Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Collaboration of PARP family members in non-cancer disease mechanism

ABSTRACT: Our work can be summarized as the establishment of protein-binding database for PARPs family as well as a comprehensive multi-omics analysis to show its potential for pathogenic mechanism study of the PARPs family. We concluded that the pathogenic role of PARPs family extends far more than cancer. Besides potential roles in neuron-degeneration diseases, results from multiple independent bio-informatic analysis indicate several PARP family members may involve in diabetes’ complication and closely related disease like types of hypertension and Systemic lupus erythematosus. The relationship between PARPs and diabetes are supported in recent reports.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Zheng Jeff

LAB HEAD: Zheng Jiefu

PROVIDER: PXD052745 | Pride | 2024-07-15

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Similar Datasets

Gene Expression Signature Shared in Autoimmune Diseases Not in Unaffected Family Members

Project description:Even though autoimmune diseases are heterogeneous, believed to result from the interaction between genetic and environmental components, patients with these disorders exhibit reproducible patterns of gene expression in their peripheral blood mononuclear cells. A portion of this gene expression profile reflects family resemblance rather than the actual presence of an autoimmune disease. Here we wanted to identify that portion of this gene expression pattern that is independent of family resemblance and determine if it is a product of disease duration, disease onset, or other factors. By increasing the number of autoimmune samples in our analysis and employing supervised clustering algorithms, we identified 100 genes whose expression profiles are shared in individuals with various autoimmune diseases but are not shared by first-degree relatives of individuals with autoimmune disease or by controls. Individuals with early disease (1 yr after onset) and established disease (10 yr after onset) exhibit a near identical expression pattern suggesting that this unique profile reflects disease onset rather than disease duration. supervised gene expression profiling were performed to a cohort sample pool: control individuals(8), unaffected family members of autoimmune diseases patients (8), and individuals with autoimmune diseases (54). we try to identify a gene expression signatures that were exclusively associated with autoimmune diseases but not infulenced by genetic components

2010-06-30 | E-GEOD-3447 | biostudies-arrayexpress

Improving Care After Inherited Cancer Testing

Project description:The IMPACT Study seeks to refine and evaluate the effectiveness of interventions on improving guideline-adherent cancer risk management (CRM) and family communication (FC) of genetic test results. These interventions will be delivered to individuals with a documented pathogenic/likely pathogenic (P/LP) variant or variant of uncertain significance (VUS) in an inherited cancer gene.

| 2368091 | ecrin-mdr-crc

Novel modifications of PARP inhibitor veliparib increase PARP1 binding to DNA breaks

Project description:The project is about studying the dynamics of PARP1 when bound to DNA and veliparib derivatives.

2024-03-19 | PXD047072 | Pride

comparative mass spectrometry analysis of the PARP1 and PAR-PARP1 interactomes

Project description:To investigate the functional outcome of PARP1 activation, we performed a pull-down assay coupled with comparative mass spectrometry (MS) analysis to identify proteins that are specifically associated with PAR-PARP1.

2022-02-14 | PXD031109 | Pride

Expression data of AI4 CD8 T cells from AI4 and Rip-B7xAI4 mice

Project description:B7x (B7-H4 or B7S1) is the seventh member of the B7 family and the in vivo function remains largely unknown. Despite new genetic data linking the B7x gene with autoimmune diseases, how exactly it contributes to peripheral tolerance and autoimmunity is unclear. Here we showed that B7x protein was not detected on antigen-presenting cells or T cells in both human and mice, which is unique in the B7 family. As B7x protein is expressed in some peripheral cells such as pancreatic b cells, we utilized a CD8 T cell-mediated diabetes model (AI4ab) in which CD8 T cells recognize an endogenous self-antigen, and found that mice lacking B7x developed more severe diabetes than control AI4ab mice. Conversely, mice overexpressing B7x in the b cells (Rip-B7xAI4ab) were diabetes free. Furthermore, adoptive transfer of effector AI4ab CD8 T cells induced diabetes in control mice, but not in Rip-B7xAI4ab mice. Mechanistic studies revealed that pathogenic effector CD8 T cells were capable of migrating to the pancreas but failed to robustly destroy tissue when encountering local B7x in Rip-B7xAI4ab mice. Although AI4ab CD8 T cells in Rip-B7xAI4ab mice and AI4ab mice showed similar cytotoxic function, cell death, and global gene expression profiles, these cells had greater proliferation in AI4ab mice than in RIP-B7xAI4ab mice. These results suggest that B7x in nonlymphoid organs prevents peripheral autoimmunity partially through inhibiting proliferation of tissue-specific CD8 T cells and that local overexpression of B7x on pancreatic b cells is sufficient to abolish CD8 T cell-induced diabetes. AI4 mice developed T1D and Rip-B7x AI4 mice were resistant to T1D. Total RNA was collected and gene expression compared between AI4 CD8 T cells from AI4 and Rip-B7xAI4 mice.

2012-08-21 | E-GEOD-40225 | biostudies-arrayexpress

Family Investigation of Nephropathy and Diabetes (FIND)

Project description:Family Investigation of Nephropathy and Diabetes (FIND)

| PRJNA75509 | ENA

Homo sapiens

Project description:Family Investigation of Nephropathy and Diabetes (FIND)

| PRJNA75511 | ENA

PARP1 and Salmonella

Project description:BACKGROUND & AIMS: The immune system comprises an innate and an adaptive immune response to combat pathogenic agents. The human enteropathogen Salmonella enterica serovar Typhimurium invades the intestinal mucosa and triggers an early innate pro-inflammatory host gene response, which results in diarrheal disease. Several host factors are involved in the acute early response to Salmonella infection. Transcription factors and transcription co-regulators have an especially important function, because they are required for the expression and synthesis of pro-inflammatory cytokines, chemokines and adhesion molecules. A central transcription factor involved in inflammation is NF-ÎºB, which requires the nuclear protein PARP1 as co-factor for the expression of some of its target genes. Here, we investigated the role of PARP1 during Salmonella infection using a mouse model for Salmonella-induced colitis. METHODS: To study enterocolitis by Salmonella Typhimurium, an established mouse model system, which relies on streptomycin-pretreatment prior to Salmonella infection, was employed. Histopathologic signs of inflammation and cecum colonization at various time-points after infection of wild type and PARP1 knockout mice were analyzed. PARP1 expression in the gut mucosa was studied by quantitative RT-PCR, Western blot and immunofluorescence. Gene expression profiles of infected and control infected mice in the wild type or PARP1 knockout background were obtained by whole mouse genome arrays and confirmed by quantitative RT-PCR. 2 genotypes (wildtype, PARP1 knockout), 2 treatments (Salmonella SB300 infection, Salmonella SB161 control infection), 2 time-points (6h, 10h). 2-3 replicates/condition.

2010-05-27 | E-GEOD-19174 | biostudies-arrayexpress

Expression data of AI4 CD8 T cells from AI4 and Rip-B7xAI4 mice

2012-08-21 | GSE40225 | GEO

HXMS on PARP1+DNA+HPF1 to study the dynamics of PARP1

Project description:The project is about studying the dynamics of PARP1 when bound to DNA and HPF1.

2022-02-17 | PXD026580 | Pride