par4 antagonist tcy nh2 Search Results


par4 agonist peptide aypgkf-nh 2  (GenScript corporation)
90
GenScript corporation par4 agonist peptide aypgkf-nh 2
RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic <t>PAR4-AP</t> (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.
Par4 Agonist Peptide Aypgkf Nh 2, 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
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par4-agonist peptide gypgqv-nh 2  (Bachem)
90
Bachem par4-agonist peptide gypgqv-nh 2
RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic <t>PAR4-AP</t> (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.
Par4 Agonist Peptide Gypgqv Nh 2, supplied by Bachem, 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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par 1and par4 antagonist peptides mpr cha  (Biosynth Carbosynth)
92
Biosynth Carbosynth par 1and par4 antagonist peptides mpr cha
RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic <t>PAR4-AP</t> (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.
Par 1and Par4 Antagonist Peptides Mpr Cha, supplied by Biosynth Carbosynth, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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par 4 antagonist tcy nh2  (Tocris)
93
Tocris par 4 antagonist tcy nh2
RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic <t>PAR4-AP</t> (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.
Par 4 Antagonist Tcy Nh2, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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par-4 pepducin p4pal-10 (palmitoyl-sgrryghalr-nh2  (GenScript corporation)
90
GenScript corporation par-4 pepducin p4pal-10 (palmitoyl-sgrryghalr-nh2
RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic <t>PAR4-AP</t> (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.
Par 4 Pepducin P4pal 10 (Palmitoyl Sgrryghalr Nh2, 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
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par4-ap aypgkf-nh2  (GL Biochem)
90
GL Biochem par4-ap aypgkf-nh2
RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic <t>PAR4-AP</t> (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.
Par4 Ap Aypgkf Nh2, supplied by GL Biochem, 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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par4 ap  (Biosynth Carbosynth)
94
Biosynth Carbosynth par4 ap
RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic <t>PAR4-AP</t> (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.
Par4 Ap, supplied by Biosynth Carbosynth, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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par4  (Biosynth Carbosynth)
86
Biosynth Carbosynth par4
RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic <t>PAR4-AP</t> (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.
Par4, supplied by Biosynth Carbosynth, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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par4-ap (gypgqv-nh2  (AnaSpec)
90
AnaSpec par4-ap (gypgqv-nh2
RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic <t>PAR4-AP</t> (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.
Par4 Ap (Gypgqv Nh2, supplied by AnaSpec, 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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ay nh2  (Tocris)
93
Tocris ay nh2
RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic <t>PAR4-AP</t> (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.
Ay Nh2, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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aypgkf-nh 2  (GenScript corporation)
90
GenScript corporation aypgkf-nh 2
RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic <t>PAR4-AP</t> (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.
Aypgkf Nh 2, 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
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aypgkf nh2  (Tocris)
93
Tocris aypgkf nh2
RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic <t>PAR4-AP</t> (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.
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Image Search Results


RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic PAR4-AP (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.

Journal: Arteriosclerosis, Thrombosis, and Vascular Biology

Article Title: PAR4 Inhibition Reduces Coronary Artery Atherosclerosis and Myocardial Fibrosis in SR-B1/LDLR Double Knockout Mice

doi: 10.1161/ATVBAHA.123.319767

Figure Lengend Snippet: RAG8 treatment impairs PAR (protease-activated receptor) 4–mediated platelet activation. A , SR-B1 (scavenger receptor class B type I)/LDLR (low-density lipoprotein receptor) double knockout (DKO) mice fed the high-fat, high-cholesterol diet containing cholate (HFCC) for 20 days and treated with the RAG8 or the inactive control SRQ8 pepducins were anesthetized, and their tails were transected across the vein ≈0.5 cm from the tip and placed in a cuvette with warm saline. The time to cessation of bleeding was monitored. Each data point represents an individual mouse (n=12, 14). B and C , SR-B1/LDLR DKO mice were fed the HFCC for 14 days and treated with the RAG8 or the inactive control SRQ8 pepducins (n=4 each). Platelets were prepared from blood collected retro-orbitally from anesthetized mice. Platelet activation was measured by treatment of platelets with either thrombin or a synthetic PAR4-AP (PAR4 agonist peptide) by flow cytometry after immunostaining with either ( B ) a FITC (fluorescein isothiocyanate)-labeled Wug-E9 antibody (for P-selectin) or ( C ) a PE (phycoerythrin)-labeled JON/A antibody for active GP IIb/IIIa (glycoprotein). Resting platelet activation levels do not differ between control SRQ8- and RAG8-treated SR-B1/LDLR DKO mice. Units are expressed as median fluorescence intensity (MFI). Bars represent means, and error bars represent SEMs. Data in A passed the normality test and were analyzed by Student t test. Data in B and C were analyzed by 2-way ANOVA with Sidak multiple comparisons post hoc test. **** P <0.0001.

Article Snippet: For pepducin-treated mouse groups, platelets (1×10 6 washed mouse platelets per reaction) were resting or activated with 1 U/mL α-thrombin (HT 1002A; Enzyme Research Laboratories, South Bend, IN) or 300 μM PAR4 agonist peptide (AYPGKF-NH 2 ; custom synthesized by Genscript, Piscataway, NJ) in the presence of 2 mM CaCl 2 .

Techniques: Activation Assay, Double Knockout, Control, Saline, Flow Cytometry, Immunostaining, Labeling, Fluorescence