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Mining Meningioma Proteomics Alterations Using IP MS

ABSTRACT: Herein we have used IP-MS based approach to identify potential interactors (PPI) that bind to Annexin A2. We have used Immunoaffinity based enrichment using antibody specific to ANXA2 followed by LC MS-MS of the Complex post running it in SDS-PAGE

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Brain, Epithelial Cell

DISEASE(S): Brain Cancer

SUBMITTER: Shuvolina Mukherjee

LAB HEAD: SANJEEVA SRIVASTAVA

PROVIDER: PXD014853 | Pride | 2021-08-30

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	IPMS.msf	Msf
	IPMS1.raw	Raw
	IPMS2.raw	Raw
	IPMS3.raw	Raw

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Publications

Comprehending Meningioma Signaling Cascades Using Multipronged Proteomics Approaches & Targeted Validation of Potential Markers.

Mukherjee Shuvolina S Biswas Deeptarup D Gadre Rucha R Jain Pooja P Syed Nelofer N Stylianou Julianna J Zeng Qingyu Q Mahadevan Anita A Epari Sridhar S Shetty Prakash P Moiyadi Aliasgar A Roy Ball Graham G Srivastava Sanjeeva S

Frontiers in oncology 20200826

Meningiomas are one of the most prevalent primary brain tumors. Our study aims to obtain mechanistic insights of meningioma pathobiology using mass spectrometry-based label-free quantitative proteome analysis to identifying druggable targets and perturbed pathways for therapeutic intervention. Label-free based proteomics study was done from peptide samples of 21 patients and 8 non-tumor controls which were followed up with Phosphoproteomics to identify the kinases and phosphorylated components o ...[more]

PMID: 32974197

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Role of annexin A2 in muscle repair

Project description:Repair of injured muscle involves repair of injured myofibers through the involvement of dysferlin and its interacting partners, including annexin. Studies with mice and patients have established that dysferlin deficit leads to chronic inflammation and adipogenic replacement of the diseased muscle. However, longitudinal analysis of annexin deficit on muscle pathology and function is lacking. Here we show that unlike annexin A1, but similar to dysferlin, lack of annexin A2 (AnxA2) causes poor myofiber repair and progressive weakening with age. However, unlike dysferlin-deficient muscle, AnxA2-deficient muscles do not exhibit chronic inflammation or adipogenic replacement. Deletion of AnxA2 in dysferlin deficient mice reduces inflammation, adipogenic replacement, and loss in muscle function caused by dysferlin deficit. These results show that: a) AnxA2 facilitates myofiber repair, b) chronic inflammation and adipogenic replacement of dysferlinopathic muscle requires AnxA2, and c) inhibiting AnxA2-mediated inflammation is a novel therapeutic avenue for dysferlinopathy.

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Annexin A2 Modulates Radiation-Sensitive Transcriptional Programming and Cell Fate

Project description:Whole genome expression profiling in the presence and absence of annexin A2 [shRNA] identified fundamentally altered transcriptional programming that changes the radioresponsive transcriptome. Bioinformatics predicted that silencing AnxA2 may enhance cell death responses to stress in association with reduced activation of pro-survival signals such as nuclear factor kappa B. This prediction was validated by demonstrating a significant increase in sensitivity toward tumor necrosis factor alpha induced cell death in annexin A2 silenced cells, relative to vector controls, associated with reduced nuclear translocation of RelA (p65) following tumor necrosis factor alpha treatment. Murine progenitor cells, JB6 cell line, were stably transformed with Annexin A2 shRNA or vector only control and then treated with ionizing radiation at two doses, 10cGy and 100cGy. Samples were collected at 2hr, 6hr and 24hr for RNA isolation. Two untreated time points were collected also: 2hr and 24hr.

2012-11-28 | E-GEOD-42547 | biostudies-arrayexpress

Annexin A2 Modulates Radiation-Sensitive Transcriptional Programming and Cell Fate

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RNA-seq analysis of transcriptomes in Wild Type and ANXA2 knockdown HK2 cells

Project description:We conducted this experiment to study the effects of Annexin A2 (ANXA2) on gene expression in human proximal tubular epithelial (HK2) cells in vitro. Short hairpin RNA targeting ANXA2 was designed and cloned into vector pGFP-B-RS for RNAi to generate the recombinant expression plasmids, which were transfected into HK2 cells. RNA-seq analysis were performed on HK2 cells, with or without ANXA2 knockdown, to reveal the differentially expressed genes (DEGs) and regulated alternative splicing events (RASEs). Then the DEGs and RASEs were validated by qRT-PCR. Using criteria of an absolute fold change of ≥2.0 or ≤ 0.5 and false discovery rate (FDR) of < 0.05 with the edgeR package, RNA-seq analysis of the transcriptomes revealed 220 upregulated and 171 downregulated genes related to ANXA2 knockdown.

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Exploring the molecular mechanism and and related signaling pathways of annexin A2 in human retinal vascular endothelial cells

Project description:To investigate the role and mechanism of ANXA2 in retinal neovascularization, we used interfering and overexpressing lentivirus to intervene in HREC cells, respectively. Divided into interference group (negative control group and positive interference group), overexpression group (negative control group, overexpression positive control group). The mechanism of action of annexin A2 in human retinal vascular endothelium was explored by real-time PCR to quantify the expression of molecular genes in samples.

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A novel tsRNA, m7G-3' tiRNA LysTTT, promotes bladder cancer malignancy via regulating ANXA2 phosphorylation

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Expression data of J3T-1, J3T-2, J3T-1shA, J3T-2A glioma

Project description:We have previously established two sibling glioma subclones, J3T-1 and J3T-2, showing distinct invasive and angiogenic phenotypes. J3T-1, expressing high annexin A2, demonstrates robust angiogenesis and tumor invasion around neovasculature. J3T-2, expressing low annexin A2, demonstrates diffuse invasion along white matter tracts. Knockdown of annexin A2 in J3T-1 (J3T-1shA) resulted in diffuse invasion pattern, and overexpression of annexin A2 in J3T-2 (J3T-2A) showed prominent angiogenesis. We used microarrays to identify genes which promote the phenotypic transition regulated by annexin A2.

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Activation of YAP-dependent Proliferation by a Small Molecule Targeting Annexin A2

Project description:The transcriptional coactivator YAP orchestrates a pro-proliferative transcriptional program that controls the fate of somatic stem cells and the regenerative responses of certain tissues. As such, agents that activate YAP may hold therapeutic potential in disease states exacerbated by insufficient proliferative repair. Here we report the discovery of a small molecule, termed PY-60, which robustly activates YAP transcriptional activity in vitro and promotes YAP-dependent expansion of epidermal keratinocytes in mouse upon topical administration of drug. Chemical proteomics revealed the relevant target of PY-60 to be Annexin A2 (ANXA2), a protein that directly associates with YAP at the cell membrane in response to increased cell density. PY-60 treatment liberates ANXA2 from the membrane, ultimately promoting a phosphatase bound, non-phosphorylated, and transcriptionally active form of YAP. This work reveals ANXA2 to be a previously undescribed, druggable component of the Hippo pathway and suggests a mechanistic rationale for promoting YAP-dependent regenerative repair in disease.

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Project description:Glioblastoma (GBM) is the most devastating tumour of the brain, endowed with a fatal prognosis. Indeed, the complete eradication of cancer cell disseminated outside the GBM mass still remains a crucial issue. Given the reported strong association existing between Annexin 2A (ANXA2) expression and cell dissemination in many cancers, we evaluated the effects exerted by the modulation of ANXA2 levels in GBM cells and assessed its potential in predicting patient outcome. Here, we show that expression of ANXA2 positively correlates with metastatic gene signatures and demonstrates to be prognostic by itself. Indeed, we prove that ANXA2 is involved in cell migration, invasion, cytoskeletal remodeling and proliferation in GBM cells. Moreover, we were able to construct a gene signature representative of ANXA2 inhibition, which showed a significant prognostic potential in different GBM patient cohorts. In this study, we demonstrate that ANXA2 acts at multiple levels in determining the disseminating and aggressive behaviour of GBM tumours. In particular, we clearly show that ANXA2 is involved in determining a migrating and disseminating phenotype of GBM cells, in controlling specific cell cycle checkpoints and a cytoskeletal remodeling associated to cell movement. These data sustain the potential of ANXA2 as a possible target and strong prognostic factor in the future management of GBM patients. Gene expression was measured on Affymetrix in 4 independent experiments of primary GBM cells treated with an ANXA2 neutralizing antibody

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