Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA119805 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Protein C (PC) deficiency increases the risk of venous thrombosis (VT) among members of Kindred Vermont II, but fails to fully account for the inheritance pattern. A genome scan of the pedigree supported the presence of a prothrombotic gene on chromosome 11q23 with weaker support on chromosomes 10p12 and 18p11.2-q11. Preliminary data from Affimetrix microarray expression analysis of Blood Outgrowth Endothelial Cells of 3 members of Kindred Vermont II compared to a well established normal control group indicated that IgsF4 was decreased in patients versus controls. In addition, both statistical and pathway analysis results suggested that these genes are associated protein C. Further studies indicated that Cell Adhesion Molecule 1 (CADM1), a member of the IgsF4 superfamily, may be associated with VT.
2009-07-15 | GSE17078 | GEO
Project description:Protein C (PC) deficiency increases the risk of venous thrombosis (VT) among members of Kindred Vermont II, but fails to fully account for the inheritance pattern. A genome scan of the pedigree supported the presence of a prothrombotic gene on chromosome 11q23 with weaker support on chromosomes 10p12 and 18p11.2-q11. Preliminary data from Affimetrix microarray expression analysis of Blood Outgrowth Endothelial Cells of 3 members of Kindred Vermont II compared to a well established normal control group indicated that IgsF4 was decreased in patients versus controls. In addition, both statistical and pathway analysis results suggested that these genes are associated protein C. Further studies indicated that Cell Adhesion Molecule 1 (CADM1), a member of the IgsF4 superfamily, may be associated with VT. Experiment Overall Design: We obtained BOEC (blood outgrowth endothelial cells) from 3 female kindred subjects (ages 56, 61, and 74) with Protein C Deficiency. We also performed microarray analysis on BOEC from 27 normal subjects of diverse ages.
2009-07-24 | E-GEOD-17078 | biostudies-arrayexpress
Project description:Arterial and venous (A/V) thrombosis constitutes the greatest source of morbidity and mortality worldwide. Long considered as distinct entities, accumulating evidence indicates that A/V thrombosis can occur in the same populations suggesting that common mechanisms are likely operative. Although hyperactivation of the immune system is a common forerunner to the genesis of thrombotic events in both vascular systems, the key molecular control points remain poorly understood. Consequently, anti-thrombotic therapies targeting the immune system for therapeutic gain are lacking. Here we show that neutrophils are key effectors of both A/V thrombosis and can be targeted via novel immunoregulatory nanoparticles. Using antiphopholipid antibody syndrome (APS) as a model for devastating A/V thrombosis, we identified the transcription factor Krüppel-like factor 2 (KLF2) as a key regulator of neutrophil activation. Upon activation via genetic loss of KLF2 or administration of antiphospholipid antibodies, neutrophils cluster P-selectin glycoprotein ligand 1 (PSGL-1) via cortical actin remodeling, thereby increasing adhesion potential at thrombosis sites. Targeting clustered PSGL-1 using designer nanoparticles attenuates neutrophil-mediated A/V thrombosis in APS and KLF2 knockout models, illustrating the importance and feasibility of targeting activated neutrophils to prevent pathological thrombosis. Together, our results demosntrate a role for activated neutrophils to prevent pathological thrombosis. Together, our results demonstrate a role for activated neutorphils in both arterial and venous thrombosis and identify key molecular events that serve as potential targets for therapeutics against diverse causes of immunothrombosis.
2022-09-12 | GSE208336 | GEO
Project description:Inactivating mutations of BAP1 are associated with an increased risk of developing metastasis in uveal melanoma (UM), but the roles of BAP1 in UM progression is unclear. To characterize BAP1’s functions in UM, we performed RNA sequencing on BAP1 wild-type and mutant UM cell lines. Differential analysis revealed that BAP1 loss is associated with an upregulated gene expression profile of multiple cell adhesion molecules (CAMs), including E-cadherin (CDH1), cell adhesion molecule 1 (CADM1), and syndecan-2 (SDC2).
2022-04-25 | GSE181194 | GEO
Project description:Coagulopathy is a hallmark finding in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is associated with an increased risk of death from venous and arterial thromboembolic complications. SARS-CoV-2 infection can lead to microvascular thrombosis that contributes to acute lung injury and respiratory failure. The molecular mechanisms leading to thrombosis in Coronavirus disease 2019 (COVID19) patients are poorly understood. Here, we study a role of the procoagulant neutrophil extracellular traps (NETs)/Factor XII (FXII) axis in COVID19-associated thromboembolism.
2021-08-20 | PXD020216 | Pride
Project description:Coagulopathy is a hallmark finding in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is associated with an increased risk of death from venous and arterial thromboembolic complications. SARS-CoV-2 infection can lead to microvascular thrombosis that contributes to acute lung injury and respiratory failure. The molecular mechanisms leading to thrombosis in Coronavirus disease 2019 (COVID19) patients are poorly understood. Here, we study a role of the procoagulant neutrophil extracellular traps (NETs)/Factor XII (FXII) axis in COVID19-associated thromboembolism.
2021-08-20 | PXD020279 | Pride
Project description:Retention of lymphocytes in the intestinal mucosa requires specialized chemokine receptors and adhesion molecules. Here we find that both CD4+CD8+ and CD4+T cells in the intestinal epithelium, as well as CD8+T cells in the intestinal mucosa and mesenteric lymph nodes, express the cell adhesion molecule Crtam upon activation, whereas the ligand of Crtam, Cadm1, is expressed on gut CD103+DCs. Lack of Crtam-Cadm1 interactions in Crtam-/- and Cadm1-/- mice results in loss of CD4+CD8+T cells, which arise from mucosal CD4+T cells that acquire a CD8 lineage expression profile. Following acute oral infection with T. gondii, both WT and Crtam-/- mice mounted a robust TH1 response, but markedly fewer TH17 cells were present in the intestinal mucosa of Crtam-/- mice. The almost exclusive TH1 response in Crtam-/- mice resulted in more efficient control of intestinal T. gondii infection. CD4+ T cells were cell sorted to analyze the differences resulting from the lack of Crtam expression during T. gondii infection.
2014-02-15 | E-GEOD-55067 | biostudies-arrayexpress
Project description:Myeloid Cell Adhesion Molecule 1 (CADM1) promotes pro-inflammatory signaling during Inflammatory Bowel Disease.
| PRJNA1139190 | ENA
Project description:Retention of lymphocytes in the intestinal mucosa requires specialized chemokine receptors and adhesion molecules. Here we find that both CD4+CD8+ and CD4+T cells in the intestinal epithelium, as well as CD8+T cells in the intestinal mucosa and mesenteric lymph nodes, express the cell adhesion molecule Crtam upon activation, whereas the ligand of Crtam, Cadm1, is expressed on gut CD103+DCs. Lack of Crtam-Cadm1 interactions in Crtam-/- and Cadm1-/- mice results in loss of CD4+CD8+T cells, which arise from mucosal CD4+T cells that acquire a CD8 lineage expression profile. Following acute oral infection with T. gondii, both WT and Crtam-/- mice mounted a robust TH1 response, but markedly fewer TH17 cells were present in the intestinal mucosa of Crtam-/- mice. The almost exclusive TH1 response in Crtam-/- mice resulted in more efficient control of intestinal T. gondii infection.
2014-02-15 | GSE55067 | GEO