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Alomone Labs tmem16a
Custom qPCR primers for determination of transcript abundance
Tmem16a, 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
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tmem16a - by Bioz Stars, 2026-03
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Custom qPCR primers for determination of transcript abundance

Journal: American Journal of Physiology - Cell Physiology

Article Title: Dextran sulfate sodium-induced chronic colitis attenuates Ca 2+ -activated Cl − secretion in murine colon by downregulating TMEM16A

doi: 10.1152/ajpcell.00328.2017

Figure Lengend Snippet: Custom qPCR primers for determination of transcript abundance

Article Snippet: PVDF membranes were then incubated in primary antibody: TMEM16A 1:500, CFTR 1:200, bestrophin-2 (BEST2) 1:500, muscarinic 3 (M 3 ) receptor 1:200 (Alomone Laboratories), inositol (1,4,5)-trisphosphate (IP 3 ) receptor 1:500, β-actin 1:1,000 (Cell Signaling, Danvers, MA) overnight at 4°C.

Techniques:

Effect of dextran sulfate sodium (DSS)-colitis on transcript abundance of Cl− channels in murine colon. Transcript abundance was determined for transmembrane protein 16A (Tmem16a; A), bestrophin-2 (Best2; B), and Cftr (C) in control (open bars) or DSS-colitis mice (closed bars). Bar graphs of summarized data represent means ± SE of 5 different animals normalized to an endogenous control, Actb. *P < 0.001, compared with their respective control.

Journal: American Journal of Physiology - Cell Physiology

Article Title: Dextran sulfate sodium-induced chronic colitis attenuates Ca 2+ -activated Cl − secretion in murine colon by downregulating TMEM16A

doi: 10.1152/ajpcell.00328.2017

Figure Lengend Snippet: Effect of dextran sulfate sodium (DSS)-colitis on transcript abundance of Cl− channels in murine colon. Transcript abundance was determined for transmembrane protein 16A (Tmem16a; A), bestrophin-2 (Best2; B), and Cftr (C) in control (open bars) or DSS-colitis mice (closed bars). Bar graphs of summarized data represent means ± SE of 5 different animals normalized to an endogenous control, Actb. *P < 0.001, compared with their respective control.

Article Snippet: PVDF membranes were then incubated in primary antibody: TMEM16A 1:500, CFTR 1:200, bestrophin-2 (BEST2) 1:500, muscarinic 3 (M 3 ) receptor 1:200 (Alomone Laboratories), inositol (1,4,5)-trisphosphate (IP 3 ) receptor 1:500, β-actin 1:1,000 (Cell Signaling, Danvers, MA) overnight at 4°C.

Techniques:

Effect of dextran sulfate sodium (DSS)-colitis on Cl− channel protein expression in murine colon. A: representative images of protein expression of the different characterized Cl− channels from epithelial lysates. BEST2, bestrophin-2. B: transmembrane protein 16A (TMEM16A) protein expression normalized to β-actin for quantification of control and DSS-colitis groups. TMEM16A expression (closed bar) is significantly decreased in DSS-colitis mice as compared with control. C and D: summarized data of Western blot quantification of BEST2 and CFTR normalized to β-actin in control and DSS-colitis mice. Neither protein was significantly altered from the control cohort. Bar graphs of summarized data represent means ± SE of 5 different animals from each respective group. *P < 0.05, compared with their respective control.

Journal: American Journal of Physiology - Cell Physiology

Article Title: Dextran sulfate sodium-induced chronic colitis attenuates Ca 2+ -activated Cl − secretion in murine colon by downregulating TMEM16A

doi: 10.1152/ajpcell.00328.2017

Figure Lengend Snippet: Effect of dextran sulfate sodium (DSS)-colitis on Cl− channel protein expression in murine colon. A: representative images of protein expression of the different characterized Cl− channels from epithelial lysates. BEST2, bestrophin-2. B: transmembrane protein 16A (TMEM16A) protein expression normalized to β-actin for quantification of control and DSS-colitis groups. TMEM16A expression (closed bar) is significantly decreased in DSS-colitis mice as compared with control. C and D: summarized data of Western blot quantification of BEST2 and CFTR normalized to β-actin in control and DSS-colitis mice. Neither protein was significantly altered from the control cohort. Bar graphs of summarized data represent means ± SE of 5 different animals from each respective group. *P < 0.05, compared with their respective control.

Article Snippet: PVDF membranes were then incubated in primary antibody: TMEM16A 1:500, CFTR 1:200, bestrophin-2 (BEST2) 1:500, muscarinic 3 (M 3 ) receptor 1:200 (Alomone Laboratories), inositol (1,4,5)-trisphosphate (IP 3 ) receptor 1:500, β-actin 1:1,000 (Cell Signaling, Danvers, MA) overnight at 4°C.

Techniques: Expressing, Western Blot

Immunohistochemistry of transmembrane protein 16A (TMEM16A) in colonic tissue sections. A: immunohistochemistry of TMEM16A in control tissue demonstrates pronounced expression and localization of the protein to surface epithelium and upper crypts (top, left). B. DSS-colitis tissue stained for TMEM16A exhibits less staining in epithelial cells and a more diffuse signal in the lamina propria (bottom, left). C and D: both cohorts of tissue were run in parallel with a control peptide specific for the anti-TMEM16A antibody. Both images demonstrate a lack of staining when coincubated with control peptide. Images were captured at ×20 magnification on the AxioImager (Carl Zeiss, Germany).

Journal: American Journal of Physiology - Cell Physiology

Article Title: Dextran sulfate sodium-induced chronic colitis attenuates Ca 2+ -activated Cl − secretion in murine colon by downregulating TMEM16A

doi: 10.1152/ajpcell.00328.2017

Figure Lengend Snippet: Immunohistochemistry of transmembrane protein 16A (TMEM16A) in colonic tissue sections. A: immunohistochemistry of TMEM16A in control tissue demonstrates pronounced expression and localization of the protein to surface epithelium and upper crypts (top, left). B. DSS-colitis tissue stained for TMEM16A exhibits less staining in epithelial cells and a more diffuse signal in the lamina propria (bottom, left). C and D: both cohorts of tissue were run in parallel with a control peptide specific for the anti-TMEM16A antibody. Both images demonstrate a lack of staining when coincubated with control peptide. Images were captured at ×20 magnification on the AxioImager (Carl Zeiss, Germany).

Article Snippet: PVDF membranes were then incubated in primary antibody: TMEM16A 1:500, CFTR 1:200, bestrophin-2 (BEST2) 1:500, muscarinic 3 (M 3 ) receptor 1:200 (Alomone Laboratories), inositol (1,4,5)-trisphosphate (IP 3 ) receptor 1:500, β-actin 1:1,000 (Cell Signaling, Danvers, MA) overnight at 4°C.

Techniques: Immunohistochemistry, Expressing, Staining