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raphani  (ATCC)
90
ATCC raphani
Raphani, supplied by ATCC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/raphani/product/ATCC
Average 90 stars, based on 1 article reviews
raphani - by Bioz Stars, 2026-03
90/100 stars
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verapamil  (Cell Signaling Technology Inc)
92
Cell Signaling Technology Inc verapamil
(A) Cholangiocytes were transfected with Poly I:C, a double-stranded RNA analog, in a dose-dependent fashion (0-50 μg) to evaluate if innate immune activation plays a role in ERK phosphorylation. Poly I:C did not phosphorylate ERK at any dosage. (B) Double-layer particles at varying dosages were used to determine the role of VP4 and VP7 in ERK phosphorylation. These particles were able to cause ERK phosphorylation despite absence of VP4 and VP7. (C) Virus like particles consisting of rotavirus proteins VP2 and VP6 (VLP 2/6) were able to induce a dose dependent ERK phosphorylation. (D) VP6 protein was assessed in a similar manner. With increasing dosages (1--5μM) of VP6, a greater ERK phosphorylation was noted compared to Maltose-binding protein (MBP) control. (E) Cholangiocytes treated with calcium free media for two hours and infected with RRV in calcium free media still demonstrated ERK phosphorylation. (F) <t>Verapamil</t> (1μg/ml) was used to block calcium channels on cholangiocytes. Following this, the cells were treated with RRV at an MOI of 160. ERK phosphorylation was noted, despite the presence of this L-type calcium channel blocker. Total p38 was used as a loading control for all studies.
Verapamil, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/verapamil/product/Cell Signaling Technology Inc
Average 92 stars, based on 1 article reviews
verapamil - by Bioz Stars, 2026-03
92/100 stars
  Buy from Supplier

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(A) Cholangiocytes were transfected with Poly I:C, a double-stranded RNA analog, in a dose-dependent fashion (0-50 μg) to evaluate if innate immune activation plays a role in ERK phosphorylation. Poly I:C did not phosphorylate ERK at any dosage. (B) Double-layer particles at varying dosages were used to determine the role of VP4 and VP7 in ERK phosphorylation. These particles were able to cause ERK phosphorylation despite absence of VP4 and VP7. (C) Virus like particles consisting of rotavirus proteins VP2 and VP6 (VLP 2/6) were able to induce a dose dependent ERK phosphorylation. (D) VP6 protein was assessed in a similar manner. With increasing dosages (1--5μM) of VP6, a greater ERK phosphorylation was noted compared to Maltose-binding protein (MBP) control. (E) Cholangiocytes treated with calcium free media for two hours and infected with RRV in calcium free media still demonstrated ERK phosphorylation. (F) Verapamil (1μg/ml) was used to block calcium channels on cholangiocytes. Following this, the cells were treated with RRV at an MOI of 160. ERK phosphorylation was noted, despite the presence of this L-type calcium channel blocker. Total p38 was used as a loading control for all studies.

Journal: Virology

Article Title: Rhesus rotavirus VP6 regulates ERK-dependent calcium influx in cholangiocytes

doi: 10.1016/j.virol.2016.09.014

Figure Lengend Snippet: (A) Cholangiocytes were transfected with Poly I:C, a double-stranded RNA analog, in a dose-dependent fashion (0-50 μg) to evaluate if innate immune activation plays a role in ERK phosphorylation. Poly I:C did not phosphorylate ERK at any dosage. (B) Double-layer particles at varying dosages were used to determine the role of VP4 and VP7 in ERK phosphorylation. These particles were able to cause ERK phosphorylation despite absence of VP4 and VP7. (C) Virus like particles consisting of rotavirus proteins VP2 and VP6 (VLP 2/6) were able to induce a dose dependent ERK phosphorylation. (D) VP6 protein was assessed in a similar manner. With increasing dosages (1--5μM) of VP6, a greater ERK phosphorylation was noted compared to Maltose-binding protein (MBP) control. (E) Cholangiocytes treated with calcium free media for two hours and infected with RRV in calcium free media still demonstrated ERK phosphorylation. (F) Verapamil (1μg/ml) was used to block calcium channels on cholangiocytes. Following this, the cells were treated with RRV at an MOI of 160. ERK phosphorylation was noted, despite the presence of this L-type calcium channel blocker. Total p38 was used as a loading control for all studies.

Article Snippet: Treatment with Calcium channel and MAPK inhibitors Cholangiocytes were pre-treated for one hour with ERK inhibitor: U0126 (ERK 1/2 inhibitor, Cell Signaling Technology), Verapamil (Ca ++ inhibitor, Sigma Aldrich) or Diltiazem HCl (Ca ++ inhibitor, Tocris bioscience, Minneapolis, MN) at concentrations of 20μmol/L and 1μg/ml, respectively.

Techniques: Transfection, Activation Assay, Phospho-proteomics, Virus, Binding Assay, Control, Infection, Blocking Assay

(A) Fluo-4 loaded cholangiocytes were treated with increasing doses of Verapamil followed by infection with RRV. This resulted in a dose dependent reduction of calcium influx into the cells. (B) Similar results were observed when cholangiocytes were treated with Diltiazem HCl, a second calcium channel inhibitor. (C) In order to determine fluo-4 loading in the presence of ERK 1/2 inhibitor and Verapamil, cells were treated with 10mM Ionomycin to open calcium channels. No reduction in the ability to fluoresce in the presence of calcium was witnessed with Verapamil or ERK inhibitor. (D) Cholangiocytes were pre-treated with calcium-free media followed by infection with RRV in calcium-free media to determine if the fluo-4 was detecting intracellular calcium release or extracellular influx. No fluorescence was observed following infection with RRV or exposure to VP6 protein in calcium-free media. (E) Cholangiocytes treated with virus-depleted stock displayed no calcium influx, while those treated with the triple-layer particles of RRV reacted similarly to the RRV virus lysate. (* = p<0.05)

Journal: Virology

Article Title: Rhesus rotavirus VP6 regulates ERK-dependent calcium influx in cholangiocytes

doi: 10.1016/j.virol.2016.09.014

Figure Lengend Snippet: (A) Fluo-4 loaded cholangiocytes were treated with increasing doses of Verapamil followed by infection with RRV. This resulted in a dose dependent reduction of calcium influx into the cells. (B) Similar results were observed when cholangiocytes were treated with Diltiazem HCl, a second calcium channel inhibitor. (C) In order to determine fluo-4 loading in the presence of ERK 1/2 inhibitor and Verapamil, cells were treated with 10mM Ionomycin to open calcium channels. No reduction in the ability to fluoresce in the presence of calcium was witnessed with Verapamil or ERK inhibitor. (D) Cholangiocytes were pre-treated with calcium-free media followed by infection with RRV in calcium-free media to determine if the fluo-4 was detecting intracellular calcium release or extracellular influx. No fluorescence was observed following infection with RRV or exposure to VP6 protein in calcium-free media. (E) Cholangiocytes treated with virus-depleted stock displayed no calcium influx, while those treated with the triple-layer particles of RRV reacted similarly to the RRV virus lysate. (* = p<0.05)

Article Snippet: Treatment with Calcium channel and MAPK inhibitors Cholangiocytes were pre-treated for one hour with ERK inhibitor: U0126 (ERK 1/2 inhibitor, Cell Signaling Technology), Verapamil (Ca ++ inhibitor, Sigma Aldrich) or Diltiazem HCl (Ca ++ inhibitor, Tocris bioscience, Minneapolis, MN) at concentrations of 20μmol/L and 1μg/ml, respectively.

Techniques: Infection, Fluorescence, Virus

(A) Dose dependent treatment of cholangiocytes with L-type calcium channel blockers Verapamil or Diltiazem HCl resulted in significant decrease in virus titers. (B) The timing of calcium channel blockade was evaluated through treatment of cholangiocytes prior to infection with RRV, after infection or both. Pre-treatment and the combination of pre- and post-treatment with 1.0uM Verapamil resulted in significant reductions in viral titers. Post-treatment with the calcium channel blocker however, did not result in a reduction of live virus. (C) The combination of pre-treatment with both ERK 1/2 inhibitor and Verapamil resulted in no further reduction of viral titer. * = p<0.05 versus control.

Journal: Virology

Article Title: Rhesus rotavirus VP6 regulates ERK-dependent calcium influx in cholangiocytes

doi: 10.1016/j.virol.2016.09.014

Figure Lengend Snippet: (A) Dose dependent treatment of cholangiocytes with L-type calcium channel blockers Verapamil or Diltiazem HCl resulted in significant decrease in virus titers. (B) The timing of calcium channel blockade was evaluated through treatment of cholangiocytes prior to infection with RRV, after infection or both. Pre-treatment and the combination of pre- and post-treatment with 1.0uM Verapamil resulted in significant reductions in viral titers. Post-treatment with the calcium channel blocker however, did not result in a reduction of live virus. (C) The combination of pre-treatment with both ERK 1/2 inhibitor and Verapamil resulted in no further reduction of viral titer. * = p<0.05 versus control.

Article Snippet: Treatment with Calcium channel and MAPK inhibitors Cholangiocytes were pre-treated for one hour with ERK inhibitor: U0126 (ERK 1/2 inhibitor, Cell Signaling Technology), Verapamil (Ca ++ inhibitor, Sigma Aldrich) or Diltiazem HCl (Ca ++ inhibitor, Tocris bioscience, Minneapolis, MN) at concentrations of 20μmol/L and 1μg/ml, respectively.

Techniques: Virus, Infection, Control