HDXMS_W215AE217A_thrombin_thrombomodulin
Ontology highlight
ABSTRACT:
INSTRUMENT(S): SYNAPT G2-Si
ORGANISM(S): Homo Sapiens (ncbitaxon:9606)
SUBMITTER: 
Elizabeth Komives
PROVIDER: MSV000088425 | MassIVE | Sun Nov 21 17:19:00 GMT 2021
REPOSITORIES: MassIVE
Similar Datasets
Project description:Human aortic smooth muscles are quiesced for 24 hours followed by treatment with thrombin for 2 hours and 8 hours in presence or absence of cyclosporin A (10 micromolar) to analyze the effect of thrombin on expression pattern of various genes in presence of cyclosporin A.
2017-10-03 | GSE104498 | GEO
Project description:Phospho-proteomic analysis of Thrombin signaling in the presence and absence of a p38 inhibitor
2020-04-06 | MSV000085235 | MassIVE
Project description:We used HDX-MS analysis to analyze the interaction between PTPN2 with a compound both in the presence and absence of the CRBN/DDB1 complex. We identified significant changes in HDX when PTPN2 was in the presence of compound. We also identified significant changes when comparing the deuteration profiles of PTPN2 in the presence of compound with and without the CRBN/DDB1 complex.
2024-08-23 | PXD053867 | Pride
Project description:Use of HDX-MS to study the allosteric and structural differences between the TRAPPII and TRAPPIII complex in the presence and absence of membrane and rab GTPases
2021-09-22 | PXD025928 | Pride
Project description:Gene expression of roots grown on MS medium versus MS+9HOT was compared. 6-day-old seedlings grown on MS were transferred to fresh plates and grown for 3- or 5- additional days in the absence or in the presence of 9-HOT (25 um). Root fragments grown after transferring to fresh plates were excised and used to compare gene expression between controls and 9-HOT treated seedlings.
2009-10-02 | E-ATMX-14 | biostudies-arrayexpress
Project description:For microarray analysis plants (Arabidopsis thaliana) were grown for 7 days in the presence or absence of 1 uM 6-benzyladenine following growth on MS medium for 7 days.
2011-12-31 | E-MEXP-3132 | biostudies-arrayexpress
Project description:Black and Hispanic American patients frequently develop earlier onset of multiple sclerosis (MS) and a more severe disease course that can be resistant to disease modifying treatments. The objectives were to identify differential methylation of genomic DNA (gDNA) associated with disease susceptibility and treatment responses in a cohort of MS patients from underrepresented minority populations. Patients with MS and controls with non-inflammatory neurologic conditions were consented and enrolled under an IRB-approved protocol. Approximately 64% of donors identified as Black or African American and 30% as White, Hispanic-Latino. Infinium MethylationEPIC bead arrays were utilized to measure epigenome-wide gDNA methylation of whole blood. Data were analyzed in the presence and absence of adjustments for unknown covariates in the dataset, some of which corresponded to disease modifying treatments. Global patterns of differential methylation associated with MS were strongest for those probes that showed relative demethylation of loci with lower M values. Pathway analysis revealed unexpected associations with shigellosis and amoebiasis. Enrichment analysis revealed an over-representation of probes in enhancer regions and an under-representation in promoters. In the presence of adjustments for covariates that included disease modifying treatments, analysis revealed 10 differentially methylated regions (DMR’s) with an FDR <1E-77. Five of these genes (ARID5B, BAZ2B, RABGAP1, SFRP2, WBP1L) are associated with cancer risk and cellular differentiation and have not been previously identified in MS studies. Hierarchical cluster and multi-dimensional scaling analysis of differential DNA methylation at 147 loci within those DMR’s was sufficient to differentiate MS donors from controls. In the absence of corrections for disease modifying treatments, differential methylation in patients treated with dimethyl fumarate was associated with immune regulatory pathways that regulate cytokine and chemokine signaling, axon guidance, and adherens junctions. These results demonstrate possible associations of gastrointestinal pathogens and regulation of cellular differentiation with MS susceptibility in our patient cohort. This work further suggests that analyses can be performed in the presence and absence of corrections for immune therapies. Because of their high representation in our patient cohort, these results may be of specific relevance in the regulation of disease susceptibility and treatment responses in Black and Hispanic Americans.
2023-02-07 | GSE219293 | GEO
Project description:Confluent human umbilical vein endothelial cells (HUVECs) were exposed to Thrombin (2 U/mL) for 2 hours. Ribosomal profiling via gradient centrifugation and fractionation was used to separate monosome, or under-translated, and polysome, or actively translated, mRNA species that were then used to probe cDNA arrays, a process known as Translation State Array Analysis (TSAA). Four samples were obtained from these experiments, Control Monosome, Control Polysome, Thrombin Monosome, and Thrombin Polysome. Using the normalized signal intensities from the GeneFilters, we calculated a translation index, or measure of movement of an mRNA molecule from the monosome to the polysome fraction upon stimulation. This calculation was made as follows: (thrombin polysome/thrombin monosome)/(control polysome/control monosome). Translational indices greater than 2.5 (upregulated) or lower than 0.4 (downregulated) were chosen for further study. TSAA data suggests that JunB is translationally regulated by thrombin stimulation. Immunocytochemistry, western blotting and RT-PCR were used to verify the results of TSAA. Keywords: Translation State Array Analysis
2006-05-31 | GSE4919 | GEO
Project description:Brain microvascular endothelial cells (BMECs) are part of the blood-brain barrier (BBB). These cells express Cacnb3 transcripts encoding the Cavβ3 protein, which is a subunit of the voltage-gated Ca2+ (Cav) channels. However, potassium depolarization and electrophysiological recordings in BMECs did not reveal a significant Cav channel function, regardless of the presence or absence of Cavβ3. In vivo, the integrity of the BBB was reduced in the absence of Cavβ3. Following induction of experimental autoimmune encephalomyelitis (EAE), Cavβ3-deficient (Cavβ3-/-) mice showed earlier disease onset with exacerbated clinical disability and increased infiltration of T-cells. In vitro, the trans-endothelial resistance of Cavβ3-/- BMEC monolayers was lower than that of wild-type, permeability to albumin and dextran was increased, and the organization of the junctional protein ZO-1 was impaired in the absence and presence of the pro-inflammatory mediator thrombin. The results suggest that Cavβ3, independent of its function as a subunit of Cav channels, tightly controls cytoplasmic [Ca2+] and Ca2+-dependent MLC phosphorylation and that this role of Cavβ3 in BMECs contributes to the integrity of the BBB and decreases severity of clinical EAE disease.
2024-07-16 | GSE268823 | GEO
Project description:Objective: Thrombin is the key serine protease of the coagulation cascade and mediates cellular responses by activation of protease-activated receptors (PARs). The predominant thrombin receptor is PAR1 and in endothelial cells (ECs) thrombin dynamically regulates a plethora of phosphorylation events. However, it has remained unclear if thrombin signaling is exclusively mediated through PAR1. Furthermore, mechanistic insight into activation and inhibition of PAR1-mediated EC signaling is lacking. In addition, signaling networks of biased PAR1 activation after differential cleavage of the PAR1 N-terminus have remained an unresolved issue.Approach and Results: Here, we used a quantitative phosphoproteomics approach to show that ‘classical’ and ‘peptide’ activation of PAR1 induce highly similar signaling, that low thrombin concentrations initiate only limited phosphoregulation, and that the PAR1 inhibitors vorapaxar and parmodulin-2 demonstrate distinct antagonistic properties. Subsequent analysis of the thrombin-regulated phosphosites in presence of PAR1 inhibitors revealed that biased activation of PAR1 is not solely linked to a specific G-protein downstream of PAR1. In addition, we showed that only the canonical thrombin PAR1 tethered ligand induces extensive early phosphoregulation in ECs.Conclusions: Our study provides detailed insight in the signaling mechanisms downstream of PAR1. Our data demonstrates that thrombin-induced EC phosphoregulation is mediated exclusively through PAR1, that thrombin and thrombin-TL peptide induce similar phosphoregulation and that only canonical PAR1 cleavage by thrombin generates a tethered ligand that potently induces early signaling. Furthermore, platelet PAR1 inhibitors directly affect EC signaling, indicating it will be a challenge to design a PAR1 antagonist that will target only those pathways responsible for tissue pathology.
2017-08-22 | PXD004264 | Pride