A5111164758- Platelet Disorders and Treatments
- Cell Adhesion Molecules Research
- Antiplatelet Therapy and Cardiovascular Diseases
- Inflammatory mediators and NSAID effects
- Protein Kinase Regulation and GTPase Signaling
- Protease and Inhibitor Mechanisms
- Biochemical and Structural Characterization
- PI3K/AKT/mTOR signaling in cancer
- Blood properties and coagulation
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Eicosanoids and Hypertension Pharmacology
- Signaling Pathways in Disease
- Complement system in diseases
- Sepsis Diagnosis and Treatment
- Analytical Methods in Pharmaceuticals
- Hemoglobinopathies and Related Disorders
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Caveolin-1 and cellular processes
- Cancer, Lipids, and Metabolism
- Bone health and treatments
- Multiple Myeloma Research and Treatments
- Mechanical Circulatory Support Devices
- Venomous Animal Envenomation and Studies
- Proteoglycans and glycosaminoglycans research
- Myeloproliferative Neoplasms: Diagnosis and Treatment
Baylor College of Medicine
2013-2025
The University of Texas at Austin
2025
Michael E. DeBakey VA Medical Center
2016-2023
University of British Columbia
2023
Children's Cancer Center
2008
Banaras Hindu University
1998
Separase is an endopeptidase that separates sister chromatids by cleaving cohesin Rad21 during the metaphase-to-anaphase transition. Conditional expression of in tetracycline-inducible diploid FSK3 mouse mammary epithelial cells with both p53 WT and mutant (Ser-233-234) alleles unknown physiological significance develops aneuploidy within 5 days induction vitro. Overexpression induces premature separation chromatids, lagging chromosomes, anaphase bridges. In vivo transplant model,...
Abstract The mechanism by which aspirin consumption is linked to significant reductions in the incidence of multiple forms cancer and metastatic spread distant tissues, resulting increased patient survival not well understood. In this study, using colon as an example, we provide both vitro (cell culture) vivo (chemically induced mouse model cancer) evidence that profound antineoplastic action may be associated with aspirin's ability irreversibly inhibit COX-1–mediated platelet activation,...
Potassium ions (K+) within the tumor microenvironment, along with dysregulation of K+ channels, play critical roles in supporting cancer cell survival and preventing their elimination. Directly monitoring changes homeostasis cells is invaluable for understanding these processes. However, achieving high selectivity over other biological metal ions, a detection dynamic range that aligns intracellular levels, broad accessibility to research laboratories remain technically challenging current...
Integrin αIIbβ3 activation is critical for platelet physiology and controlled by signal transduction through kinases phosphatases. Compared with kinases, a role phosphatases in integrin signaling less understood. We report that the catalytic subunit of protein phosphatase 2A (PP2Ac) associates constitutively resting platelets human embryonal kidney 293 cells expressing αIIbβ3. The membrane proximal KVGFFKR sequence within cytoplasmic domain αIIb sufficient to support direct interaction...
Thrombosis is caused by the activation of platelets at site ruptured atherosclerotic plaques. This involves engagement G protein–coupled receptors (GPCR) on that promote their aggregation. Although it known protein kinases and phosphatases modulate GPCR signaling, how serine/threonine integrate with signaling pathways less understood. Because subcellular localization substrate specificity catalytic subunit phosphatase 1 (PP1c) dictated PP1c-interacting proteins, here we sought to identify...
Background Hemostasis and thrombosis are regulated by agonist-induced activation of platelet integrin αIIbβ3. Integrin activation, in turn is mediated cellular signaling via protein kinases phosphatases. Although the catalytic subunit phosphatase 1 (PP1c) interacts with αIIbβ3, role PP1c reactivity unclear. Methodology/Principal Findings Using γ isoform deficient mice (PP1cγ−/−), we show that platelets have moderately decreased soluble fibrinogen binding aggregation to low concentrations...
Essentials Platelet adhesion to von Willebrand factor (VWF) is critical for hemostasis and thrombosis. Whether VWF can undergo phosphorylation unknown. Family with sequence similarity 20 kinase phosphorylates A2 domain at S1517 S1613. Phosphorylation of A1A2A3 S1613 enhances platelet adhesion. SUMMARY: Background mediates contributes sites vascular injury as well arterial The domains contain important that differentially participate in supporting FAM20c (family 20, member C) has emerged a...
Sepsis-induced coagulopathy leading to disseminated microvascular thrombosis is associated with high mortality and has no existing therapy. Despite the prevalence of Gram-positive bacterial sepsis, especially methicillin-resistant
Although protein kinases and phosphatases participate in integrin αIIbβ3 signalling, whether functions are regulated by the catalytic subunit of phosphatase 1(PP1c)isoforms unclear. We show that siRNA mediated knockdown all PP1c isoforms(α, β γ1)in 293 cells decreased adhesion to immobilised fibrinogen fibrin clot retraction. Selective only PP1cγ1 did not alter or retraction, while depletion PP1cβ both functions. Unexpectedly, PP1cα enhanced Protein interaction studies revealed isoforms can...
Hyperferritinemia is associated with poor outcomes in critically ill patients sepsis, hemophagocytic lymphohistiocytosis (HLH), macrophage activation syndromes (MAS) and coronavirus disease 19 (COVID-19). Autopsies of hyperferritinemic that succumbed to either HLH, MAS or COVID-19 have revealed disseminated microvascular thromboses von Willebrand factor (VWF)-, platelets-, and/or fibrin-rich microthrombi. It unknown whether high plasma ferritin concentration actively promotes thrombosis,...
Sepsis can lead to coagulopathy and microvascular thrombosis. Prior studies, including ours, reported an increased level of extracellular vimentin in blood derived from septic patients. Moreover, we identified the contribution fibrin formation clot structure ex vivo plasma Here, tested status its impact on clots using our recently described swine model methicillin-resistant Staphylococcus aureus (MRSA) sepsis-induced coagulopathy.
Bashir, Dalia; Nguyen, Trung; Da, Qi; Cruz, Miguel; Allen, Carl; Lam, Fong; Pradhan, Subhashree; Vijayan, Vinod