Proteins interacting with SRBSDV P6 by Co-IP and mass spectrometry
Ontology highlight
ABSTRACT:
INSTRUMENT(S): LTQ Orbitrap Elite
ORGANISM(S): Oryza Sativa (rice)
TISSUE(S): Leaf, Shoot
SUBMITTER: 
Ming Zeng
LAB HEAD: Ming Zeng
PROVIDER: PXD059146 | Pride | 2025-07-16
REPOSITORIES: pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Raw_data.raw | Raw | |||
| Search.msf | Msf | |||
| checksum.txt | Txt |
Items per page: 5 1 - 3 of 3 |
Similar Datasets
Project description:We found that USF2 is repressor of lysosomal genes. To find the interacting co-repressor complex of USF2, we performed USF2 complex purification and mass spectrography.
2024-09-11 | PXD050434 | Pride
Project description:Analysis of Rosa Damascena Stem Cell-derived Exosome
2023-08-21 | PXD043169 | Pride
Project description:Condensation (C) domains are the key component linking different monomers together, typically forming peptide bonds and occasionally ester bonds, during the nonribosomal peptide synthetase (NRPS). While A domains have been well characterised due to their role in selectivity of the monomers and functioning as a gate keeper in the NRPS biosynthesis, C domains have been a subject of debate as they have not demonstrated signs of “A-domain like” side chain selectivity of its acceptor side. Here, we report our biochemical and structural characterisation of the selectivity of the fuscachelin C3-domain showing that it is not broadly flexible for monomers at the acceptor site, suggesting the need to consider C-domain mutation regarding future NRPS engineering.
2023-06-02 | PXD040334 | Pride
Project description:Cardiac hypertrophy and failure are accompanied by a reprogramming of gene expression that involves transcription factors and chromatin remodeling enzymes. Little is known about the role of histone methylation and demethylation in this process. To understand the role of JMJD2A, a trimethyl demethylase for histone 3 lysine 9 and 36, in cardiac hypertrophy, we generated heart specific JMJD2A deletion (JMJD2A hKO) and overexpression (JMJD2A-Tg) mouse lines. JMJD2A hKO and JMJD2A-Tg mice are viable and have no overt baseline phenotype. However, they have altered responses to cardiac stresses. While inactivation of JMJD2A in hKO mice resulted in an attenuated hypertrophic response to transverse aortic constriction (TAC)-induced pressure overload compared to that of control littermates, JMJD2A-Tg mice have exacerbated cardiac hypertrophy after TAC. We identified four-and-a-half LIM domains 1 (FHL1) as a novel target of JMJD2A. JMJD2A binds to the FHL1 promoter in response to TAC and upregulates the expression of FHL1. Binding of JMJD2A to the FHL1 promoter is associated with downregulation of trimethylated H3K9. Upregulation of FHL1 by JMJD2A is mediated through SRF and myocardin, and requires its demethylase activity. The expression of JMJD2A is upregulated in human hypertrophic cardiomyopathy patients. Our studies reveal that JMJD2A promotes cardiac hypertrophy by synergistically upregulating SRF/myocardin-targeted genes and suggest a novel mechanism of reprogramming of gene expression involved in cardiac hypertrophy. Six to eight years old wildtype and JMJD2A heart specific transgnic mice were undergone either sham or TAC surgery. After 3 weeks, mice were sarcirificed to harvest heart. RNA was extracted from heart samples and treated with DNase, followed by biotin-labeling and microarray hybridization.
2011-06-02 | E-GEOD-27689 | biostudies-arrayexpress
Project description:Aims/hypothesis AGEs are considered environmental contributors of type 1 diabetes, but the exact role AGEs play early in pathogenesis of the disease, remains unidentified. We aimed to reduce AGEs with the pharmacotherapy alagebrium chloride in MIN6N8 cells and early in life in NOD mice to determine its impact on beta cell immunogenicity, function, and disease progression. Methods MIN6N8 cells were cultured with AGEs with or without short-term alagebrium therapy to determine the effect on ER stress and beta cell antigen presentation via a reporter assay for protein responses in the unfolded protein response, the enzymatic activity of endoplasmic reticulum aminopeptidase-1 (ERAP1) and the immunopeptidome. To determine the effect of short-term alagebrium therapy on beta cells in vivo, female NOD mice were treated with alagebrium and insulin secretion, insulitis, and immune cell repertoire were studied. Adoptive transfer studies and diabetes progression studies were used to consider the impact of alagebrium on immune cell function and disease outcome. Results In MIN6N8 cells, alagebrium therapy inhibited the induction of endoplasmic reticulum (ER) stress and the activity of ERAP1 by AGE-modified proteins. Alagebrium treated-MIN6N8 cells did not change the MHC Class I presentation of known beta cell antigens but did induce proteomic changes related to ER homeostatic pathways. Prior to overt autoimmune diabetes, female NOD mice treated with alagebrium for 30-40 days had improved insulin secretion, reduced insulitis and amplified proportions of pancreatic CD8+ T cells, mature B cells and F4/80+ macrophages. Splenocytes from alagebrium-treated mice adoptively transferred disease to NODscid recipients and maintained interferon production in vitro. While partial protection of islets by alagebrium was seen following the adoptive transfer of activated NOD G9C8 transgenic TCR CD8+ T cells, alagebrium therapy in NOD mice did not reduce diabetes progression. Conclusions/interpretation Our data suggests that in experimental models of diabetes, short-term alagebrium treatment allows for beta cell improvement, and maintenance of immune cell function, which does not fully mitigate diabetes progression.
2021-06-29 | PXD025998 | Pride
Project description:Peptide vaccination remains a viable approach to induce T-cell mediated killing of tumours. To identify potential T-cell targets for Triple-Negative Breast Cancer (TNBC) vaccination, we examined the effect of the pro-inflammatory cytokine interferon-γ (IFNγ) on the transcriptome, proteome and immunopeptidome of the TNBC cell line MDA-MB-231. Using high resolution mass spectrometry, we identified a total of 84,131 peptides from 9,647 source proteins presented by human leukocyte antigen (HLA)-I and HLA-II alleles. Treatment with IFNγ resulted in a remarkable remoulding of the immunopeptidome, with only a 34% overlap between untreated and treated cells across the HLA-I immunopeptidome, and expression of HLA-II only on treated cells. IFNγ increased the overall number, diversity and abundance of the immunopeptidome, as well as the proportion of coverage of source antigens. The suite of peptides displayed under conditions of IFNγ treatment included many known tumour associated antigens, with the HLA-II repertoire sampling 265 breast cancer associated antigens absent from those sampled by HLA-I. Quantitative analysis of the transcriptome (10,248 transcripts) and proteome (6783 proteins) of these cells revealed 229 proteins and transcripts were commonly differentially expressed, most of which involved in downstream targets of IFNγ signalling including components of the antigen processing machinery such as tapasin and HLA. However, these changes in protein expression did not explain the dramatic modulation of the immunopeptidome following IFNγ treatment. These results demonstrate the high degree of plasticity in the immunopeptidome TNBC cells following cytokine stimulation and provide evidence that under pro-inflammatory conditions a greater variety of HLA-I and HLA-II vaccine targets are unveiled to the immune system. This has important implications for the development of personalised cancer vaccination strategies.
2021-05-13 | PXD023044 | Pride
Project description:We have analysed a patinet derived mesothelioma cell line by immuniopeptidomics and identified cancer antignes in this line immunopeptidome.
2025-05-06 | PXD037845 | Pride
Project description:Magnaporthe oryzae snodprot1 homologous protein (MSP1) has been shown to act as a pathogen-associated molecular pattern (PAMPs) and trigger PAMP-triggered immunity (PTI) response involving programmed cell death and expression of various defense-related genes in rice. The involvement of several post-translational modifications (PTMs) in the regulation of plant immune response, especially PTI, during pathogen infection is well established, however, the information on the regulatory roles of these PTMs in response to MSP1-induced signaling in rice is currently elusive. Here, we report the phosphoproteome, ubiquitinome, and acetylproteome to investigate the MSP1-induced PTMs alterations in MSP1 overexpressed rice. Our analysis identified a total of 4,666 PTM modified sites in rice leaves including 4,292 phosphosites, 189 ubiquitin sites, and 185 acetylation sites. Among these, PTM status of 437 phosphorylated, 53 ubiquitinated, and 68 acetylated peptides were significantly changed by MSP1. Functional annotation of MSP1 modulated peptides by MapMan analysis revealed that these were majorly associated with cellular immune responses such as signaling, transcription factors, DNA and RNA regulation, and protein metabolism, among others. Taken together, this study uncovers the MSP1-induced PTMs changes in rice proteins and identified several novel components of rice-MSP1 interaction.
2023-07-21 | PXD039997 | Pride
Project description:Previous studies in Leishmania mexicana have identified the cytoskeletal protein KHARON as being important for both flagellar trafficking of the glucose transporter GT1 and for successful cytokinesis and survival of infectious amastigote forms inside mammalian macrophages. KHARON is located in three distinct regions of the cytoskeleton: the base of the flagellum, the subpellicular microtubules, and the mitotic spindle. To deconvolve the different functions for KHARON, we have identified two partner proteins, KHAP1 and KHAP2, that associate with KHARON. KHAP1 is located only in the subpellicular microtubules, while KHAP2 is located at the subpellicular microtubules and the base of the flagellum. Both the KHAP1 and KHAP2 null mutants are unable to execute cytokinesis but are able to traffic GT1 to the flagellum. These results confirm that KHARON assembles into distinct functional complexes and that the subpellicular complex is essential for cytokinesis and viability of disease-causing amastigotes but not for flagellar membrane trafficking.
2020-08-17 | PXD019032 | Pride
Project description:The SAGA-like complex SLIK is a modified version of the Spt-Ada-Gcn5-Acetyltransferase (SAGA) complex. SLIK is formed through C-terminal truncation of the Spt7 SAGA subunit, causing loss of Spt8 that interacts with the TATA-binding protein. SLIK and SAGA are both coactivators of RNA polymerase II transcription in yeast. In addition, both SAGA and SLIK perform chromatin modifications and the two complexes have been speculated to uniquely contribute to transcription regulation. To test the respective contribution of SAGA vs. SLIK in transcription regulation, we assayed the chromatin modifying functions of SAGA vs. SLIK, revealing identical kinetics on minimal substrates in vitro. Furthermore, we determined a low-resolution cryo-EM structure of SLIK, revealing a modular architecture identical to SAGA. Finally, we performed a comprehensive study of DNA-binding properties of both coactivators. Purified SAGA and SLIK both associate with ssDNA and dsDNA with high affinity (KD = 10-17 nM) and the binding is sequence-independent. In conclusion, our study shows that the cleavage of Spt7 and the absence of Spt8 subunit in SLIK neither drive any major conformational differences in its structure compared to SAGA, nor significantly affect HAT, DUB or DNA binding activities in vitro.
2021-04-19 | PXD024640 | Pride