNB1 fragment capable of binding to miR‐195. The gene was co‐transfected with miR‐195 into HEK293 cells, and miR‐195 reduced the activity of the luciferase reporter gene, ** P
    Kir2 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 80/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/kir2 1/product/Alomone Labs
    Average 80 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    kir2 1 - by Bioz Stars, 2021-12
    80/100 stars
    		  Buy from Supplier

    Image Search Results


    The increase in rubidium ion (Rb + ) uptake in wild-type (WT) cells exposed to capsaicin (1 µM) was prevented by A889425 (1 µM), a TRPV1 antagonist ( A ), and bumetanide, a sodium-potassium/two-chloride cotransporter (NKCC1) inhibitor ( B ). Added alone, bumetanide reduced Rb + uptake. The increase in Rb + uptake in capsaicin-treated cells was prevented by 10 nM bumetanide as well as 10 μM bumetanide. Data are the mean ± SE of results from 6 to 12 independent experiments. * P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: TRPV1 activation stimulates NKCC1 and increases hydrostatic pressure in the mouse lens

    doi: 10.1152/ajpcell.00391.2019

    Figure Lengend Snippet: The increase in rubidium ion (Rb + ) uptake in wild-type (WT) cells exposed to capsaicin (1 µM) was prevented by A889425 (1 µM), a TRPV1 antagonist ( A ), and bumetanide, a sodium-potassium/two-chloride cotransporter (NKCC1) inhibitor ( B ). Added alone, bumetanide reduced Rb + uptake. The increase in Rb + uptake in capsaicin-treated cells was prevented by 10 nM bumetanide as well as 10 μM bumetanide. Data are the mean ± SE of results from 6 to 12 independent experiments. * P

    Article Snippet: A889425 was purchased from Alomone Laboratories (Jerusalem, Israel).

    Techniques:

    Effect of Na-K-2Cl cotransporter (NKCC) inhibitor bumetanide (Bum; A ) and transient receptor potential vanilloid 1 (TRPV1) antagonist A889425 (A88; B ) on the Rb uptake response to capsaicin (Cap, 100nM). Intact lenses were preincubated 20 min with or without bumetanide (10 µM) or A889425 (1.0 µM) in isosmotic Krebs solution and then transferred to RbCl-containing Krebs solution with or without (Control, Con) capsaicin for 10 min in the continued presence or absence of bumetanide or A889425. Each value is the mean ± SE of results from 5–6 lenses. *** P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: Activation of TRPV1 channels leads to stimulation of NKCC1 cotransport in the lens

    doi: 10.1152/ajpcell.00252.2018

    Figure Lengend Snippet: Effect of Na-K-2Cl cotransporter (NKCC) inhibitor bumetanide (Bum; A ) and transient receptor potential vanilloid 1 (TRPV1) antagonist A889425 (A88; B ) on the Rb uptake response to capsaicin (Cap, 100nM). Intact lenses were preincubated 20 min with or without bumetanide (10 µM) or A889425 (1.0 µM) in isosmotic Krebs solution and then transferred to RbCl-containing Krebs solution with or without (Control, Con) capsaicin for 10 min in the continued presence or absence of bumetanide or A889425. Each value is the mean ± SE of results from 5–6 lenses. *** P

    Article Snippet: A889425 was purchased from Alomone Laboratory (Hadassah Ein Kerem, Jerusalem BioPark, Israel). with-no-lysine kinase (WNK)463 was purchased from Sellekchem (Houston, TX).

    Techniques:

    Effect of transient receptor potential vanilloid 1 (TRPV1) antagonist A889425 (A88) on the Na-K-2Cl cotransporter 1 (NKCC1) phosphorylation response to hyperosmotic solution (Hyper; A ) and capsaicin (Cap; B ). Intact lenses were preincubated in Krebs solution (300 mosM) with or without A889425 (1 µM) for 20 min and then exposed to capsaicin (100 nM) or hyperosmotic solution (350 mosM) for 10 min in the continued presence or absence of A889425. The capsule epithelium was then removed for Western blot analysis. Figures show bands for phospho-(p)NKCC1 detected using a rabbit polyclonal anti-phospho-NKCC1 (Thr 212/217 ) antibody; figures also show bands for β-actin. Band density of active (phosphorylated) NKCC1 was normalized to β-actin band density. In each panel a representative blot is presented along with a bar graph that shows densitometric analysis (means ± SE) of results from 3 independent experiments. *Significant difference ( P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: Activation of TRPV1 channels leads to stimulation of NKCC1 cotransport in the lens

    doi: 10.1152/ajpcell.00252.2018

    Figure Lengend Snippet: Effect of transient receptor potential vanilloid 1 (TRPV1) antagonist A889425 (A88) on the Na-K-2Cl cotransporter 1 (NKCC1) phosphorylation response to hyperosmotic solution (Hyper; A ) and capsaicin (Cap; B ). Intact lenses were preincubated in Krebs solution (300 mosM) with or without A889425 (1 µM) for 20 min and then exposed to capsaicin (100 nM) or hyperosmotic solution (350 mosM) for 10 min in the continued presence or absence of A889425. The capsule epithelium was then removed for Western blot analysis. Figures show bands for phospho-(p)NKCC1 detected using a rabbit polyclonal anti-phospho-NKCC1 (Thr 212/217 ) antibody; figures also show bands for β-actin. Band density of active (phosphorylated) NKCC1 was normalized to β-actin band density. In each panel a representative blot is presented along with a bar graph that shows densitometric analysis (means ± SE) of results from 3 independent experiments. *Significant difference ( P

    Article Snippet: A889425 was purchased from Alomone Laboratory (Hadassah Ein Kerem, Jerusalem BioPark, Israel). with-no-lysine kinase (WNK)463 was purchased from Sellekchem (Houston, TX).

    Techniques: Western Blot

    Effect of Na-K-2Cl cotransporter (NKCC) inhibitor bumetanide (Bum; A ) and transient receptor potential vanilloid 1 (TRPV1) antagonist A889425 (A88; B ) on the Rb uptake response to hyperosmotic solution. Intact lenses were preincubated 20 min with or without bumetanide (10 µM) or A889425 (1.0 µM) in isosmotic Krebs solution and then transferred to RbCl-containing control (300 mosM) or hyperosmotic (350 mosM) Krebs solution for 10 min in the continued presence or absence (Control, Con, of bumetanide or A889425. Each value is the mean ± SE of results from 5–6 lenses. ***Significant difference ( P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: Activation of TRPV1 channels leads to stimulation of NKCC1 cotransport in the lens

    doi: 10.1152/ajpcell.00252.2018

    Figure Lengend Snippet: Effect of Na-K-2Cl cotransporter (NKCC) inhibitor bumetanide (Bum; A ) and transient receptor potential vanilloid 1 (TRPV1) antagonist A889425 (A88; B ) on the Rb uptake response to hyperosmotic solution. Intact lenses were preincubated 20 min with or without bumetanide (10 µM) or A889425 (1.0 µM) in isosmotic Krebs solution and then transferred to RbCl-containing control (300 mosM) or hyperosmotic (350 mosM) Krebs solution for 10 min in the continued presence or absence (Control, Con, of bumetanide or A889425. Each value is the mean ± SE of results from 5–6 lenses. ***Significant difference ( P

    Article Snippet: A889425 was purchased from Alomone Laboratory (Hadassah Ein Kerem, Jerusalem BioPark, Israel). with-no-lysine kinase (WNK)463 was purchased from Sellekchem (Houston, TX).

    Techniques:

    The inhibitory influence of a TRPV1 antagonist A889425 on the ERK activation response to hyperosmotic solution and also the response to capsaicin. Intact lenses were pre-incubated for 20 min in the presence of absence of A889425 (1 μM) and then treated for 5 min with either hyperosmotic Krebs solution (350 mOsm) (Panel A) or capsaicin (100 nM) (Panel B) in the continued presence/absence of A889425. The epithelium was then removed for analysis of ERK1/2 phosphorylation. The bar graph in each panel shows mean ± SEM of 3 independent experiments. * (p

    Journal: Experimental eye research

    Article Title: TRPV1-dependent ERK1/2 activation in porcine lens epithelium

    doi: 10.1016/j.exer.2018.04.006

    Figure Lengend Snippet: The inhibitory influence of a TRPV1 antagonist A889425 on the ERK activation response to hyperosmotic solution and also the response to capsaicin. Intact lenses were pre-incubated for 20 min in the presence of absence of A889425 (1 μM) and then treated for 5 min with either hyperosmotic Krebs solution (350 mOsm) (Panel A) or capsaicin (100 nM) (Panel B) in the continued presence/absence of A889425. The epithelium was then removed for analysis of ERK1/2 phosphorylation. The bar graph in each panel shows mean ± SEM of 3 independent experiments. * (p

    Article Snippet: A889425 was purchased from Alomone Labs (Hadassah Ein Kerem, Jerusalem BioPark, Israel).

    Techniques: Activation Assay, Incubation

    Direct interaction between miR‐195 and Cavβ1, Kir2.1 and Kv4.3. (A) Direct interaction between miR‐195 and Cavβ1. A fragment of miR‐195 that binds to CACNB1. miR‐195 is complementary to the CACNB1 gene 943‐949, which encodes Cavβ1, and the corresponding mutant sequence is designed based on the binding site. (B) Luciferase reporter with a CACNB1 fragment capable of binding to miR‐195. The gene was co‐transfected with miR‐195 into HEK293 cells, and miR‐195 reduced the activity of the luciferase reporter gene, ** P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Up‐regulation of miR‐195 contributes to cardiac hypertrophy‐induced arrhythmia by targeting calcium and potassium channels, et al. Up‐regulation of miR‐195 contributes to cardiac hypertrophy‐induced arrhythmia by targeting calcium and potassium channels

    doi: 10.1111/jcmm.15431

    Figure Lengend Snippet: Direct interaction between miR‐195 and Cavβ1, Kir2.1 and Kv4.3. (A) Direct interaction between miR‐195 and Cavβ1. A fragment of miR‐195 that binds to CACNB1. miR‐195 is complementary to the CACNB1 gene 943‐949, which encodes Cavβ1, and the corresponding mutant sequence is designed based on the binding site. (B) Luciferase reporter with a CACNB1 fragment capable of binding to miR‐195. The gene was co‐transfected with miR‐195 into HEK293 cells, and miR‐195 reduced the activity of the luciferase reporter gene, ** P

    Article Snippet: After the addition of the miR‐195 inhibitor, the down‐regulation of Cavβ1 (#P < .05 vs. miR‐195 mimics), Kir2.1 (#P < .05 vs. miR‐195) and Kv4.3 (#P < .05 vs. miR‐195) was restored to normal level (Figure ,E).

    Techniques: Mutagenesis, Sequencing, Binding Assay, Luciferase, Transfection, Activity Assay

    miR‐195 inhibits the expression of Cavβ1, Kir2.1 and Kv4.3 in cardiomyocytes by immunofluorescence and Western blot. (A) Effects of miR‐195 on protein levels of endogenous Cavβ1 in primary cultured cardiomyocytes by Western blot analysis. miR‐195 effectively inhibited the expression of Cavβ1 relative to control group, whereas the scrambled NC miRNA failed to affect the protein levels. In contrast, AMO‐195 rescued the down‐regulation of Cavβ1 elicited by miR‐195. * P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Up‐regulation of miR‐195 contributes to cardiac hypertrophy‐induced arrhythmia by targeting calcium and potassium channels, et al. Up‐regulation of miR‐195 contributes to cardiac hypertrophy‐induced arrhythmia by targeting calcium and potassium channels

    doi: 10.1111/jcmm.15431

    Figure Lengend Snippet: miR‐195 inhibits the expression of Cavβ1, Kir2.1 and Kv4.3 in cardiomyocytes by immunofluorescence and Western blot. (A) Effects of miR‐195 on protein levels of endogenous Cavβ1 in primary cultured cardiomyocytes by Western blot analysis. miR‐195 effectively inhibited the expression of Cavβ1 relative to control group, whereas the scrambled NC miRNA failed to affect the protein levels. In contrast, AMO‐195 rescued the down‐regulation of Cavβ1 elicited by miR‐195. * P

    Article Snippet: After the addition of the miR‐195 inhibitor, the down‐regulation of Cavβ1 (#P < .05 vs. miR‐195 mimics), Kir2.1 (#P < .05 vs. miR‐195) and Kv4.3 (#P < .05 vs. miR‐195) was restored to normal level (Figure ,E).

    Techniques: Expressing, Immunofluorescence, Western Blot, Cell Culture

    miR‐195 inhibits the protein expression of Cavβ1, Kir2.1 and Kv4.3 in vivo. (A‐C) qPCR showed the changes of CACNB1/KCNJ2/KCND3 transcripts in cardiac tissues from overexpressing miR‐195 mice, n = 5‐9. (D) Verification of the specificity of miR‐195 on Cavβ1. Compared with NC, the expression of Cavβ1 protein in the overexpressed miR‐195 group was decreased. ** P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Up‐regulation of miR‐195 contributes to cardiac hypertrophy‐induced arrhythmia by targeting calcium and potassium channels, et al. Up‐regulation of miR‐195 contributes to cardiac hypertrophy‐induced arrhythmia by targeting calcium and potassium channels

    doi: 10.1111/jcmm.15431

    Figure Lengend Snippet: miR‐195 inhibits the protein expression of Cavβ1, Kir2.1 and Kv4.3 in vivo. (A‐C) qPCR showed the changes of CACNB1/KCNJ2/KCND3 transcripts in cardiac tissues from overexpressing miR‐195 mice, n = 5‐9. (D) Verification of the specificity of miR‐195 on Cavβ1. Compared with NC, the expression of Cavβ1 protein in the overexpressed miR‐195 group was decreased. ** P

    Article Snippet: After the addition of the miR‐195 inhibitor, the down‐regulation of Cavβ1 (#P < .05 vs. miR‐195 mimics), Kir2.1 (#P < .05 vs. miR‐195) and Kv4.3 (#P < .05 vs. miR‐195) was restored to normal level (Figure ,E).

    Techniques: Expressing, In Vivo, Real-time Polymerase Chain Reaction, Mouse Assay