inactive analogue for src inhibitor pp3 Search Results


inactive analogue pp3  (Cosmo Bio USA)
90
Cosmo Bio USA inactive analogue pp3
Inactive Analogue Pp3, supplied by Cosmo Bio USA, 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/inactive+analogue+for+src+inhibitor+pp3/inactive+analogue+pp3/pm40533081-127-10-20
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inactive analogue pp3 - by Bioz Stars, 2026-09
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pp3  (Santa Cruz Biotechnology)
90
Santa Cruz Biotechnology pp3
The Tyr-kinase Fyn is the link between PrP C and SOCE. (A) PrP C reduces the level of active Fyn, as evident from both the representative WB (upper panel) of PrP-Tg and PrP-KO CGN probed with an antibody to p-SFK or total Fyn (both run in duplicate), under SOCE-activating conditions (Ca 2+ -depleted stores), and the corresponding densitometric analysis of p-SFK immunosignals normalized to that of total Fyn (lower panel). Contrary to other neuronal SFK members (Supplementary Figure 4), the identical apparent mass of p-SFK and Fyn indicates that the Fyn band corresponds to the p-SFK band. Similar results were obtained under basal conditions, i.e., with Ca 2+ -filled stores (see Supplementary Figure 3). (B,C) Addition (+) of the SFK inhibitors saracatinib (sara, 5 μM) and PP2 (10 μM), but not of <t>PP3</t> (10 μM), reduces the level of both p-SFK (B) and total Tyr-phosphorylated (p-Tyr) proteins (C) of CGN compared to the untreated (−) samples. (B) The upper panel reports a representative WB of the two neuronal genotypes treated with, or without, the SFK inhibitors, and immunostained as in (A) , while the lower panel shows the corresponding densitometric analysis of p-SFK normalized to the band intensity of total Fyn. Veh (vehicle) indicates the control experiment run in the presence of DMSO (0.1%). (C) The upper panel reports the WB of total p-Tyr proteins present in the two CGN genotypes treated as in (B) . In the corresponding densitometric analysis (lowest panel), the p-Tyr band intensity was normalized to that of the Coomassie blue-stained bands (middle panel). (D) Only saracatinib and PP2 decrease SOCE-induced [Ca 2+ ] pm peaks, and abrogate the difference observed in control (veh-treated) PrP-Tg and PrP-KO CGN. (E) STIM1 is more abundantly Tyr-phosphorylated in PrP-KO CGN than in PrP-Tg CGN under SOCE-stimulating conditions. This is evident from the representative WB (left panel) of immunoprecipitated (IP) STIM1 probed with an antibody to either p-Tyr or total STIM1 (arrow), and from the corresponding densitometric analysis (right panel) reported as the ratio between the p-Tyr band intensity and the STIM1 band intensity. The arrowhead in the left panels indicates the immunosignal of the mouse IgG used in the immunoprecipitation assay. On the left of the WB, MW standards are indicated. * p < 0.05, ** p < 0.01, *** p < 0.001, Student’s t -test. The analysis of the statistical significance ( p -value, Student’s t -test) of data for the comparison between different treatments within each PrP genotype (B–D) is reported in Supplementary Table 2. Other details are as in the legend to Figure .
Pp3, supplied by Santa Cruz Biotechnology, 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/inactive+analogue+for+src+inhibitor+pp3/PP+3/pmc04623396-60-21-24
Average 90 stars, based on 1 article reviews
pp3 - by Bioz Stars, 2026-09
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multidentate phosphine ligand tris(2(diphenylphosphino)ethyl)-phosphine  (Verlag GmbH)
90
Verlag GmbH multidentate phosphine ligand tris(2(diphenylphosphino)ethyl)-phosphine
The Tyr-kinase Fyn is the link between PrP C and SOCE. (A) PrP C reduces the level of active Fyn, as evident from both the representative WB (upper panel) of PrP-Tg and PrP-KO CGN probed with an antibody to p-SFK or total Fyn (both run in duplicate), under SOCE-activating conditions (Ca 2+ -depleted stores), and the corresponding densitometric analysis of p-SFK immunosignals normalized to that of total Fyn (lower panel). Contrary to other neuronal SFK members (Supplementary Figure 4), the identical apparent mass of p-SFK and Fyn indicates that the Fyn band corresponds to the p-SFK band. Similar results were obtained under basal conditions, i.e., with Ca 2+ -filled stores (see Supplementary Figure 3). (B,C) Addition (+) of the SFK inhibitors saracatinib (sara, 5 μM) and PP2 (10 μM), but not of <t>PP3</t> (10 μM), reduces the level of both p-SFK (B) and total Tyr-phosphorylated (p-Tyr) proteins (C) of CGN compared to the untreated (−) samples. (B) The upper panel reports a representative WB of the two neuronal genotypes treated with, or without, the SFK inhibitors, and immunostained as in (A) , while the lower panel shows the corresponding densitometric analysis of p-SFK normalized to the band intensity of total Fyn. Veh (vehicle) indicates the control experiment run in the presence of DMSO (0.1%). (C) The upper panel reports the WB of total p-Tyr proteins present in the two CGN genotypes treated as in (B) . In the corresponding densitometric analysis (lowest panel), the p-Tyr band intensity was normalized to that of the Coomassie blue-stained bands (middle panel). (D) Only saracatinib and PP2 decrease SOCE-induced [Ca 2+ ] pm peaks, and abrogate the difference observed in control (veh-treated) PrP-Tg and PrP-KO CGN. (E) STIM1 is more abundantly Tyr-phosphorylated in PrP-KO CGN than in PrP-Tg CGN under SOCE-stimulating conditions. This is evident from the representative WB (left panel) of immunoprecipitated (IP) STIM1 probed with an antibody to either p-Tyr or total STIM1 (arrow), and from the corresponding densitometric analysis (right panel) reported as the ratio between the p-Tyr band intensity and the STIM1 band intensity. The arrowhead in the left panels indicates the immunosignal of the mouse IgG used in the immunoprecipitation assay. On the left of the WB, MW standards are indicated. * p < 0.05, ** p < 0.01, *** p < 0.001, Student’s t -test. The analysis of the statistical significance ( p -value, Student’s t -test) of data for the comparison between different treatments within each PrP genotype (B–D) is reported in Supplementary Table 2. Other details are as in the legend to Figure .
Multidentate Phosphine Ligand Tris(2(diphenylphosphino)ethyl) Phosphine, supplied by Verlag GmbH, 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/inactive+analogue+for+src+inhibitor+pp3/tris+2+carboxyethyl+phosphine++tcep+/10__1002_slash_ppsc__201900043-277-13-3
Average 90 stars, based on 1 article reviews
multidentate phosphine ligand tris(2(diphenylphosphino)ethyl)-phosphine - by Bioz Stars, 2026-09
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pp2 and pp3  (Biomol GmbH)
90
Biomol GmbH pp2 and pp3
The Tyr-kinase Fyn is the link between PrP C and SOCE. (A) PrP C reduces the level of active Fyn, as evident from both the representative WB (upper panel) of PrP-Tg and PrP-KO CGN probed with an antibody to p-SFK or total Fyn (both run in duplicate), under SOCE-activating conditions (Ca 2+ -depleted stores), and the corresponding densitometric analysis of p-SFK immunosignals normalized to that of total Fyn (lower panel). Contrary to other neuronal SFK members (Supplementary Figure 4), the identical apparent mass of p-SFK and Fyn indicates that the Fyn band corresponds to the p-SFK band. Similar results were obtained under basal conditions, i.e., with Ca 2+ -filled stores (see Supplementary Figure 3). (B,C) Addition (+) of the SFK inhibitors saracatinib (sara, 5 μM) and PP2 (10 μM), but not of <t>PP3</t> (10 μM), reduces the level of both p-SFK (B) and total Tyr-phosphorylated (p-Tyr) proteins (C) of CGN compared to the untreated (−) samples. (B) The upper panel reports a representative WB of the two neuronal genotypes treated with, or without, the SFK inhibitors, and immunostained as in (A) , while the lower panel shows the corresponding densitometric analysis of p-SFK normalized to the band intensity of total Fyn. Veh (vehicle) indicates the control experiment run in the presence of DMSO (0.1%). (C) The upper panel reports the WB of total p-Tyr proteins present in the two CGN genotypes treated as in (B) . In the corresponding densitometric analysis (lowest panel), the p-Tyr band intensity was normalized to that of the Coomassie blue-stained bands (middle panel). (D) Only saracatinib and PP2 decrease SOCE-induced [Ca 2+ ] pm peaks, and abrogate the difference observed in control (veh-treated) PrP-Tg and PrP-KO CGN. (E) STIM1 is more abundantly Tyr-phosphorylated in PrP-KO CGN than in PrP-Tg CGN under SOCE-stimulating conditions. This is evident from the representative WB (left panel) of immunoprecipitated (IP) STIM1 probed with an antibody to either p-Tyr or total STIM1 (arrow), and from the corresponding densitometric analysis (right panel) reported as the ratio between the p-Tyr band intensity and the STIM1 band intensity. The arrowhead in the left panels indicates the immunosignal of the mouse IgG used in the immunoprecipitation assay. On the left of the WB, MW standards are indicated. * p < 0.05, ** p < 0.01, *** p < 0.001, Student’s t -test. The analysis of the statistical significance ( p -value, Student’s t -test) of data for the comparison between different treatments within each PrP genotype (B–D) is reported in Supplementary Table 2. Other details are as in the legend to Figure .
Pp2 And Pp3, supplied by Biomol GmbH, 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/inactive+analogue+for+src+inhibitor+pp3/pp2/pmc03037367-143-2-6
Average 90 stars, based on 1 article reviews
pp2 and pp3 - by Bioz Stars, 2026-09
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pp3  (Biomol GmbH)
90
Biomol GmbH pp3
The Tyr-kinase Fyn is the link between PrP C and SOCE. (A) PrP C reduces the level of active Fyn, as evident from both the representative WB (upper panel) of PrP-Tg and PrP-KO CGN probed with an antibody to p-SFK or total Fyn (both run in duplicate), under SOCE-activating conditions (Ca 2+ -depleted stores), and the corresponding densitometric analysis of p-SFK immunosignals normalized to that of total Fyn (lower panel). Contrary to other neuronal SFK members (Supplementary Figure 4), the identical apparent mass of p-SFK and Fyn indicates that the Fyn band corresponds to the p-SFK band. Similar results were obtained under basal conditions, i.e., with Ca 2+ -filled stores (see Supplementary Figure 3). (B,C) Addition (+) of the SFK inhibitors saracatinib (sara, 5 μM) and PP2 (10 μM), but not of <t>PP3</t> (10 μM), reduces the level of both p-SFK (B) and total Tyr-phosphorylated (p-Tyr) proteins (C) of CGN compared to the untreated (−) samples. (B) The upper panel reports a representative WB of the two neuronal genotypes treated with, or without, the SFK inhibitors, and immunostained as in (A) , while the lower panel shows the corresponding densitometric analysis of p-SFK normalized to the band intensity of total Fyn. Veh (vehicle) indicates the control experiment run in the presence of DMSO (0.1%). (C) The upper panel reports the WB of total p-Tyr proteins present in the two CGN genotypes treated as in (B) . In the corresponding densitometric analysis (lowest panel), the p-Tyr band intensity was normalized to that of the Coomassie blue-stained bands (middle panel). (D) Only saracatinib and PP2 decrease SOCE-induced [Ca 2+ ] pm peaks, and abrogate the difference observed in control (veh-treated) PrP-Tg and PrP-KO CGN. (E) STIM1 is more abundantly Tyr-phosphorylated in PrP-KO CGN than in PrP-Tg CGN under SOCE-stimulating conditions. This is evident from the representative WB (left panel) of immunoprecipitated (IP) STIM1 probed with an antibody to either p-Tyr or total STIM1 (arrow), and from the corresponding densitometric analysis (right panel) reported as the ratio between the p-Tyr band intensity and the STIM1 band intensity. The arrowhead in the left panels indicates the immunosignal of the mouse IgG used in the immunoprecipitation assay. On the left of the WB, MW standards are indicated. * p < 0.05, ** p < 0.01, *** p < 0.001, Student’s t -test. The analysis of the statistical significance ( p -value, Student’s t -test) of data for the comparison between different treatments within each PrP genotype (B–D) is reported in Supplementary Table 2. Other details are as in the legend to Figure .
Pp3, supplied by Biomol GmbH, 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/inactive+analogue+for+src+inhibitor+pp3/pp3/10__1074_slash_jbc__m114__629527-70-2-8
Average 90 stars, based on 1 article reviews
pp3 - by Bioz Stars, 2026-09
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pp3 difco  (Difco)
86
Difco pp3 difco
The Tyr-kinase Fyn is the link between PrP C and SOCE. (A) PrP C reduces the level of active Fyn, as evident from both the representative WB (upper panel) of PrP-Tg and PrP-KO CGN probed with an antibody to p-SFK or total Fyn (both run in duplicate), under SOCE-activating conditions (Ca 2+ -depleted stores), and the corresponding densitometric analysis of p-SFK immunosignals normalized to that of total Fyn (lower panel). Contrary to other neuronal SFK members (Supplementary Figure 4), the identical apparent mass of p-SFK and Fyn indicates that the Fyn band corresponds to the p-SFK band. Similar results were obtained under basal conditions, i.e., with Ca 2+ -filled stores (see Supplementary Figure 3). (B,C) Addition (+) of the SFK inhibitors saracatinib (sara, 5 μM) and PP2 (10 μM), but not of <t>PP3</t> (10 μM), reduces the level of both p-SFK (B) and total Tyr-phosphorylated (p-Tyr) proteins (C) of CGN compared to the untreated (−) samples. (B) The upper panel reports a representative WB of the two neuronal genotypes treated with, or without, the SFK inhibitors, and immunostained as in (A) , while the lower panel shows the corresponding densitometric analysis of p-SFK normalized to the band intensity of total Fyn. Veh (vehicle) indicates the control experiment run in the presence of DMSO (0.1%). (C) The upper panel reports the WB of total p-Tyr proteins present in the two CGN genotypes treated as in (B) . In the corresponding densitometric analysis (lowest panel), the p-Tyr band intensity was normalized to that of the Coomassie blue-stained bands (middle panel). (D) Only saracatinib and PP2 decrease SOCE-induced [Ca 2+ ] pm peaks, and abrogate the difference observed in control (veh-treated) PrP-Tg and PrP-KO CGN. (E) STIM1 is more abundantly Tyr-phosphorylated in PrP-KO CGN than in PrP-Tg CGN under SOCE-stimulating conditions. This is evident from the representative WB (left panel) of immunoprecipitated (IP) STIM1 probed with an antibody to either p-Tyr or total STIM1 (arrow), and from the corresponding densitometric analysis (right panel) reported as the ratio between the p-Tyr band intensity and the STIM1 band intensity. The arrowhead in the left panels indicates the immunosignal of the mouse IgG used in the immunoprecipitation assay. On the left of the WB, MW standards are indicated. * p < 0.05, ** p < 0.01, *** p < 0.001, Student’s t -test. The analysis of the statistical significance ( p -value, Student’s t -test) of data for the comparison between different treatments within each PrP genotype (B–D) is reported in Supplementary Table 2. Other details are as in the legend to Figure .
Pp3 Difco, supplied by Difco, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/inactive+analogue+for+src+inhibitor+pp3/difco+pp3/10__1074_slash_jbc__274__14__9836-46-26-27
Average 86 stars, based on 1 article reviews
pp3 difco - by Bioz Stars, 2026-09
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pp3 (10 m; a.g. scientific, inc)  (AG Scientific)
90
AG Scientific pp3 (10 m; a.g. scientific, inc)
The Tyr-kinase Fyn is the link between PrP C and SOCE. (A) PrP C reduces the level of active Fyn, as evident from both the representative WB (upper panel) of PrP-Tg and PrP-KO CGN probed with an antibody to p-SFK or total Fyn (both run in duplicate), under SOCE-activating conditions (Ca 2+ -depleted stores), and the corresponding densitometric analysis of p-SFK immunosignals normalized to that of total Fyn (lower panel). Contrary to other neuronal SFK members (Supplementary Figure 4), the identical apparent mass of p-SFK and Fyn indicates that the Fyn band corresponds to the p-SFK band. Similar results were obtained under basal conditions, i.e., with Ca 2+ -filled stores (see Supplementary Figure 3). (B,C) Addition (+) of the SFK inhibitors saracatinib (sara, 5 μM) and PP2 (10 μM), but not of <t>PP3</t> (10 μM), reduces the level of both p-SFK (B) and total Tyr-phosphorylated (p-Tyr) proteins (C) of CGN compared to the untreated (−) samples. (B) The upper panel reports a representative WB of the two neuronal genotypes treated with, or without, the SFK inhibitors, and immunostained as in (A) , while the lower panel shows the corresponding densitometric analysis of p-SFK normalized to the band intensity of total Fyn. Veh (vehicle) indicates the control experiment run in the presence of DMSO (0.1%). (C) The upper panel reports the WB of total p-Tyr proteins present in the two CGN genotypes treated as in (B) . In the corresponding densitometric analysis (lowest panel), the p-Tyr band intensity was normalized to that of the Coomassie blue-stained bands (middle panel). (D) Only saracatinib and PP2 decrease SOCE-induced [Ca 2+ ] pm peaks, and abrogate the difference observed in control (veh-treated) PrP-Tg and PrP-KO CGN. (E) STIM1 is more abundantly Tyr-phosphorylated in PrP-KO CGN than in PrP-Tg CGN under SOCE-stimulating conditions. This is evident from the representative WB (left panel) of immunoprecipitated (IP) STIM1 probed with an antibody to either p-Tyr or total STIM1 (arrow), and from the corresponding densitometric analysis (right panel) reported as the ratio between the p-Tyr band intensity and the STIM1 band intensity. The arrowhead in the left panels indicates the immunosignal of the mouse IgG used in the immunoprecipitation assay. On the left of the WB, MW standards are indicated. * p < 0.05, ** p < 0.01, *** p < 0.001, Student’s t -test. The analysis of the statistical significance ( p -value, Student’s t -test) of data for the comparison between different treatments within each PrP genotype (B–D) is reported in Supplementary Table 2. Other details are as in the legend to Figure .
Pp3 (10 M; A.G. Scientific, Inc), supplied by AG Scientific, 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/inactive+analogue+for+src+inhibitor+pp3/pp3/10__1074_slash_jbc__m708300200-40-48-51
Average 90 stars, based on 1 article reviews
pp3 (10 m; a.g. scientific, inc) - by Bioz Stars, 2026-09
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peptides pp1, pp2, pp3, pp4 and 23  (GenScript corporation)
90
GenScript corporation peptides pp1, pp2, pp3, pp4 and 23
The Tyr-kinase Fyn is the link between PrP C and SOCE. (A) PrP C reduces the level of active Fyn, as evident from both the representative WB (upper panel) of PrP-Tg and PrP-KO CGN probed with an antibody to p-SFK or total Fyn (both run in duplicate), under SOCE-activating conditions (Ca 2+ -depleted stores), and the corresponding densitometric analysis of p-SFK immunosignals normalized to that of total Fyn (lower panel). Contrary to other neuronal SFK members (Supplementary Figure 4), the identical apparent mass of p-SFK and Fyn indicates that the Fyn band corresponds to the p-SFK band. Similar results were obtained under basal conditions, i.e., with Ca 2+ -filled stores (see Supplementary Figure 3). (B,C) Addition (+) of the SFK inhibitors saracatinib (sara, 5 μM) and PP2 (10 μM), but not of <t>PP3</t> (10 μM), reduces the level of both p-SFK (B) and total Tyr-phosphorylated (p-Tyr) proteins (C) of CGN compared to the untreated (−) samples. (B) The upper panel reports a representative WB of the two neuronal genotypes treated with, or without, the SFK inhibitors, and immunostained as in (A) , while the lower panel shows the corresponding densitometric analysis of p-SFK normalized to the band intensity of total Fyn. Veh (vehicle) indicates the control experiment run in the presence of DMSO (0.1%). (C) The upper panel reports the WB of total p-Tyr proteins present in the two CGN genotypes treated as in (B) . In the corresponding densitometric analysis (lowest panel), the p-Tyr band intensity was normalized to that of the Coomassie blue-stained bands (middle panel). (D) Only saracatinib and PP2 decrease SOCE-induced [Ca 2+ ] pm peaks, and abrogate the difference observed in control (veh-treated) PrP-Tg and PrP-KO CGN. (E) STIM1 is more abundantly Tyr-phosphorylated in PrP-KO CGN than in PrP-Tg CGN under SOCE-stimulating conditions. This is evident from the representative WB (left panel) of immunoprecipitated (IP) STIM1 probed with an antibody to either p-Tyr or total STIM1 (arrow), and from the corresponding densitometric analysis (right panel) reported as the ratio between the p-Tyr band intensity and the STIM1 band intensity. The arrowhead in the left panels indicates the immunosignal of the mouse IgG used in the immunoprecipitation assay. On the left of the WB, MW standards are indicated. * p < 0.05, ** p < 0.01, *** p < 0.001, Student’s t -test. The analysis of the statistical significance ( p -value, Student’s t -test) of data for the comparison between different treatments within each PrP genotype (B–D) is reported in Supplementary Table 2. Other details are as in the legend to Figure .
Peptides Pp1, Pp2, Pp3, Pp4 And 23, supplied by GenScript corporation, 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/inactive+analogue+for+src+inhibitor+pp3/peptides+pp1++pp2++pp3++pp4+and+23/pmc04168794__cb500374f_si_001-40-3-10
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peptides pp1, pp2, pp3, pp4 and 23 - by Bioz Stars, 2026-09
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pp3  (Merck KGaA)
90
Merck KGaA pp3
The Tyr-kinase Fyn is the link between PrP C and SOCE. (A) PrP C reduces the level of active Fyn, as evident from both the representative WB (upper panel) of PrP-Tg and PrP-KO CGN probed with an antibody to p-SFK or total Fyn (both run in duplicate), under SOCE-activating conditions (Ca 2+ -depleted stores), and the corresponding densitometric analysis of p-SFK immunosignals normalized to that of total Fyn (lower panel). Contrary to other neuronal SFK members (Supplementary Figure 4), the identical apparent mass of p-SFK and Fyn indicates that the Fyn band corresponds to the p-SFK band. Similar results were obtained under basal conditions, i.e., with Ca 2+ -filled stores (see Supplementary Figure 3). (B,C) Addition (+) of the SFK inhibitors saracatinib (sara, 5 μM) and PP2 (10 μM), but not of <t>PP3</t> (10 μM), reduces the level of both p-SFK (B) and total Tyr-phosphorylated (p-Tyr) proteins (C) of CGN compared to the untreated (−) samples. (B) The upper panel reports a representative WB of the two neuronal genotypes treated with, or without, the SFK inhibitors, and immunostained as in (A) , while the lower panel shows the corresponding densitometric analysis of p-SFK normalized to the band intensity of total Fyn. Veh (vehicle) indicates the control experiment run in the presence of DMSO (0.1%). (C) The upper panel reports the WB of total p-Tyr proteins present in the two CGN genotypes treated as in (B) . In the corresponding densitometric analysis (lowest panel), the p-Tyr band intensity was normalized to that of the Coomassie blue-stained bands (middle panel). (D) Only saracatinib and PP2 decrease SOCE-induced [Ca 2+ ] pm peaks, and abrogate the difference observed in control (veh-treated) PrP-Tg and PrP-KO CGN. (E) STIM1 is more abundantly Tyr-phosphorylated in PrP-KO CGN than in PrP-Tg CGN under SOCE-stimulating conditions. This is evident from the representative WB (left panel) of immunoprecipitated (IP) STIM1 probed with an antibody to either p-Tyr or total STIM1 (arrow), and from the corresponding densitometric analysis (right panel) reported as the ratio between the p-Tyr band intensity and the STIM1 band intensity. The arrowhead in the left panels indicates the immunosignal of the mouse IgG used in the immunoprecipitation assay. On the left of the WB, MW standards are indicated. * p < 0.05, ** p < 0.01, *** p < 0.001, Student’s t -test. The analysis of the statistical significance ( p -value, Student’s t -test) of data for the comparison between different treatments within each PrP genotype (B–D) is reported in Supplementary Table 2. Other details are as in the legend to Figure .
Pp3, supplied by Merck KGaA, 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/inactive+analogue+for+src+inhibitor+pp3/pp3/pm33883672-231-3-8
Average 90 stars, based on 1 article reviews
pp3 - by Bioz Stars, 2026-09
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pp3  (ClinGen Resource)
90
ClinGen Resource pp3
The Tyr-kinase Fyn is the link between PrP C and SOCE. (A) PrP C reduces the level of active Fyn, as evident from both the representative WB (upper panel) of PrP-Tg and PrP-KO CGN probed with an antibody to p-SFK or total Fyn (both run in duplicate), under SOCE-activating conditions (Ca 2+ -depleted stores), and the corresponding densitometric analysis of p-SFK immunosignals normalized to that of total Fyn (lower panel). Contrary to other neuronal SFK members (Supplementary Figure 4), the identical apparent mass of p-SFK and Fyn indicates that the Fyn band corresponds to the p-SFK band. Similar results were obtained under basal conditions, i.e., with Ca 2+ -filled stores (see Supplementary Figure 3). (B,C) Addition (+) of the SFK inhibitors saracatinib (sara, 5 μM) and PP2 (10 μM), but not of <t>PP3</t> (10 μM), reduces the level of both p-SFK (B) and total Tyr-phosphorylated (p-Tyr) proteins (C) of CGN compared to the untreated (−) samples. (B) The upper panel reports a representative WB of the two neuronal genotypes treated with, or without, the SFK inhibitors, and immunostained as in (A) , while the lower panel shows the corresponding densitometric analysis of p-SFK normalized to the band intensity of total Fyn. Veh (vehicle) indicates the control experiment run in the presence of DMSO (0.1%). (C) The upper panel reports the WB of total p-Tyr proteins present in the two CGN genotypes treated as in (B) . In the corresponding densitometric analysis (lowest panel), the p-Tyr band intensity was normalized to that of the Coomassie blue-stained bands (middle panel). (D) Only saracatinib and PP2 decrease SOCE-induced [Ca 2+ ] pm peaks, and abrogate the difference observed in control (veh-treated) PrP-Tg and PrP-KO CGN. (E) STIM1 is more abundantly Tyr-phosphorylated in PrP-KO CGN than in PrP-Tg CGN under SOCE-stimulating conditions. This is evident from the representative WB (left panel) of immunoprecipitated (IP) STIM1 probed with an antibody to either p-Tyr or total STIM1 (arrow), and from the corresponding densitometric analysis (right panel) reported as the ratio between the p-Tyr band intensity and the STIM1 band intensity. The arrowhead in the left panels indicates the immunosignal of the mouse IgG used in the immunoprecipitation assay. On the left of the WB, MW standards are indicated. * p < 0.05, ** p < 0.01, *** p < 0.001, Student’s t -test. The analysis of the statistical significance ( p -value, Student’s t -test) of data for the comparison between different treatments within each PrP genotype (B–D) is reported in Supplementary Table 2. Other details are as in the legend to Figure .
Pp3, supplied by ClinGen Resource, 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/inactive+analogue+for+src+inhibitor+pp3/pp3/ppr0247163-354-0-14
Average 90 stars, based on 1 article reviews
pp3 - by Bioz Stars, 2026-09
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pp3 protein  (Johns Hopkins HealthCare)
90
Johns Hopkins HealthCare pp3 protein
The Tyr-kinase Fyn is the link between PrP C and SOCE. (A) PrP C reduces the level of active Fyn, as evident from both the representative WB (upper panel) of PrP-Tg and PrP-KO CGN probed with an antibody to p-SFK or total Fyn (both run in duplicate), under SOCE-activating conditions (Ca 2+ -depleted stores), and the corresponding densitometric analysis of p-SFK immunosignals normalized to that of total Fyn (lower panel). Contrary to other neuronal SFK members (Supplementary Figure 4), the identical apparent mass of p-SFK and Fyn indicates that the Fyn band corresponds to the p-SFK band. Similar results were obtained under basal conditions, i.e., with Ca 2+ -filled stores (see Supplementary Figure 3). (B,C) Addition (+) of the SFK inhibitors saracatinib (sara, 5 μM) and PP2 (10 μM), but not of <t>PP3</t> (10 μM), reduces the level of both p-SFK (B) and total Tyr-phosphorylated (p-Tyr) proteins (C) of CGN compared to the untreated (−) samples. (B) The upper panel reports a representative WB of the two neuronal genotypes treated with, or without, the SFK inhibitors, and immunostained as in (A) , while the lower panel shows the corresponding densitometric analysis of p-SFK normalized to the band intensity of total Fyn. Veh (vehicle) indicates the control experiment run in the presence of DMSO (0.1%). (C) The upper panel reports the WB of total p-Tyr proteins present in the two CGN genotypes treated as in (B) . In the corresponding densitometric analysis (lowest panel), the p-Tyr band intensity was normalized to that of the Coomassie blue-stained bands (middle panel). (D) Only saracatinib and PP2 decrease SOCE-induced [Ca 2+ ] pm peaks, and abrogate the difference observed in control (veh-treated) PrP-Tg and PrP-KO CGN. (E) STIM1 is more abundantly Tyr-phosphorylated in PrP-KO CGN than in PrP-Tg CGN under SOCE-stimulating conditions. This is evident from the representative WB (left panel) of immunoprecipitated (IP) STIM1 probed with an antibody to either p-Tyr or total STIM1 (arrow), and from the corresponding densitometric analysis (right panel) reported as the ratio between the p-Tyr band intensity and the STIM1 band intensity. The arrowhead in the left panels indicates the immunosignal of the mouse IgG used in the immunoprecipitation assay. On the left of the WB, MW standards are indicated. * p < 0.05, ** p < 0.01, *** p < 0.001, Student’s t -test. The analysis of the statistical significance ( p -value, Student’s t -test) of data for the comparison between different treatments within each PrP genotype (B–D) is reported in Supplementary Table 2. Other details are as in the legend to Figure .
Pp3 Protein, supplied by Johns Hopkins HealthCare, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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pp3 1- phenyl- 1h- pyrazolo[3,4- d]pyrimidin- 4- amine  (Merck KGaA)
90
Merck KGaA pp3 1- phenyl- 1h- pyrazolo[3,4- d]pyrimidin- 4- amine
The Tyr-kinase Fyn is the link between PrP C and SOCE. (A) PrP C reduces the level of active Fyn, as evident from both the representative WB (upper panel) of PrP-Tg and PrP-KO CGN probed with an antibody to p-SFK or total Fyn (both run in duplicate), under SOCE-activating conditions (Ca 2+ -depleted stores), and the corresponding densitometric analysis of p-SFK immunosignals normalized to that of total Fyn (lower panel). Contrary to other neuronal SFK members (Supplementary Figure 4), the identical apparent mass of p-SFK and Fyn indicates that the Fyn band corresponds to the p-SFK band. Similar results were obtained under basal conditions, i.e., with Ca 2+ -filled stores (see Supplementary Figure 3). (B,C) Addition (+) of the SFK inhibitors saracatinib (sara, 5 μM) and PP2 (10 μM), but not of <t>PP3</t> (10 μM), reduces the level of both p-SFK (B) and total Tyr-phosphorylated (p-Tyr) proteins (C) of CGN compared to the untreated (−) samples. (B) The upper panel reports a representative WB of the two neuronal genotypes treated with, or without, the SFK inhibitors, and immunostained as in (A) , while the lower panel shows the corresponding densitometric analysis of p-SFK normalized to the band intensity of total Fyn. Veh (vehicle) indicates the control experiment run in the presence of DMSO (0.1%). (C) The upper panel reports the WB of total p-Tyr proteins present in the two CGN genotypes treated as in (B) . In the corresponding densitometric analysis (lowest panel), the p-Tyr band intensity was normalized to that of the Coomassie blue-stained bands (middle panel). (D) Only saracatinib and PP2 decrease SOCE-induced [Ca 2+ ] pm peaks, and abrogate the difference observed in control (veh-treated) PrP-Tg and PrP-KO CGN. (E) STIM1 is more abundantly Tyr-phosphorylated in PrP-KO CGN than in PrP-Tg CGN under SOCE-stimulating conditions. This is evident from the representative WB (left panel) of immunoprecipitated (IP) STIM1 probed with an antibody to either p-Tyr or total STIM1 (arrow), and from the corresponding densitometric analysis (right panel) reported as the ratio between the p-Tyr band intensity and the STIM1 band intensity. The arrowhead in the left panels indicates the immunosignal of the mouse IgG used in the immunoprecipitation assay. On the left of the WB, MW standards are indicated. * p < 0.05, ** p < 0.01, *** p < 0.001, Student’s t -test. The analysis of the statistical significance ( p -value, Student’s t -test) of data for the comparison between different treatments within each PrP genotype (B–D) is reported in Supplementary Table 2. Other details are as in the legend to Figure .
Pp3 1 Phenyl 1h Pyrazolo[3,4 D]Pyrimidin 4 Amine, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


The Tyr-kinase Fyn is the link between PrP C and SOCE. (A) PrP C reduces the level of active Fyn, as evident from both the representative WB (upper panel) of PrP-Tg and PrP-KO CGN probed with an antibody to p-SFK or total Fyn (both run in duplicate), under SOCE-activating conditions (Ca 2+ -depleted stores), and the corresponding densitometric analysis of p-SFK immunosignals normalized to that of total Fyn (lower panel). Contrary to other neuronal SFK members (Supplementary Figure 4), the identical apparent mass of p-SFK and Fyn indicates that the Fyn band corresponds to the p-SFK band. Similar results were obtained under basal conditions, i.e., with Ca 2+ -filled stores (see Supplementary Figure 3). (B,C) Addition (+) of the SFK inhibitors saracatinib (sara, 5 μM) and PP2 (10 μM), but not of PP3 (10 μM), reduces the level of both p-SFK (B) and total Tyr-phosphorylated (p-Tyr) proteins (C) of CGN compared to the untreated (−) samples. (B) The upper panel reports a representative WB of the two neuronal genotypes treated with, or without, the SFK inhibitors, and immunostained as in (A) , while the lower panel shows the corresponding densitometric analysis of p-SFK normalized to the band intensity of total Fyn. Veh (vehicle) indicates the control experiment run in the presence of DMSO (0.1%). (C) The upper panel reports the WB of total p-Tyr proteins present in the two CGN genotypes treated as in (B) . In the corresponding densitometric analysis (lowest panel), the p-Tyr band intensity was normalized to that of the Coomassie blue-stained bands (middle panel). (D) Only saracatinib and PP2 decrease SOCE-induced [Ca 2+ ] pm peaks, and abrogate the difference observed in control (veh-treated) PrP-Tg and PrP-KO CGN. (E) STIM1 is more abundantly Tyr-phosphorylated in PrP-KO CGN than in PrP-Tg CGN under SOCE-stimulating conditions. This is evident from the representative WB (left panel) of immunoprecipitated (IP) STIM1 probed with an antibody to either p-Tyr or total STIM1 (arrow), and from the corresponding densitometric analysis (right panel) reported as the ratio between the p-Tyr band intensity and the STIM1 band intensity. The arrowhead in the left panels indicates the immunosignal of the mouse IgG used in the immunoprecipitation assay. On the left of the WB, MW standards are indicated. * p < 0.05, ** p < 0.01, *** p < 0.001, Student’s t -test. The analysis of the statistical significance ( p -value, Student’s t -test) of data for the comparison between different treatments within each PrP genotype (B–D) is reported in Supplementary Table 2. Other details are as in the legend to Figure .

Journal: Frontiers in Cellular Neuroscience

Article Title: The prion protein constitutively controls neuronal store-operated Ca 2+ entry through Fyn kinase

doi: 10.3389/fncel.2015.00416

Figure Lengend Snippet: The Tyr-kinase Fyn is the link between PrP C and SOCE. (A) PrP C reduces the level of active Fyn, as evident from both the representative WB (upper panel) of PrP-Tg and PrP-KO CGN probed with an antibody to p-SFK or total Fyn (both run in duplicate), under SOCE-activating conditions (Ca 2+ -depleted stores), and the corresponding densitometric analysis of p-SFK immunosignals normalized to that of total Fyn (lower panel). Contrary to other neuronal SFK members (Supplementary Figure 4), the identical apparent mass of p-SFK and Fyn indicates that the Fyn band corresponds to the p-SFK band. Similar results were obtained under basal conditions, i.e., with Ca 2+ -filled stores (see Supplementary Figure 3). (B,C) Addition (+) of the SFK inhibitors saracatinib (sara, 5 μM) and PP2 (10 μM), but not of PP3 (10 μM), reduces the level of both p-SFK (B) and total Tyr-phosphorylated (p-Tyr) proteins (C) of CGN compared to the untreated (−) samples. (B) The upper panel reports a representative WB of the two neuronal genotypes treated with, or without, the SFK inhibitors, and immunostained as in (A) , while the lower panel shows the corresponding densitometric analysis of p-SFK normalized to the band intensity of total Fyn. Veh (vehicle) indicates the control experiment run in the presence of DMSO (0.1%). (C) The upper panel reports the WB of total p-Tyr proteins present in the two CGN genotypes treated as in (B) . In the corresponding densitometric analysis (lowest panel), the p-Tyr band intensity was normalized to that of the Coomassie blue-stained bands (middle panel). (D) Only saracatinib and PP2 decrease SOCE-induced [Ca 2+ ] pm peaks, and abrogate the difference observed in control (veh-treated) PrP-Tg and PrP-KO CGN. (E) STIM1 is more abundantly Tyr-phosphorylated in PrP-KO CGN than in PrP-Tg CGN under SOCE-stimulating conditions. This is evident from the representative WB (left panel) of immunoprecipitated (IP) STIM1 probed with an antibody to either p-Tyr or total STIM1 (arrow), and from the corresponding densitometric analysis (right panel) reported as the ratio between the p-Tyr band intensity and the STIM1 band intensity. The arrowhead in the left panels indicates the immunosignal of the mouse IgG used in the immunoprecipitation assay. On the left of the WB, MW standards are indicated. * p < 0.05, ** p < 0.01, *** p < 0.001, Student’s t -test. The analysis of the statistical significance ( p -value, Student’s t -test) of data for the comparison between different treatments within each PrP genotype (B–D) is reported in Supplementary Table 2. Other details are as in the legend to Figure .

Article Snippet: Instead, the SFK inhibitors [PP2 (10 μM, Tocris) and saracatinib (5 μM, Santa Cruz Biotechnology)], and the negative control of PP2, PP3 (10 μM, Santa Cruz Biotechnology), were added during the reconstitution step, and kept in the perfusion buffer throughout the entire experiment.

Techniques: Control, Staining, Immunoprecipitation, Comparison