Deficiency in TMX1 potentiates platelet function and thrombosis and shortens bleeding times in mice. Convulxin-induced (A) and thrombin-induced (C) aggregation and convulxin-induced ATP release (B) for platelets from wild-type (TMX1^+/+) and TMX1-deficient (TMX1^−/−) mice. (C) rTMX1 (2 μM) was added to TMX1-null platelets 5 minutes prior to platelet activation. Representative tracings (left panels) and combined results (right panel); data are mean ± standard error of the mean (SEM), n = 4 (A-B), n = 5 (C). *P < .05, **P < .01, Student t test (A-B), analysis of variance (C). TMX1-deficient platelets have enhanced convulxin-induced activation of αIIbβ3 (detected by the JON/A activation-dependent antibody) (D) and P-selectin expression (E). Adding rTMX1 (2 μM) 5 minutes prior to platelet activation reverses the increased aggregation and P-selectin expression. Representative line graphs (left panels) and combined results (right panels); data are mean ± SEM, n = 4. Platelets from wild-type littermate control or TMX1-deficient mice were stimulated with convulxin for 5 minutes, followed by flow cytometry analysis. ***P < .001, analysis of variance. (F) Incorporation of platelets into a growing thrombus in TMX1^+/+ and TMX1^−/− mice was detected by Alexa Fluor–488 anti-CD41 after an FeCl₃ (3.5%)–induced mesenteric arterial injury. Images were taken at 3, 7, 12, and 20 minutes. Dashed lines mark the vessel wall. Scale bars, 200 μm. Mean vessel diameters: TMX1^+/+ mice, 94.34 ± 3.20 μm; TMX1^−/− mice, 93.71 ± 5.71 μm (P = not significant). (G) Composite of fluorescent intensity per area (FI/μm²) in TMX1^+/+ mice (n = 13 from 4 mice) and TMX1^−/− mice (n = 13 from 3 mice); data are mean ± SEM. **P < .01, ***P < .001, Student t test. (H) Tail bleeding time in TMX1^+/+ and TMX1^−/− mice; data are mean ± SEM. ***P < .001, Student t test. NS, not significant.