Hs_Thyroid_gland
Ontology highlight
ABSTRACT:
REANALYSIS of: PXD000865
INSTRUMENT(S): LTQ Orbitrap Elite
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Others
SUBMITTER: Wilhelm et al.
PROVIDER: PAe005037 | PeptideAtlas | 2014-12-31
REPOSITORIES: PeptideAtlas
Publications
Mass-spectrometry-based draft of the human proteome.
Wilhelm Mathias M Schlegl Judith J Hahne Hannes H Gholami Amin Moghaddas AM Lieberenz Marcus M Savitski Mikhail M MM Ziegler Emanuel E Butzmann Lars L Gessulat Siegfried S Marx Harald H Mathieson Toby T Lemeer Simone S Schnatbaum Karsten K Reimer Ulf U Wenschuh Holger H Mollenhauer Martin M Slotta-Huspenina Julia J Boese Joos-Hendrik JH Bantscheff Marcus M Gerstmair Anja A Faerber Franz F Kuster Bernhard B
Nature 20140501 7502
Proteomes are characterized by large protein-abundance differences, cell-type- and time-dependent expression patterns and post-translational modifications, all of which carry biological information that is not accessible by genomics or transcriptomics. Here we present a mass-spectrometry-based draft of the human proteome and a public, high-performance, in-memory database for real-time analysis of terabytes of big data, called ProteomicsDB. The information assembled from human tissues, cell lines ...[more]
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-07-24 | GSE180743 | GEO
Project description:We developed three different protein arrays to measure IgG autoantibodies associated with Connective Tissue Diseases (CTDs), Anti-Cytokine Antibodies (ACA), and anti-viral antibody responses in 147 hospitalized COVID-19 patients in three different centers.
2021-07-24 | GSE180742 | GEO
Project description:Aberrant activation of PI3K pathway is frequently observed in triple negative breast cancer (TNBC). However single agent PI3K inhibitors have shown limited anti-tumor activity. To investigate biomarkers of response and resistance mechanisms, we tested 17 TNBC patient-derived xenograft (PDX) models representing diverse genomic backgrounds and varying degrees of PI3K pathway signaling activities for their tumor growth response to the pan-PI3K inhibitor BKM120. Baseline and post-treatment PDX tumors harvested following 3 days of BKM120 or vehicle administration were subjected to reverse phase protein array (RPPA) to identify protein markers associated with tumor growth response. While BKM120 consistently reduced PI3K pathway activity, as demonstrated by reduced levels of phosphorylated AKT, percentage tumor growth inhibition (%TGI) ranged from 35% in the least sensitive to 84% in the most sensitive PDX model at the completion of approximately 3-4 weeks of treatment. Several biomarkers showed significant association with resistance, including elevated baseline levels of growth factor receptors (EGFR, pHER3 Y1197), PI3Kp85 regulatory subunit, anti-apoptotic protein BclXL, EMT (Vimentin, MMP9, IntegrinaV), NFKB pathway (IkappaB, RANKL), and intracellular signaling molecules including Caveolin, CBP, and KLF4, as well as treatment-induced increase in the levels of phosphorylated forms of Aurora kinases. Sensitivity to BKM120 was associated with higher baseline levels of proapoptotic markers (Bak and Caspase 3) and a greater number of markers differentially changed following BKM120 therapy. Interestingly, markers indicating PI3K pathway signaling activation or PTEN loss at baseline were not significantly correlated to %TGI. These results provide important insights into biomarker development for PI3K inhibitors in TNBC.
2021-01-27 | GSE149720 | GEO
Project description:To compare the cell signaling events between PC-3 cells and MDA-MB-468 cells, we performed a Reverse Phase of Protein Array (RPPA) profiling on 468 and PC-3 Cells that treated with DMSO, AZD5363, MS21 at 1µM for 24hr respectively.
2019-11-27 | GSE141079 | GEO
Project description:Systemic lupus erythematosus is a chronic autoimmune disease with multifactorial ethiopathogenesis. The complement system is involved in both the early and late stages of disease development and organ damage. To better understand autoantibody mediated complement consumption the GAPAID consortium examined ex vivo immune complex formation on autoantigen arrays. We recruited patients with SLE (n=211), with other systemic autoimmune diseases (n=65) and non-autoimmune control subjects (n=149) in two rheumatology tertiary care centers. Standard clinical and laboratory data were collected from all subjects and serum complement levels were determined in SLE patients. The genotype of SNP rs1143679 in the ITGAM gene was also determined. On-chip formation of immune complexes was examined using a functional immunoassay on autoantigen microarray. The amount of antigen-bound IgM, IgG and complement C4 and C3 was quantified on autoantigens comprising nucleic acids, proteins and lipids. Our results show that the relatively high complement consumption of nucleic acids is further increased upon binding of IgM and IgG. This is true even when serum complement levels are decreased due to complement consumption in SLE patients. A negative correlation between serum complement levels and ex vivo complement deposition on nucleic acid autoantigens is demonstrated. On the contrary, most protein and lipid autoantigens show positive correlation with C4 and C3 levels. Genetic analysis reveals that the non-synonymous variant rs1143679 in complement receptor type 3 is associated with an increased production of anti-dsDNA IgG antibodies. Notwithstanding, homozygous carriers of the previously reported susceptible allele (AA) have lower levels of dsDNA specific IgM among SLE patients. Regarding organ involvement we find that besides anti-C1q IgG, low levels of dsDNA specific IgM and low complement C4 binding to C1q are also associated with renal injury. In summary, nucleic acids maintain a skewed complement deposition balance when bound by IgG and IgM, depleting the early classical complement pathway from other physiological processes. Dysfunction of the receptor responsible for complement-mediated apoptotic debris removal promotes the development of autoantibodies targeting nucleic acids. These observations provide serological and genetic evidence for complement-mediated clearance deficiency of apoptotic debris in lupus.
2016-03-07 | GSE69366 | GEO
Project description:Primary lymphoma of the central nervous system (PCNSL) is a diffuse large B cell lymphoma confined to the CNS. In order to elucidate its peculiar organ tropism, we generated recombinant antibodies (recAb) identical with the BCR of a series of 23 PCNSL from immunocompetent patients. While none of the recAb showed self-reactivity upon testing with common autoantigens, they recognized 1547 proteins present on a large-scale protein microarray. Interestingly, proteins recognized by the recAb are physiologically expressed by CNS neurons (GRINL1A, centaurin-α, BAIAP2). Furthermore, 87% (20/23) of the recAb including all antibodies derived from IGHV4 34 using PCNSL recognized galectin-3, which was upregulated on microglia/macrophages, astrocytes, and cerebral endothelial cells upon CNS invasion by PCNSL. Thus, PCNSL Ig may recognize CNS proteins as self-antigens. Their interaction may contribute to BCR signaling with sustained NF-κB activation and, ultimately, may foster tumor cell proliferation and survival. These data may also explain, at least in part, the affinity of the tumor cells of PCNSL to the CNS.
2015-07-01 | GSE61556 | GEO
Project description:Overall, this work describes the largest cohort of patients with RAG mutations and an associated phenotype consisting of combined immunodeficiency and granulomatous lesions and/or autoimmunity (CID-G/AI). By using multiple methods (microarray, ELISA and multiplex bead technology), we have consistently identified a distinctive signature of anti-cytokine antibodies in patients with RAG-dependent immunodeficiencies, especially in those with CID-G/AI and a history of severe viral infections. These autoantibodies were not detected in a large panel of patients with other forms of primary immunodeficiency, and may therefore represent a novel biomarker panel of this condition.
2015-07-08 | GSE70618 | GEO
Project description:The pathogenesis of Chlamydophila (C.) psittaci negative ocular adnexal extranodal marginal zone lymphomas (OAEMZLs) is poorly understood. OAEMZLs are monoclonal tumors expressing a biased repertoire of mutated surface immunoglobulins. Antigenic activation of the B cell receptor (BCR) may play a role in the pathogenesis of these lymphomas. We have analyzed the reactivity of recombinant OAEMZL immunoglobulins. OAEMZL antibodies reacted with self-human antigens, as demonstrated by enzyme-linked immunosorbent assays, HEp-2 immunofluorescence and human protein microarrays. All the analyzed recombinant antibodies (rAbs) exhibited polyreactivity by comprehensive protein array antibody reactivity and some rAbs also demonstrated rheumatoid factor activity. The identity of several reactive antigens was confirmed by microcapillary reverse-phase HPLC nano-electrospray tandem mass spectrometry. The tested rAbs frequently reacted with shared intracellular and extracellular self-antigens (e.g. galectin-3). Furthermore, these self-antigens induced BCR signaling in B cells expressing cognate surface immunoglobulins derived from OAEMZLs. These findings suggest that interactions between self-antigens and cognate OAEMZL tumor-derived BCRs are functional, inducing intracellular signaling. Overall our findings suggest that self-antigen-induced BCR stimulation may be implicated in the pathogenesis of C. psittaci negative OAEMZLs.
2015-01-30 | GSE65443 | GEO
Project description:Leptospirosis is the most widespread zoonotic disease in the world. The lack of an adequate laboratory test is a major barrier for the diagnosis, especially during the early stages of illness, when antibiotic therapy is most effective. Therefore, there is a critical need for an efficient diagnostic test for this life threatening disease. In order to identify new targets that could be used as diagnostic makers for leptopirosis, we constructed a protein microarray chip comprising 61% of Leptospira interrogans proteome and investigated the IgG response against leptospiral antigens from 274 individuals, including 80 acute-, 80 convalescent-phase patients and 114 healthy control subjects from regions with endemic, high endemic and no endemic transmission of leptospirosis. A nitrocellulose line blot assay was performed to validate the accuracy of the protein microarray results. We found 16 antigens that can discriminate between acute cases and healthy individuals from a region with high endemic transmission of leptospirosis, and 18 antigens that distinguish convalescent cases. Some of the antigens identified in this study, such as LipL32, the non-identical domains of the Lig proteins, GroEL and Loa22 are already known to be recognized by sera from human patients, thus serving as a proof-of-concept for the serodiagnostic antigen discovery approach. Several novel antigens were identified, including the hypothetical protein LIC10215 which showed good sensitivity and specificity rates for both acute- and convalescent-phase patients. Our study is the first large-scale evaluation of immunodominant antigens associated with naturally acquired leptospiral infection and novel as well as known serodiagnostic leptospiral antigens that are recognized by antibodies in the sera of leptospirosis cases were identified. The novel antigens identified here may have potential use in both the development of new tests and the improvement of currently available assays for diagnosing this neglected tropical disease. Further research is needed to assess the accuracy of these antigens in more appropriate diagnostic platforms.
2012-12-04 | GSE42720 | GEO
Project description:Humoral immune responses are traditionally characterized by determining the presence and quality of antibodies specific for certain antigens. Arraying of large numbers of antigens allows the parallel measurement of antibodies, generating patterns called antibody profiles. Functional characterization of these antibodies could help draw an even more informative map of an immune response. To generate functional antibody profiles we simultaneously tested not only IgM, IgG and IgA binding to but also complement activation by a panel of endogenous and exogenous antigens printed as microarrays, using normal and autoimmune human sera. We show that complement activation by a particular antigen in a given individual cannot be predicted by the measurement of antigen specific antibodies, in spite of a general correlation between the amount of antigen-bound antibody and the deposited C3 fragments. This is due to both differences in the isotypes that dominate in the recognition of an antigen and individual variations for a given isotype, resulting in altered complement activation potential. Thus, antigen specific C3 deposition can be used as an additional parameter in immune response monitoring. This is exemplified by comparing the coordinates of antigens, used for the diagnosis of systemic lupus erythematosus, of normal and autoimmune serum samples in a two-dimensional space derived from C3 deposition and antibody binding. Since cleavage fragments of C3 mediate important immunological processes we propose that measurement of their deposition on antigen microarrays, in addition to antibody profiling, can provide useful functional signature about the tested serum. Keywords: IgM immuneprofile, antigen array
2008-12-01 | GSE12943 | GEO