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Dynamic response of annexin A11-associated gene expression to cisplatin treatment

ABSTRACT: Based on a time-course study of cisplatin response in ovarian cancer cells with/without suppression of annexin A11 expression using whole genome oligonucleotide microarrays, we identified a set of differentially expressed genes associated with annexin A11 expression and patterns of gene expressions in response to cisplatin exposure. Keywords: human ovarian cancer cell lines 2008 cells (one ovarian cancer cell line) were transfected with ANXA11_RNAi or control_RNAi for 2 days and then treated with 10 ÂµM cisplatin (Sigma) for 0, 8, 16, 24 hours. Total RNA of 8 samples were prepared for gene expression profiling using the Agilent 44K whole genome oligonucleotide microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Jin Song

PROVIDER: E-GEOD-13893 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Dynamic response of annexin A11-associated gene expression to cisplatin treatment

Project description:Based on a time-course study of cisplatin response in ovarian cancer cells with/without suppression of annexin A11 expression using whole genome oligonucleotide microarrays, we identified a set of differentially expressed genes associated with annexin A11 expression and patterns of gene expressions in response to cisplatin exposure. Keywords: human ovarian cancer cell lines

2009-12-01 | GSE13893 | GEO

Proteinase K digestion of Annexin A11 fibrils

Project description:Human Annexin A11 (Uniprot accession no. P50995) head domain (residues 2-196) was recombinantly expressed, purified, fibrilized, and digested by proteinase K. Products were analyzed by LC/MS/MS.

2023-01-20 | MSV000091107 | MassIVE

Homo sapiens

Project description:Dynamic response of annexin A11-associated gene expression to cisplatin treatment

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Annexin 10 promotes invasion in QBC-939 cell

Project description:Annexin family is the largest category of eukaryotic calcium and phospholipid-binding proteins and plays important roles in various physiological processes, including cell differentiation and proliferation. More than 160 Annexin proteins are classified into 65 different speciesAs a new member of Annexin family, the role of ANXA10 in cancer progression is rarely investigated, and its expression and function in CCA need more experiments to reveal.

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Gene Expression Profile of Cisplatin Resistance in Ovarian Cancer Cell Lines

Project description:To determine the signaling networks that are dysregulated in platinum-resistant ovarian cancer, gene expression data were obtained from, and compared between, the ovarian cancer cell line, A2780, and its cisplatin-resistant derivative, A2780cis. Gene expression data from a cisplatin-sensitive ovarian cancer cell line (A2780) were collected and compared to gene expression data from a cisplatin-resistant cell line (A2780cis). 6 independent experiments were completed for both the sensitive and resistant cell lines.

2011-11-05 | E-GEOD-33482 | biostudies-arrayexpress

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.

2016-10-04 | GSE87557 | GEO

Annexin A1 exerts renoprotective effects in experimental crescentic glomerulonephritis

Project description:The glucocorticoid-inducible protein annexin A1 has been shown to function as key-regulator of the resolution phase of inflammation but its role in immune-mediated crescentic glomerulonephritis has not been studied so far. Acute crescentic glomerulonephritis was induced in annexin A1 deficient and wildtype mice using a sheep serum against rat glomerular basement membrane constituents. Alterations in gene expression were determined by RNA-Seq and gene ontology analysis. Intrinsic annexin A1 has a protective effect in reducing pro-inflammatory signals and infiltration of neutrophil granulocytes during crescentic GN. The annexin A1 signaling cascade may therefore provide novel targets for the treatment of inflammatory kidney disease.

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Galectin-3 and prohibitin 1 are autoantigens in IgG4-related cholangitis without protective effects against toxic bile acids

Project description:IgG4-related cholangitis (IRC) is the hepatobiliary manifestation of IgG4-related disease, a systemic B-cell-driven fibroinflammatory disorder. Four autoantigens have recently been described in IgG4-RD; annexin A11, galectin-3, laminin 511-E8, and prohibitin 1. We have previously reported a protective role of annexin A11 and laminin 511-E8 in human cholangiocytes against toxic bile acids. Here we explored a potentially protective role of the carbohydrate binding lectin galectin-3 and the scaffold proteins prohibitin 1 and 2.

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Investigation of over-expressing Annexin receptor cell line with and without agonists

Project description:The therapeutic potential of pro-resolution factors in determining the outcome of inflammatory events has gained ground over the past decade. However, the attention has been focused on the non-genomic effects of these endogenous, anti-inflammatory substances. In this study, we have focused our attention on identifying specific annexin 1 (AnxA1) protein/ALX receptor mediated gene activation, in an effort to identify down-stream genomic targets of this well-known, glucocorticoid induced, pro-resolution factor. In this study, we used four different types of samples (with 2 replicates each):1)cells transfected with the empty pGEX-4T-327 vector and vehicle (PBS) treated; 2)cells transfected with the annexin receptor ALXR (also known as FPR2) and vehicle (PBS) treated; 3)cells transfected with the annexin receptor ALXR and treated with 10uM Ac-26 peptide for 4 hours; 4) cells transfected with the annexin receptor ALXR and treated with 0.5uM Annexin 1 for 4 hours. After the treatments, cells were collected for RNA extraction.

2010-09-28 | E-GEOD-14807 | biostudies-arrayexpress

Regulation of somatosensory mechanotransduction by Annexin A6

Project description:Sensory neuron mechanically-activated slowly adapting currents have been linked to noxious mechanosensation. We identified a Conotoxin, Noxious Mechanosensation Blocker -1, that blocks such currents selectively. Using an active biotinylated form of the toxin we identified 67 binding proteins in sensory neurons and sensory neuron-derived cell lines using mass spectrometry. Annexin A6 was the most frequently identified binding protein. Annexin A6 knockout mice showed an enhanced sensitivity to mechanical stimuli. Rapidly adapting currents were enhanced and slowly adapting channels diminished. The percentage of neurons expressing slowly adapting currents fell and non-responsive neurons increased. Conversely, overexpression of annexin A6 in DRG neurons inhibited rapidly adapting currents without effects on slowly adapting currents. Co-expression of annexin A6 with Piezo 2 led to an inhibition of Piezo-mediated rapidly adapting currents. AAV-mediated gene delivery of annexin A6 to sensory neurons in a mouse model of osteoarthritis attenuated mechanical pain. These data demonstrate a role for annexin A6 in somatosensory mechanotransduction.

2018-04-17 | PXD005718 | Pride

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