human prorenin Search Results


elisa kits  (R&D Systems)
95
R&D Systems elisa kits
Elisa Kits, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+prorenin/Human+Renin+Quantikine+ELISA+Kit/10__3390_slash_ijms26051789-223-16-27
Average 95 stars, based on 1 article reviews
elisa kits - by Bioz Stars, 2026-11
95/100 stars
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ren propeptide  (R&D Systems)
90
R&D Systems ren propeptide
Ren Propeptide, supplied by R&D Systems, 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/product/human+prorenin/Human+Renin+Propeptide+Antibody/10__1530_slash_ec___16___0082-65-63-65
Average 90 stars, based on 1 article reviews
ren propeptide - by Bioz Stars, 2026-11
90/100 stars
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renin sirna  (OriGene)
93
OriGene renin sirna
LX‐2 derived EV contain renin activity that stimulates delayed platelet activation. (A) The aspartyl protease inhibitor pepstatin suppresses LX2 induced platelet activation. LX‐2 cell EV were preincubated with pepstatin (10 μg/mL, 10 min), or not, prior to assessing platelet activation induced by LX‐2 EV. HBSS buffer the EV were resuspended in was the negative control. *** p < 0.001 unpaired T test, N = 5 biologic replicates. (B) Renin enzymatic activity underlies platelet stimulation by LX‐2 EV. Freshly isolated human platelets were incubated (10 min, 1000 rpm) in aggregometer cuvettes with the stated concentrations of the DRI Aliskiren. Aggregation was then initiated by the addition of LX‐2 EV at t = 0. N = 7 biologic replicates. *** p < 0.001 by one way ANOVA. (C) The Direct Renin Inhibitor VTP23999 and Aliskiren inhibit HSC EV‐induced platelet aggregation. Platelets stirring in aggregometer cuvettes were pretreated, or not, with VTP23999 (40 μM) or Aliskiren (40 μM) prior to the addition of buffer or washed EV recovered from LX‐2 cell conditioned media. VTP23999 N = 15 biologic replicates **** p < 0.0001; Aliskiren N = 14 biologic replicates unpaired T test p < 0.0001. (D) Renin mRNA accumulates during iPSC maturation to initiate HSC. Transcript levels of the REN gene quantified by RT‐qPCR were assessed as human iPSC cells were differentiated to quiescent and then initiated HSC. mean ± SD using a two‐tailed unpaired t ‐test with Welch's corrections to calculate exact p ‐values from 4 independent replicates. (E) Renin enzymatic activity promotes platelet aggregation in response to EV from iPSC‐derived initiated HSC. Platelet aggregation induced by media conditioned by iPSC matured to initiated HSC in the presence or absence of 40 μM Aliskiren ( N = 4 biologic replicates) or VTP23999 ( N = 3 biologic replicates) ** p < 0.01 with p = 0.0012. (F) LX‐2 cell derived EV contain prorenin while platelets abundantly express the prorenin receptor (p)RR. ( left ) Western blot for renin (37.5 kDa) and prorenin (~42–45 kDa) in EV isolated by ultracentrifugation from LX‐2 cell conditioned media, and ( right ) prorenin receptor (apparent ~42 kDa mobility) expressed by LX‐2 cells or washed human platelets. (G) The combination of platelets incubated with LX‐2 EV develops renin enzymatic activity. Renin enzymatic activity was assayed using a fluorogenic TF3/TQ3‐labeled peptide substrate (Abcam) to assess fluorescent resonant energy transfer over time as platelets were incubated with or without purified LX‐2 EV. N = 5 assay replicates. Unpaired T test p = 0.0172. (H) Renin knockdown in LX‐2 cells reduces EV‐associated renin and suppresses LX‐2 EV‐induced platelet aggregation. LX‐2 cells were incubated overnight with REN <t>siRNA</t> or a universal scrambled control siRNAs, <t>the</t> <t>transfection</t> media was removed and the cells were incubated with complete MEM overnight, this was removed and discarded and the cells incubated overnight for a second time before this conditioned media was collected, cleared by centrifugation, and concentrated by Centricon filtration. EV from knockdown or scrambled control cells were added to stirring platelets at t = 0 with aggregation assessed by clearing as before. The amount of aggregation after 35 min of incubation was quantitated with REN siRNA EV significantly less effective than EV from scrambled control‐treated cells. N = 5 biologic replicates **** p < 0.0001.
Renin Sirna, supplied by OriGene, 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/product/human+prorenin/Renin+(REN)+Human+siRNA+Oligo+Duplex/pmc12521956-122-3-5
Average 93 stars, based on 1 article reviews
renin sirna - by Bioz Stars, 2026-11
93/100 stars
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human renin cdna untagged  (OriGene)
91
OriGene human renin cdna untagged
LX‐2 derived EV contain renin activity that stimulates delayed platelet activation. (A) The aspartyl protease inhibitor pepstatin suppresses LX2 induced platelet activation. LX‐2 cell EV were preincubated with pepstatin (10 μg/mL, 10 min), or not, prior to assessing platelet activation induced by LX‐2 EV. HBSS buffer the EV were resuspended in was the negative control. *** p < 0.001 unpaired T test, N = 5 biologic replicates. (B) Renin enzymatic activity underlies platelet stimulation by LX‐2 EV. Freshly isolated human platelets were incubated (10 min, 1000 rpm) in aggregometer cuvettes with the stated concentrations of the DRI Aliskiren. Aggregation was then initiated by the addition of LX‐2 EV at t = 0. N = 7 biologic replicates. *** p < 0.001 by one way ANOVA. (C) The Direct Renin Inhibitor VTP23999 and Aliskiren inhibit HSC EV‐induced platelet aggregation. Platelets stirring in aggregometer cuvettes were pretreated, or not, with VTP23999 (40 μM) or Aliskiren (40 μM) prior to the addition of buffer or washed EV recovered from LX‐2 cell conditioned media. VTP23999 N = 15 biologic replicates **** p < 0.0001; Aliskiren N = 14 biologic replicates unpaired T test p < 0.0001. (D) Renin mRNA accumulates during iPSC maturation to initiate HSC. Transcript levels of the REN gene quantified by RT‐qPCR were assessed as human iPSC cells were differentiated to quiescent and then initiated HSC. mean ± SD using a two‐tailed unpaired t ‐test with Welch's corrections to calculate exact p ‐values from 4 independent replicates. (E) Renin enzymatic activity promotes platelet aggregation in response to EV from iPSC‐derived initiated HSC. Platelet aggregation induced by media conditioned by iPSC matured to initiated HSC in the presence or absence of 40 μM Aliskiren ( N = 4 biologic replicates) or VTP23999 ( N = 3 biologic replicates) ** p < 0.01 with p = 0.0012. (F) LX‐2 cell derived EV contain prorenin while platelets abundantly express the prorenin receptor (p)RR. ( left ) Western blot for renin (37.5 kDa) and prorenin (~42–45 kDa) in EV isolated by ultracentrifugation from LX‐2 cell conditioned media, and ( right ) prorenin receptor (apparent ~42 kDa mobility) expressed by LX‐2 cells or washed human platelets. (G) The combination of platelets incubated with LX‐2 EV develops renin enzymatic activity. Renin enzymatic activity was assayed using a fluorogenic TF3/TQ3‐labeled peptide substrate (Abcam) to assess fluorescent resonant energy transfer over time as platelets were incubated with or without purified LX‐2 EV. N = 5 assay replicates. Unpaired T test p = 0.0172. (H) Renin knockdown in LX‐2 cells reduces EV‐associated renin and suppresses LX‐2 EV‐induced platelet aggregation. LX‐2 cells were incubated overnight with REN <t>siRNA</t> or a universal scrambled control siRNAs, <t>the</t> <t>transfection</t> media was removed and the cells were incubated with complete MEM overnight, this was removed and discarded and the cells incubated overnight for a second time before this conditioned media was collected, cleared by centrifugation, and concentrated by Centricon filtration. EV from knockdown or scrambled control cells were added to stirring platelets at t = 0 with aggregation assessed by clearing as before. The amount of aggregation after 35 min of incubation was quantitated with REN siRNA EV significantly less effective than EV from scrambled control‐treated cells. N = 5 biologic replicates **** p < 0.0001.
Human Renin Cdna Untagged, supplied by OriGene, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+prorenin/Renin+(REN)+(NM_000537)+Human+Untagged+Clone/pmc06691008__41598_2019_48014_MOESM1_ESM-1-0-9
Average 91 stars, based on 1 article reviews
human renin cdna untagged - by Bioz Stars, 2026-11
91/100 stars
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tris buffered saline tbs  (R&D Systems)
92
R&D Systems tris buffered saline tbs
LX‐2 derived EV contain renin activity that stimulates delayed platelet activation. (A) The aspartyl protease inhibitor pepstatin suppresses LX2 induced platelet activation. LX‐2 cell EV were preincubated with pepstatin (10 μg/mL, 10 min), or not, prior to assessing platelet activation induced by LX‐2 EV. HBSS buffer the EV were resuspended in was the negative control. *** p < 0.001 unpaired T test, N = 5 biologic replicates. (B) Renin enzymatic activity underlies platelet stimulation by LX‐2 EV. Freshly isolated human platelets were incubated (10 min, 1000 rpm) in aggregometer cuvettes with the stated concentrations of the DRI Aliskiren. Aggregation was then initiated by the addition of LX‐2 EV at t = 0. N = 7 biologic replicates. *** p < 0.001 by one way ANOVA. (C) The Direct Renin Inhibitor VTP23999 and Aliskiren inhibit HSC EV‐induced platelet aggregation. Platelets stirring in aggregometer cuvettes were pretreated, or not, with VTP23999 (40 μM) or Aliskiren (40 μM) prior to the addition of buffer or washed EV recovered from LX‐2 cell conditioned media. VTP23999 N = 15 biologic replicates **** p < 0.0001; Aliskiren N = 14 biologic replicates unpaired T test p < 0.0001. (D) Renin mRNA accumulates during iPSC maturation to initiate HSC. Transcript levels of the REN gene quantified by RT‐qPCR were assessed as human iPSC cells were differentiated to quiescent and then initiated HSC. mean ± SD using a two‐tailed unpaired t ‐test with Welch's corrections to calculate exact p ‐values from 4 independent replicates. (E) Renin enzymatic activity promotes platelet aggregation in response to EV from iPSC‐derived initiated HSC. Platelet aggregation induced by media conditioned by iPSC matured to initiated HSC in the presence or absence of 40 μM Aliskiren ( N = 4 biologic replicates) or VTP23999 ( N = 3 biologic replicates) ** p < 0.01 with p = 0.0012. (F) LX‐2 cell derived EV contain prorenin while platelets abundantly express the prorenin receptor (p)RR. ( left ) Western blot for renin (37.5 kDa) and prorenin (~42–45 kDa) in EV isolated by ultracentrifugation from LX‐2 cell conditioned media, and ( right ) prorenin receptor (apparent ~42 kDa mobility) expressed by LX‐2 cells or washed human platelets. (G) The combination of platelets incubated with LX‐2 EV develops renin enzymatic activity. Renin enzymatic activity was assayed using a fluorogenic TF3/TQ3‐labeled peptide substrate (Abcam) to assess fluorescent resonant energy transfer over time as platelets were incubated with or without purified LX‐2 EV. N = 5 assay replicates. Unpaired T test p = 0.0172. (H) Renin knockdown in LX‐2 cells reduces EV‐associated renin and suppresses LX‐2 EV‐induced platelet aggregation. LX‐2 cells were incubated overnight with REN <t>siRNA</t> or a universal scrambled control siRNAs, <t>the</t> <t>transfection</t> media was removed and the cells were incubated with complete MEM overnight, this was removed and discarded and the cells incubated overnight for a second time before this conditioned media was collected, cleared by centrifugation, and concentrated by Centricon filtration. EV from knockdown or scrambled control cells were added to stirring platelets at t = 0 with aggregation assessed by clearing as before. The amount of aggregation after 35 min of incubation was quantitated with REN siRNA EV significantly less effective than EV from scrambled control‐treated cells. N = 5 biologic replicates **** p < 0.0001.
Tris Buffered Saline Tbs, supplied by R&D Systems, 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/product/human+prorenin/Human+Renin+Propeptide+Antibody/pm25902786-94-9-25
Average 92 stars, based on 1 article reviews
tris buffered saline tbs - by Bioz Stars, 2026-11
92/100 stars
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human elisa kits  (Shanghai Korain Biotech Co Ltd)
94
Shanghai Korain Biotech Co Ltd human elisa kits
LX‐2 derived EV contain renin activity that stimulates delayed platelet activation. (A) The aspartyl protease inhibitor pepstatin suppresses LX2 induced platelet activation. LX‐2 cell EV were preincubated with pepstatin (10 μg/mL, 10 min), or not, prior to assessing platelet activation induced by LX‐2 EV. HBSS buffer the EV were resuspended in was the negative control. *** p < 0.001 unpaired T test, N = 5 biologic replicates. (B) Renin enzymatic activity underlies platelet stimulation by LX‐2 EV. Freshly isolated human platelets were incubated (10 min, 1000 rpm) in aggregometer cuvettes with the stated concentrations of the DRI Aliskiren. Aggregation was then initiated by the addition of LX‐2 EV at t = 0. N = 7 biologic replicates. *** p < 0.001 by one way ANOVA. (C) The Direct Renin Inhibitor VTP23999 and Aliskiren inhibit HSC EV‐induced platelet aggregation. Platelets stirring in aggregometer cuvettes were pretreated, or not, with VTP23999 (40 μM) or Aliskiren (40 μM) prior to the addition of buffer or washed EV recovered from LX‐2 cell conditioned media. VTP23999 N = 15 biologic replicates **** p < 0.0001; Aliskiren N = 14 biologic replicates unpaired T test p < 0.0001. (D) Renin mRNA accumulates during iPSC maturation to initiate HSC. Transcript levels of the REN gene quantified by RT‐qPCR were assessed as human iPSC cells were differentiated to quiescent and then initiated HSC. mean ± SD using a two‐tailed unpaired t ‐test with Welch's corrections to calculate exact p ‐values from 4 independent replicates. (E) Renin enzymatic activity promotes platelet aggregation in response to EV from iPSC‐derived initiated HSC. Platelet aggregation induced by media conditioned by iPSC matured to initiated HSC in the presence or absence of 40 μM Aliskiren ( N = 4 biologic replicates) or VTP23999 ( N = 3 biologic replicates) ** p < 0.01 with p = 0.0012. (F) LX‐2 cell derived EV contain prorenin while platelets abundantly express the prorenin receptor (p)RR. ( left ) Western blot for renin (37.5 kDa) and prorenin (~42–45 kDa) in EV isolated by ultracentrifugation from LX‐2 cell conditioned media, and ( right ) prorenin receptor (apparent ~42 kDa mobility) expressed by LX‐2 cells or washed human platelets. (G) The combination of platelets incubated with LX‐2 EV develops renin enzymatic activity. Renin enzymatic activity was assayed using a fluorogenic TF3/TQ3‐labeled peptide substrate (Abcam) to assess fluorescent resonant energy transfer over time as platelets were incubated with or without purified LX‐2 EV. N = 5 assay replicates. Unpaired T test p = 0.0172. (H) Renin knockdown in LX‐2 cells reduces EV‐associated renin and suppresses LX‐2 EV‐induced platelet aggregation. LX‐2 cells were incubated overnight with REN <t>siRNA</t> or a universal scrambled control siRNAs, <t>the</t> <t>transfection</t> media was removed and the cells were incubated with complete MEM overnight, this was removed and discarded and the cells incubated overnight for a second time before this conditioned media was collected, cleared by centrifugation, and concentrated by Centricon filtration. EV from knockdown or scrambled control cells were added to stirring platelets at t = 0 with aggregation assessed by clearing as before. The amount of aggregation after 35 min of incubation was quantitated with REN siRNA EV significantly less effective than EV from scrambled control‐treated cells. N = 5 biologic replicates **** p < 0.0001.
Human Elisa Kits, supplied by Shanghai Korain Biotech Co Ltd, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+prorenin/Human+Renin+ELISA+Kit/pmc13113473-122-9-12
Average 94 stars, based on 1 article reviews
human elisa kits - by Bioz Stars, 2026-11
94/100 stars
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polyclonal anti human renin sheep antibody  (R&D Systems)
90
R&D Systems polyclonal anti human renin sheep antibody
LX‐2 derived EV contain renin activity that stimulates delayed platelet activation. (A) The aspartyl protease inhibitor pepstatin suppresses LX2 induced platelet activation. LX‐2 cell EV were preincubated with pepstatin (10 μg/mL, 10 min), or not, prior to assessing platelet activation induced by LX‐2 EV. HBSS buffer the EV were resuspended in was the negative control. *** p < 0.001 unpaired T test, N = 5 biologic replicates. (B) Renin enzymatic activity underlies platelet stimulation by LX‐2 EV. Freshly isolated human platelets were incubated (10 min, 1000 rpm) in aggregometer cuvettes with the stated concentrations of the DRI Aliskiren. Aggregation was then initiated by the addition of LX‐2 EV at t = 0. N = 7 biologic replicates. *** p < 0.001 by one way ANOVA. (C) The Direct Renin Inhibitor VTP23999 and Aliskiren inhibit HSC EV‐induced platelet aggregation. Platelets stirring in aggregometer cuvettes were pretreated, or not, with VTP23999 (40 μM) or Aliskiren (40 μM) prior to the addition of buffer or washed EV recovered from LX‐2 cell conditioned media. VTP23999 N = 15 biologic replicates **** p < 0.0001; Aliskiren N = 14 biologic replicates unpaired T test p < 0.0001. (D) Renin mRNA accumulates during iPSC maturation to initiate HSC. Transcript levels of the REN gene quantified by RT‐qPCR were assessed as human iPSC cells were differentiated to quiescent and then initiated HSC. mean ± SD using a two‐tailed unpaired t ‐test with Welch's corrections to calculate exact p ‐values from 4 independent replicates. (E) Renin enzymatic activity promotes platelet aggregation in response to EV from iPSC‐derived initiated HSC. Platelet aggregation induced by media conditioned by iPSC matured to initiated HSC in the presence or absence of 40 μM Aliskiren ( N = 4 biologic replicates) or VTP23999 ( N = 3 biologic replicates) ** p < 0.01 with p = 0.0012. (F) LX‐2 cell derived EV contain prorenin while platelets abundantly express the prorenin receptor (p)RR. ( left ) Western blot for renin (37.5 kDa) and prorenin (~42–45 kDa) in EV isolated by ultracentrifugation from LX‐2 cell conditioned media, and ( right ) prorenin receptor (apparent ~42 kDa mobility) expressed by LX‐2 cells or washed human platelets. (G) The combination of platelets incubated with LX‐2 EV develops renin enzymatic activity. Renin enzymatic activity was assayed using a fluorogenic TF3/TQ3‐labeled peptide substrate (Abcam) to assess fluorescent resonant energy transfer over time as platelets were incubated with or without purified LX‐2 EV. N = 5 assay replicates. Unpaired T test p = 0.0172. (H) Renin knockdown in LX‐2 cells reduces EV‐associated renin and suppresses LX‐2 EV‐induced platelet aggregation. LX‐2 cells were incubated overnight with REN <t>siRNA</t> or a universal scrambled control siRNAs, <t>the</t> <t>transfection</t> media was removed and the cells were incubated with complete MEM overnight, this was removed and discarded and the cells incubated overnight for a second time before this conditioned media was collected, cleared by centrifugation, and concentrated by Centricon filtration. EV from knockdown or scrambled control cells were added to stirring platelets at t = 0 with aggregation assessed by clearing as before. The amount of aggregation after 35 min of incubation was quantitated with REN siRNA EV significantly less effective than EV from scrambled control‐treated cells. N = 5 biologic replicates **** p < 0.0001.
Polyclonal Anti Human Renin Sheep Antibody, supplied by R&D Systems, 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/product/human+prorenin/Human+Renin+Antibody/pm31945766-88-5-10
Average 90 stars, based on 1 article reviews
polyclonal anti human renin sheep antibody - by Bioz Stars, 2026-11
90/100 stars
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human renin precursor elisa kit  (Cusabio)
90
Cusabio human renin precursor elisa kit
LX‐2 derived EV contain renin activity that stimulates delayed platelet activation. (A) The aspartyl protease inhibitor pepstatin suppresses LX2 induced platelet activation. LX‐2 cell EV were preincubated with pepstatin (10 μg/mL, 10 min), or not, prior to assessing platelet activation induced by LX‐2 EV. HBSS buffer the EV were resuspended in was the negative control. *** p < 0.001 unpaired T test, N = 5 biologic replicates. (B) Renin enzymatic activity underlies platelet stimulation by LX‐2 EV. Freshly isolated human platelets were incubated (10 min, 1000 rpm) in aggregometer cuvettes with the stated concentrations of the DRI Aliskiren. Aggregation was then initiated by the addition of LX‐2 EV at t = 0. N = 7 biologic replicates. *** p < 0.001 by one way ANOVA. (C) The Direct Renin Inhibitor VTP23999 and Aliskiren inhibit HSC EV‐induced platelet aggregation. Platelets stirring in aggregometer cuvettes were pretreated, or not, with VTP23999 (40 μM) or Aliskiren (40 μM) prior to the addition of buffer or washed EV recovered from LX‐2 cell conditioned media. VTP23999 N = 15 biologic replicates **** p < 0.0001; Aliskiren N = 14 biologic replicates unpaired T test p < 0.0001. (D) Renin mRNA accumulates during iPSC maturation to initiate HSC. Transcript levels of the REN gene quantified by RT‐qPCR were assessed as human iPSC cells were differentiated to quiescent and then initiated HSC. mean ± SD using a two‐tailed unpaired t ‐test with Welch's corrections to calculate exact p ‐values from 4 independent replicates. (E) Renin enzymatic activity promotes platelet aggregation in response to EV from iPSC‐derived initiated HSC. Platelet aggregation induced by media conditioned by iPSC matured to initiated HSC in the presence or absence of 40 μM Aliskiren ( N = 4 biologic replicates) or VTP23999 ( N = 3 biologic replicates) ** p < 0.01 with p = 0.0012. (F) LX‐2 cell derived EV contain prorenin while platelets abundantly express the prorenin receptor (p)RR. ( left ) Western blot for renin (37.5 kDa) and prorenin (~42–45 kDa) in EV isolated by ultracentrifugation from LX‐2 cell conditioned media, and ( right ) prorenin receptor (apparent ~42 kDa mobility) expressed by LX‐2 cells or washed human platelets. (G) The combination of platelets incubated with LX‐2 EV develops renin enzymatic activity. Renin enzymatic activity was assayed using a fluorogenic TF3/TQ3‐labeled peptide substrate (Abcam) to assess fluorescent resonant energy transfer over time as platelets were incubated with or without purified LX‐2 EV. N = 5 assay replicates. Unpaired T test p = 0.0172. (H) Renin knockdown in LX‐2 cells reduces EV‐associated renin and suppresses LX‐2 EV‐induced platelet aggregation. LX‐2 cells were incubated overnight with REN <t>siRNA</t> or a universal scrambled control siRNAs, <t>the</t> <t>transfection</t> media was removed and the cells were incubated with complete MEM overnight, this was removed and discarded and the cells incubated overnight for a second time before this conditioned media was collected, cleared by centrifugation, and concentrated by Centricon filtration. EV from knockdown or scrambled control cells were added to stirring platelets at t = 0 with aggregation assessed by clearing as before. The amount of aggregation after 35 min of incubation was quantitated with REN siRNA EV significantly less effective than EV from scrambled control‐treated cells. N = 5 biologic replicates **** p < 0.0001.
Human Renin Precursor Elisa Kit, supplied by Cusabio, 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/product/human+prorenin/Human+renin+(REN)+ELISA+Kit/pmc06676210-75-22-31
Average 90 stars, based on 1 article reviews
human renin precursor elisa kit - by Bioz Stars, 2026-11
90/100 stars
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immunosorbent assay elisa kit  (R&D Systems)
94
R&D Systems immunosorbent assay elisa kit
LX‐2 derived EV contain renin activity that stimulates delayed platelet activation. (A) The aspartyl protease inhibitor pepstatin suppresses LX2 induced platelet activation. LX‐2 cell EV were preincubated with pepstatin (10 μg/mL, 10 min), or not, prior to assessing platelet activation induced by LX‐2 EV. HBSS buffer the EV were resuspended in was the negative control. *** p < 0.001 unpaired T test, N = 5 biologic replicates. (B) Renin enzymatic activity underlies platelet stimulation by LX‐2 EV. Freshly isolated human platelets were incubated (10 min, 1000 rpm) in aggregometer cuvettes with the stated concentrations of the DRI Aliskiren. Aggregation was then initiated by the addition of LX‐2 EV at t = 0. N = 7 biologic replicates. *** p < 0.001 by one way ANOVA. (C) The Direct Renin Inhibitor VTP23999 and Aliskiren inhibit HSC EV‐induced platelet aggregation. Platelets stirring in aggregometer cuvettes were pretreated, or not, with VTP23999 (40 μM) or Aliskiren (40 μM) prior to the addition of buffer or washed EV recovered from LX‐2 cell conditioned media. VTP23999 N = 15 biologic replicates **** p < 0.0001; Aliskiren N = 14 biologic replicates unpaired T test p < 0.0001. (D) Renin mRNA accumulates during iPSC maturation to initiate HSC. Transcript levels of the REN gene quantified by RT‐qPCR were assessed as human iPSC cells were differentiated to quiescent and then initiated HSC. mean ± SD using a two‐tailed unpaired t ‐test with Welch's corrections to calculate exact p ‐values from 4 independent replicates. (E) Renin enzymatic activity promotes platelet aggregation in response to EV from iPSC‐derived initiated HSC. Platelet aggregation induced by media conditioned by iPSC matured to initiated HSC in the presence or absence of 40 μM Aliskiren ( N = 4 biologic replicates) or VTP23999 ( N = 3 biologic replicates) ** p < 0.01 with p = 0.0012. (F) LX‐2 cell derived EV contain prorenin while platelets abundantly express the prorenin receptor (p)RR. ( left ) Western blot for renin (37.5 kDa) and prorenin (~42–45 kDa) in EV isolated by ultracentrifugation from LX‐2 cell conditioned media, and ( right ) prorenin receptor (apparent ~42 kDa mobility) expressed by LX‐2 cells or washed human platelets. (G) The combination of platelets incubated with LX‐2 EV develops renin enzymatic activity. Renin enzymatic activity was assayed using a fluorogenic TF3/TQ3‐labeled peptide substrate (Abcam) to assess fluorescent resonant energy transfer over time as platelets were incubated with or without purified LX‐2 EV. N = 5 assay replicates. Unpaired T test p = 0.0172. (H) Renin knockdown in LX‐2 cells reduces EV‐associated renin and suppresses LX‐2 EV‐induced platelet aggregation. LX‐2 cells were incubated overnight with REN <t>siRNA</t> or a universal scrambled control siRNAs, <t>the</t> <t>transfection</t> media was removed and the cells were incubated with complete MEM overnight, this was removed and discarded and the cells incubated overnight for a second time before this conditioned media was collected, cleared by centrifugation, and concentrated by Centricon filtration. EV from knockdown or scrambled control cells were added to stirring platelets at t = 0 with aggregation assessed by clearing as before. The amount of aggregation after 35 min of incubation was quantitated with REN siRNA EV significantly less effective than EV from scrambled control‐treated cells. N = 5 biologic replicates **** p < 0.0001.
Immunosorbent Assay Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+prorenin/Human+Renin+Quantikine+ELISA+Kit/pmc08425233-81-17-26
Average 94 stars, based on 1 article reviews
immunosorbent assay elisa kit - by Bioz Stars, 2026-11
94/100 stars
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a human renin r polyclonal antibody  (R&D Systems)
91
R&D Systems a human renin r polyclonal antibody
LX‐2 derived EV contain renin activity that stimulates delayed platelet activation. (A) The aspartyl protease inhibitor pepstatin suppresses LX2 induced platelet activation. LX‐2 cell EV were preincubated with pepstatin (10 μg/mL, 10 min), or not, prior to assessing platelet activation induced by LX‐2 EV. HBSS buffer the EV were resuspended in was the negative control. *** p < 0.001 unpaired T test, N = 5 biologic replicates. (B) Renin enzymatic activity underlies platelet stimulation by LX‐2 EV. Freshly isolated human platelets were incubated (10 min, 1000 rpm) in aggregometer cuvettes with the stated concentrations of the DRI Aliskiren. Aggregation was then initiated by the addition of LX‐2 EV at t = 0. N = 7 biologic replicates. *** p < 0.001 by one way ANOVA. (C) The Direct Renin Inhibitor VTP23999 and Aliskiren inhibit HSC EV‐induced platelet aggregation. Platelets stirring in aggregometer cuvettes were pretreated, or not, with VTP23999 (40 μM) or Aliskiren (40 μM) prior to the addition of buffer or washed EV recovered from LX‐2 cell conditioned media. VTP23999 N = 15 biologic replicates **** p < 0.0001; Aliskiren N = 14 biologic replicates unpaired T test p < 0.0001. (D) Renin mRNA accumulates during iPSC maturation to initiate HSC. Transcript levels of the REN gene quantified by RT‐qPCR were assessed as human iPSC cells were differentiated to quiescent and then initiated HSC. mean ± SD using a two‐tailed unpaired t ‐test with Welch's corrections to calculate exact p ‐values from 4 independent replicates. (E) Renin enzymatic activity promotes platelet aggregation in response to EV from iPSC‐derived initiated HSC. Platelet aggregation induced by media conditioned by iPSC matured to initiated HSC in the presence or absence of 40 μM Aliskiren ( N = 4 biologic replicates) or VTP23999 ( N = 3 biologic replicates) ** p < 0.01 with p = 0.0012. (F) LX‐2 cell derived EV contain prorenin while platelets abundantly express the prorenin receptor (p)RR. ( left ) Western blot for renin (37.5 kDa) and prorenin (~42–45 kDa) in EV isolated by ultracentrifugation from LX‐2 cell conditioned media, and ( right ) prorenin receptor (apparent ~42 kDa mobility) expressed by LX‐2 cells or washed human platelets. (G) The combination of platelets incubated with LX‐2 EV develops renin enzymatic activity. Renin enzymatic activity was assayed using a fluorogenic TF3/TQ3‐labeled peptide substrate (Abcam) to assess fluorescent resonant energy transfer over time as platelets were incubated with or without purified LX‐2 EV. N = 5 assay replicates. Unpaired T test p = 0.0172. (H) Renin knockdown in LX‐2 cells reduces EV‐associated renin and suppresses LX‐2 EV‐induced platelet aggregation. LX‐2 cells were incubated overnight with REN <t>siRNA</t> or a universal scrambled control siRNAs, <t>the</t> <t>transfection</t> media was removed and the cells were incubated with complete MEM overnight, this was removed and discarded and the cells incubated overnight for a second time before this conditioned media was collected, cleared by centrifugation, and concentrated by Centricon filtration. EV from knockdown or scrambled control cells were added to stirring platelets at t = 0 with aggregation assessed by clearing as before. The amount of aggregation after 35 min of incubation was quantitated with REN siRNA EV significantly less effective than EV from scrambled control‐treated cells. N = 5 biologic replicates **** p < 0.0001.
A Human Renin R Polyclonal Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+prorenin/Human+Renin+Antibody/pm21412241-33-11-22
Average 91 stars, based on 1 article reviews
a human renin r polyclonal antibody - by Bioz Stars, 2026-11
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atp6ap2 primary antibody  (R&D Systems)
91
R&D Systems atp6ap2 primary antibody
<t>ATP6AP2</t> siRNA transfection in HTR-8/SVneo cells. HTR-8/SVneo cells were treated with 5 nM ATP6AP2 siRNA and cultured for 48 h. ATP6AP2 siRNA successfully decreased both (A) ATP6AP2 mRNA expression; and (B) (P)RR protein levels compared with negative control siRNA treated cells. (C) ATP6AP2 siRNA significantly decreased proliferation, migration, and invasion of HTR-8/SVneo cells when compared with the negative control siRNA. ***: p < 0.0005, ****: p < 0.0001 indicate significant differences between ATP6AP2 and negative control siRNA treatment groups. β-actin (ACTB) was used as a loading control in the representative immunoblot. Data were analysed by Mann-Whitney test and are presented mean +/- SEM. N = 3 experiments conducted in technical triplicates.
Atp6ap2 Primary Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+prorenin/Human%2FMouse+Renin+R+Antibody/pmc10427116-149-6-11
Average 91 stars, based on 1 article reviews
atp6ap2 primary antibody - by Bioz Stars, 2026-11
91/100 stars
  Buy from Supplier

Image Search Results


LX‐2 derived EV contain renin activity that stimulates delayed platelet activation. (A) The aspartyl protease inhibitor pepstatin suppresses LX2 induced platelet activation. LX‐2 cell EV were preincubated with pepstatin (10 μg/mL, 10 min), or not, prior to assessing platelet activation induced by LX‐2 EV. HBSS buffer the EV were resuspended in was the negative control. *** p < 0.001 unpaired T test, N = 5 biologic replicates. (B) Renin enzymatic activity underlies platelet stimulation by LX‐2 EV. Freshly isolated human platelets were incubated (10 min, 1000 rpm) in aggregometer cuvettes with the stated concentrations of the DRI Aliskiren. Aggregation was then initiated by the addition of LX‐2 EV at t = 0. N = 7 biologic replicates. *** p < 0.001 by one way ANOVA. (C) The Direct Renin Inhibitor VTP23999 and Aliskiren inhibit HSC EV‐induced platelet aggregation. Platelets stirring in aggregometer cuvettes were pretreated, or not, with VTP23999 (40 μM) or Aliskiren (40 μM) prior to the addition of buffer or washed EV recovered from LX‐2 cell conditioned media. VTP23999 N = 15 biologic replicates **** p < 0.0001; Aliskiren N = 14 biologic replicates unpaired T test p < 0.0001. (D) Renin mRNA accumulates during iPSC maturation to initiate HSC. Transcript levels of the REN gene quantified by RT‐qPCR were assessed as human iPSC cells were differentiated to quiescent and then initiated HSC. mean ± SD using a two‐tailed unpaired t ‐test with Welch's corrections to calculate exact p ‐values from 4 independent replicates. (E) Renin enzymatic activity promotes platelet aggregation in response to EV from iPSC‐derived initiated HSC. Platelet aggregation induced by media conditioned by iPSC matured to initiated HSC in the presence or absence of 40 μM Aliskiren ( N = 4 biologic replicates) or VTP23999 ( N = 3 biologic replicates) ** p < 0.01 with p = 0.0012. (F) LX‐2 cell derived EV contain prorenin while platelets abundantly express the prorenin receptor (p)RR. ( left ) Western blot for renin (37.5 kDa) and prorenin (~42–45 kDa) in EV isolated by ultracentrifugation from LX‐2 cell conditioned media, and ( right ) prorenin receptor (apparent ~42 kDa mobility) expressed by LX‐2 cells or washed human platelets. (G) The combination of platelets incubated with LX‐2 EV develops renin enzymatic activity. Renin enzymatic activity was assayed using a fluorogenic TF3/TQ3‐labeled peptide substrate (Abcam) to assess fluorescent resonant energy transfer over time as platelets were incubated with or without purified LX‐2 EV. N = 5 assay replicates. Unpaired T test p = 0.0172. (H) Renin knockdown in LX‐2 cells reduces EV‐associated renin and suppresses LX‐2 EV‐induced platelet aggregation. LX‐2 cells were incubated overnight with REN siRNA or a universal scrambled control siRNAs, the transfection media was removed and the cells were incubated with complete MEM overnight, this was removed and discarded and the cells incubated overnight for a second time before this conditioned media was collected, cleared by centrifugation, and concentrated by Centricon filtration. EV from knockdown or scrambled control cells were added to stirring platelets at t = 0 with aggregation assessed by clearing as before. The amount of aggregation after 35 min of incubation was quantitated with REN siRNA EV significantly less effective than EV from scrambled control‐treated cells. N = 5 biologic replicates **** p < 0.0001.

Journal: The FASEB Journal

Article Title: Prorenin in Hepatic Stellate Cell Extracellular Vesicles Induces Platelet‐Dependent Thrombin Formation and Release of Profibrotic TGF ‐β

doi: 10.1096/fj.202501902R

Figure Lengend Snippet: LX‐2 derived EV contain renin activity that stimulates delayed platelet activation. (A) The aspartyl protease inhibitor pepstatin suppresses LX2 induced platelet activation. LX‐2 cell EV were preincubated with pepstatin (10 μg/mL, 10 min), or not, prior to assessing platelet activation induced by LX‐2 EV. HBSS buffer the EV were resuspended in was the negative control. *** p < 0.001 unpaired T test, N = 5 biologic replicates. (B) Renin enzymatic activity underlies platelet stimulation by LX‐2 EV. Freshly isolated human platelets were incubated (10 min, 1000 rpm) in aggregometer cuvettes with the stated concentrations of the DRI Aliskiren. Aggregation was then initiated by the addition of LX‐2 EV at t = 0. N = 7 biologic replicates. *** p < 0.001 by one way ANOVA. (C) The Direct Renin Inhibitor VTP23999 and Aliskiren inhibit HSC EV‐induced platelet aggregation. Platelets stirring in aggregometer cuvettes were pretreated, or not, with VTP23999 (40 μM) or Aliskiren (40 μM) prior to the addition of buffer or washed EV recovered from LX‐2 cell conditioned media. VTP23999 N = 15 biologic replicates **** p < 0.0001; Aliskiren N = 14 biologic replicates unpaired T test p < 0.0001. (D) Renin mRNA accumulates during iPSC maturation to initiate HSC. Transcript levels of the REN gene quantified by RT‐qPCR were assessed as human iPSC cells were differentiated to quiescent and then initiated HSC. mean ± SD using a two‐tailed unpaired t ‐test with Welch's corrections to calculate exact p ‐values from 4 independent replicates. (E) Renin enzymatic activity promotes platelet aggregation in response to EV from iPSC‐derived initiated HSC. Platelet aggregation induced by media conditioned by iPSC matured to initiated HSC in the presence or absence of 40 μM Aliskiren ( N = 4 biologic replicates) or VTP23999 ( N = 3 biologic replicates) ** p < 0.01 with p = 0.0012. (F) LX‐2 cell derived EV contain prorenin while platelets abundantly express the prorenin receptor (p)RR. ( left ) Western blot for renin (37.5 kDa) and prorenin (~42–45 kDa) in EV isolated by ultracentrifugation from LX‐2 cell conditioned media, and ( right ) prorenin receptor (apparent ~42 kDa mobility) expressed by LX‐2 cells or washed human platelets. (G) The combination of platelets incubated with LX‐2 EV develops renin enzymatic activity. Renin enzymatic activity was assayed using a fluorogenic TF3/TQ3‐labeled peptide substrate (Abcam) to assess fluorescent resonant energy transfer over time as platelets were incubated with or without purified LX‐2 EV. N = 5 assay replicates. Unpaired T test p = 0.0172. (H) Renin knockdown in LX‐2 cells reduces EV‐associated renin and suppresses LX‐2 EV‐induced platelet aggregation. LX‐2 cells were incubated overnight with REN siRNA or a universal scrambled control siRNAs, the transfection media was removed and the cells were incubated with complete MEM overnight, this was removed and discarded and the cells incubated overnight for a second time before this conditioned media was collected, cleared by centrifugation, and concentrated by Centricon filtration. EV from knockdown or scrambled control cells were added to stirring platelets at t = 0 with aggregation assessed by clearing as before. The amount of aggregation after 35 min of incubation was quantitated with REN siRNA EV significantly less effective than EV from scrambled control‐treated cells. N = 5 biologic replicates **** p < 0.0001.

Article Snippet: Stock solutions of Renin siRNA (ORIGENE Technologies SR 304032) and universal control siTran (2.0 siRNA) transfection reagents were made to 5 μM that was diluted 45× with the supplied transfection buffer before addition of siTran 2.0 reagent and addition to the target cells prior to incubation at 37° for 18 h. This media was replaced with serum‐free MEM and again cultured overnight before this media was replaced and the cells were again incubated overnight before this medium was collected, cleared by centrifugation at 10 000 × g for 30 min at 4°, and concentrated by filtration with a 3.0 Centricon.

Techniques: Derivative Assay, Activity Assay, Activation Assay, Protease Inhibitor, Negative Control, Isolation, Incubation, Quantitative RT-PCR, Two Tailed Test, Western Blot, Labeling, Purification, Knockdown, Control, Transfection, Centrifugation, Filtration

ATP6AP2 siRNA transfection in HTR-8/SVneo cells. HTR-8/SVneo cells were treated with 5 nM ATP6AP2 siRNA and cultured for 48 h. ATP6AP2 siRNA successfully decreased both (A) ATP6AP2 mRNA expression; and (B) (P)RR protein levels compared with negative control siRNA treated cells. (C) ATP6AP2 siRNA significantly decreased proliferation, migration, and invasion of HTR-8/SVneo cells when compared with the negative control siRNA. ***: p < 0.0005, ****: p < 0.0001 indicate significant differences between ATP6AP2 and negative control siRNA treatment groups. β-actin (ACTB) was used as a loading control in the representative immunoblot. Data were analysed by Mann-Whitney test and are presented mean +/- SEM. N = 3 experiments conducted in technical triplicates.

Journal: Frontiers in Cell and Developmental Biology

Article Title: Placental deficiency of the (pro)renin receptor ((P)RR) reduces placental development and functional capacity

doi: 10.3389/fcell.2023.1212898

Figure Lengend Snippet: ATP6AP2 siRNA transfection in HTR-8/SVneo cells. HTR-8/SVneo cells were treated with 5 nM ATP6AP2 siRNA and cultured for 48 h. ATP6AP2 siRNA successfully decreased both (A) ATP6AP2 mRNA expression; and (B) (P)RR protein levels compared with negative control siRNA treated cells. (C) ATP6AP2 siRNA significantly decreased proliferation, migration, and invasion of HTR-8/SVneo cells when compared with the negative control siRNA. ***: p < 0.0005, ****: p < 0.0001 indicate significant differences between ATP6AP2 and negative control siRNA treatment groups. β-actin (ACTB) was used as a loading control in the representative immunoblot. Data were analysed by Mann-Whitney test and are presented mean +/- SEM. N = 3 experiments conducted in technical triplicates.

Article Snippet: After which, slides were incubated with ATP6AP2 primary antibody (1 μg/mL; RnD Systems; AF5716, Minneapolis United States) in 1% BSA/PBS overnight at 4°C., before being incubated with a 1:300 dilution of anti-goat secondary antibody (HAF017, R&D systems) in 1% BSA/PBS for 1 h at RT.

Techniques: Transfection, Cell Culture, Expressing, Negative Control, Migration, Control, Western Blot, MANN-WHITNEY

The effect of lentiviral APT6AP2 transfection on mouse blastocyst outgrowth in vitro . (A) Blastocysts were outgrown for 120 h and visual assessment of GFP was undertaken. GFP expression in blastocysts confirmed that there was successful infection of the lentivirus in the control lentivirus (CV) and the ATP6AP2 siRNA lentivirus (KV) groups. (B) Blastocysts were cultured for 96 or 120 h and outgrowth area was measured in cm 2 . Blastocyst outgrowth area was significantly reduced in the KV compared to the CV group. Outgrowth area was also significantly reduced in the CV group compared to the no lentiviral group (NV). BF: Bright field, GFP: Green fluorescent protein. **: p < 0.005, denotes significant differences between treatments. Individual blastocysts within each image and their outgrowth are outlined in white. Images were acquired at 2.5x magnification. Scale bar: 1000 μm. Data were analysed by Dunnett’s multiple comparisons test and are presented as mean +/- SEM. 96 hrs N = 15–24 blastocysts, 120 hrs N = 9 blastocysts. Biological replicates (96 hrs n = 9–13, 120 hrs n = 6 mice), total number of blastocysts analysed (96 hrs n = 15–24, 120 hrs n = 9).

Journal: Frontiers in Cell and Developmental Biology

Article Title: Placental deficiency of the (pro)renin receptor ((P)RR) reduces placental development and functional capacity

doi: 10.3389/fcell.2023.1212898

Figure Lengend Snippet: The effect of lentiviral APT6AP2 transfection on mouse blastocyst outgrowth in vitro . (A) Blastocysts were outgrown for 120 h and visual assessment of GFP was undertaken. GFP expression in blastocysts confirmed that there was successful infection of the lentivirus in the control lentivirus (CV) and the ATP6AP2 siRNA lentivirus (KV) groups. (B) Blastocysts were cultured for 96 or 120 h and outgrowth area was measured in cm 2 . Blastocyst outgrowth area was significantly reduced in the KV compared to the CV group. Outgrowth area was also significantly reduced in the CV group compared to the no lentiviral group (NV). BF: Bright field, GFP: Green fluorescent protein. **: p < 0.005, denotes significant differences between treatments. Individual blastocysts within each image and their outgrowth are outlined in white. Images were acquired at 2.5x magnification. Scale bar: 1000 μm. Data were analysed by Dunnett’s multiple comparisons test and are presented as mean +/- SEM. 96 hrs N = 15–24 blastocysts, 120 hrs N = 9 blastocysts. Biological replicates (96 hrs n = 9–13, 120 hrs n = 6 mice), total number of blastocysts analysed (96 hrs n = 15–24, 120 hrs n = 9).

Article Snippet: After which, slides were incubated with ATP6AP2 primary antibody (1 μg/mL; RnD Systems; AF5716, Minneapolis United States) in 1% BSA/PBS overnight at 4°C., before being incubated with a 1:300 dilution of anti-goat secondary antibody (HAF017, R&D systems) in 1% BSA/PBS for 1 h at RT.

Techniques: Transfection, In Vitro, Expressing, Infection, Control, Cell Culture

Placental (pro)renin receptor ((P)RR/ATP6AP2) expression in a mouse model of early placental (P)RR deficiency. (A) Green fluorescent protein (GFP) immunofluorescent staining of embryonic age (EA) 10 mouse placenta where Pl: placenta and Fe: mouse fetus. EA 18 transfected mouse placentae were separated into the labyrinth and junctional zones. (B) ATP6AP2 mRNA expression and (C) (P)RR protein levels were significantly reduced in the labyrinth zone of ATP6AP2 lentivirus infected placentae (KV) when compared with the control lentivirus infected placentae (CV). A representative immunoblot of (P)RR protein levels in mouse placenta is shown, ponceau was used as a loading control. NV: No lentivirus, CV: Control lentivirus, KV: ATP6AP2 lentivirus. *: p < 0.05 **: p < 0.005, denotes significant differences between treatments. Data are presented as mean +/- SEM. NV: n = 9 litters with 1–4 fetuses and placentae per litter (21 pups). CV: n = 6 litters with 1–5 fetuses and placentae per litter (13 pups). KV: n = 6 litters with 1–2 fetuses and placentae per litter (8 pups). Scale bar (white line) = 200 μm.

Journal: Frontiers in Cell and Developmental Biology

Article Title: Placental deficiency of the (pro)renin receptor ((P)RR) reduces placental development and functional capacity

doi: 10.3389/fcell.2023.1212898

Figure Lengend Snippet: Placental (pro)renin receptor ((P)RR/ATP6AP2) expression in a mouse model of early placental (P)RR deficiency. (A) Green fluorescent protein (GFP) immunofluorescent staining of embryonic age (EA) 10 mouse placenta where Pl: placenta and Fe: mouse fetus. EA 18 transfected mouse placentae were separated into the labyrinth and junctional zones. (B) ATP6AP2 mRNA expression and (C) (P)RR protein levels were significantly reduced in the labyrinth zone of ATP6AP2 lentivirus infected placentae (KV) when compared with the control lentivirus infected placentae (CV). A representative immunoblot of (P)RR protein levels in mouse placenta is shown, ponceau was used as a loading control. NV: No lentivirus, CV: Control lentivirus, KV: ATP6AP2 lentivirus. *: p < 0.05 **: p < 0.005, denotes significant differences between treatments. Data are presented as mean +/- SEM. NV: n = 9 litters with 1–4 fetuses and placentae per litter (21 pups). CV: n = 6 litters with 1–5 fetuses and placentae per litter (13 pups). KV: n = 6 litters with 1–2 fetuses and placentae per litter (8 pups). Scale bar (white line) = 200 μm.

Article Snippet: After which, slides were incubated with ATP6AP2 primary antibody (1 μg/mL; RnD Systems; AF5716, Minneapolis United States) in 1% BSA/PBS overnight at 4°C., before being incubated with a 1:300 dilution of anti-goat secondary antibody (HAF017, R&D systems) in 1% BSA/PBS for 1 h at RT.

Techniques: Expressing, Staining, Transfection, Infection, Control, Western Blot

Placental localisation of the (pro)renin receptor ((P)RR). (P)RR immunohistochemical staining of embryonic age 18 mouse placental labyrinth regions. (P)RR antibody staining (brown) in (A) no lentivirus infected placentae; (B) control lentivirus infected placentae; (C) ATP6AP2 lentiviral infected placentae; and (D), no primary antibody control. Inset top right: Whole placenta pictures with red boxes highlighting regions of interest. Scale bar: 50 μM at 25x magnification.

Journal: Frontiers in Cell and Developmental Biology

Article Title: Placental deficiency of the (pro)renin receptor ((P)RR) reduces placental development and functional capacity

doi: 10.3389/fcell.2023.1212898

Figure Lengend Snippet: Placental localisation of the (pro)renin receptor ((P)RR). (P)RR immunohistochemical staining of embryonic age 18 mouse placental labyrinth regions. (P)RR antibody staining (brown) in (A) no lentivirus infected placentae; (B) control lentivirus infected placentae; (C) ATP6AP2 lentiviral infected placentae; and (D), no primary antibody control. Inset top right: Whole placenta pictures with red boxes highlighting regions of interest. Scale bar: 50 μM at 25x magnification.

Article Snippet: After which, slides were incubated with ATP6AP2 primary antibody (1 μg/mL; RnD Systems; AF5716, Minneapolis United States) in 1% BSA/PBS overnight at 4°C., before being incubated with a 1:300 dilution of anti-goat secondary antibody (HAF017, R&D systems) in 1% BSA/PBS for 1 h at RT.

Techniques: Immunohistochemical staining, Staining, Infection, Control

Maternal weights and pregnancy success.

Journal: Frontiers in Cell and Developmental Biology

Article Title: Placental deficiency of the (pro)renin receptor ((P)RR) reduces placental development and functional capacity

doi: 10.3389/fcell.2023.1212898

Figure Lengend Snippet: Maternal weights and pregnancy success.

Article Snippet: After which, slides were incubated with ATP6AP2 primary antibody (1 μg/mL; RnD Systems; AF5716, Minneapolis United States) in 1% BSA/PBS overnight at 4°C., before being incubated with a 1:300 dilution of anti-goat secondary antibody (HAF017, R&D systems) in 1% BSA/PBS for 1 h at RT.

Techniques: Control, shRNA

Fetal/placental characteristics.

Journal: Frontiers in Cell and Developmental Biology

Article Title: Placental deficiency of the (pro)renin receptor ((P)RR) reduces placental development and functional capacity

doi: 10.3389/fcell.2023.1212898

Figure Lengend Snippet: Fetal/placental characteristics.

Article Snippet: After which, slides were incubated with ATP6AP2 primary antibody (1 μg/mL; RnD Systems; AF5716, Minneapolis United States) in 1% BSA/PBS overnight at 4°C., before being incubated with a 1:300 dilution of anti-goat secondary antibody (HAF017, R&D systems) in 1% BSA/PBS for 1 h at RT.

Techniques: Control, shRNA