Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mechanism of lacritin-dependent production of the important dry eye mucin 'MUC16'

ABSTRACT: Lacritin targets its coreceptor 'syndecan-1' in lacritin-dependent production of the important dry eye mucin 'MUC16'. Real-time PCR analysis suggests that this effect is post-transcriptional. In contrast, serum stimulation of MUC16 by these cells is transcriptionally dependent. Our goal is to determine whether this regulation is global to other heavily O-glycosylated proteins, and if so, if it is dependent on transcription of a Golgi glycosyltransferases. If not, the mechanism might be microRNA dependent.

ORGANISM(S): Homo sapiens

PROVIDER: GSE31930 | GEO | 2011/09/06

SECONDARY ACCESSION(S): PRJNA145025

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Mechanism of lacritin-dependent production of the important dry eye mucin 'MUC16'

Project description:Lacritin targets its coreceptor 'syndecan-1' in lacritin-dependent production of the important dry eye mucin 'MUC16'. Real-time PCR analysis suggests that this effect is post-transcriptional. In contrast, serum stimulation of MUC16 by these cells is transcriptionally dependent. Our goal is to determine whether this regulation is global to other heavily O-glycosylated proteins, and if so, if it is dependent on transcription of a Golgi glycosyltransferases. If not, the mechanism might be microRNA dependent. Among other glycogenes, expression of heparanases, sulfotransferases and epimerase are also of interest. Heparanase is required for lacritin binding to its co-receptor syndecan-1 and this binding site may require a sulfated iduronic acid. In request 1705, we recently asked core D whether they could generate this sulfate iduronic acid-containing glycan (iduronic acid (2-O-sulfated)-N-acetylglucosamine-glucuronic acid-N-acetylglucosamine-[glucuronic acid-N-acetylglucosamine]5-glucuronic acid-galactose-galactose-SERINE) to test as a competitive inhibitor in binding studies. Our experiment is to compare Glyco-gene expression by human corneal epithelial cells in response to cell communication glycoprotein 'lacritin' versus negative control deletion construct 'C-25 lacritin' and versus positive control serum.

2011-09-05 | E-GEOD-31930 | biostudies-arrayexpress

MUC16 is a critical molecule for the pancreatic tumor microenvironment and metastasis in PDAC

Project description:Investigate the cooperative action of MUC16 with other defined oncogenic mutations in the metastasis of PC using Muc16–/– mice

2022-10-22 | GSE212777 | GEO

Influence of the MUC16 on gene expression of cancer cells from PDAC

Project description:To investigate the differentially expressed genes and the pathways they might alter upon loss of MUC16 and subsequent perturbation of its downstream signaling We performed gene expression profiling analysis using data obtained from RNA-seq of the two different conditions (WT versus MUC16-knockout) (three replicates each).

2024-11-30 | GSE247666 | GEO

Immunoaffinity-free chromatographic purification of ovarian cancer biomarker CA125 (MUC16) from blood serum

Project description:The present work developed a non-affinity-based chromatographic method to enrich MUC16 from serum. The enriched MUC16 sample was further processed using a Midi Top 14 abundant protein depletion column. Peptides identified using bottom-up proteomics yielded 1–8% coverage of MUC16. Additionally, MUC16 was detected in samples containing less than the clinical cut-off level of CA125 (35 U/mL), suggesting that this strategy of enrichment and bottom-up proteomics can enable analysis of CA125 from serum of individuals with early-stage ovarian cancer and those whose tumors express CA125 (MUC16) at low levels.

2024-10-17 | PXD053289 | Pride

A revised molecular model of ovarian cancer biomarker CA125 (MUC16) enabled by long-read sequencing

Project description:The biomarker CA125, a peptide epitope located in several tandem repeats of the mucin MUC16, is the gold-standard for monitoring regression and recurrence of high-grade serous ovarian cancer in response to therapy. However, the CA125 epitope along with several structural features of the MUC16 molecule are ill-defined. One central aspect still unresolved is the number of tandem repeats in MUC16 and how many of these contain the CA125 epitope. Studies from the early 2000s assembled short DNA reads to estimate that MUC16 contained 63 repeats. Here, we conduct Nanopore long-read sequencing of MUC16 transcripts from three primary ovarian tumors and established cell lines (OVCAR3, OVCAR5, and Kuramochi) for a more exhaustive and accurate estimation and sequencing of the MUC16 tandem repeats. The consensus sequence derived from these six sources was confirmed by proteomics validation and agrees with recent additions to the NCBI database. We propose a model of MUC16 containing 19—not 63—tandem repeats. Additionally, we predict the structure of the tandem repeat domain using the deep-learning algorithm, AlphaFold. The predicted structure displays an SEA domain and unstructured linker region rich in proline, serine, and threonine residues in all 19 tandem repeats. Our studies now pave the way for a detailed characterization of the CA125 epitope. Sequencing and modeling of the MUC16 tandem repeats along with their glycoproteomic characterization, currently underway in our laboratories, will help identify novel epitopes in the MUC16 molecule that improve on the sensitivity and clinical utility of the current CA125 assay.

2024-05-21 | PXD044117 | Pride

Focus on Molecules: human mucin MUC16.

Project description: Not available

| S-EPMC2586928 | biostudies-literature

Interferon-gamma/TNF-treated human corneal epithelial cells

Project description:Our experiment is to compare Glyco-gene expression by interferon-gamma/TNF-treated human corneal epithelial cells also treated either with cell communication glycoprotein 'lacritin' or negative control deletion construct 'C-25 lacritin'. In a newly developing story, lacritin but not C-25 protects human corneal epithelial cells from INFG/TNF-induced cell death. This expression array will help work out the mechanism of protection to complement phosphoblotting and shRNA approaches currently underway. Lacritin targets its coreceptor 'syndecan-1' in lacritin-dependent cell proliferation and secretion. Lacritin appears to be important in human 'dry eye' and in promoting corneal epithelial cell survival in the presence of inflammatory cytokines.

2011-09-05 | E-GEOD-31931 | biostudies-arrayexpress

Glycogene expression in control and tumor-bearing mouse muscles

Project description:We have observed aberrant glycosylation in membrane proteins in mouse skeletal muscles undergoing cachexia ( muscle wasting) in a tumor bearing condition. Since multiple proteins were glycosylated in this tumor state, we are interested in looking at the glycochip array that includes glycosyltransferases to observe any possible induction of these transferases.

2011-04-29 | GSE28930 | GEO

Fibronectin regulates Wnt7a signaling and satellite cell expansion

Project description:The influence of the extracellular matrix (ECM) within the stem cell niche remains poorly understood. We found that Syndecan-4 (Sdc4) and Frizzled-7 (Fzd7) form a coreceptor complex in satellite cells and that binding of the ECM glycoprotein Fibronectin (FN) to Sdc4 stimulates the ability of Wnt7a to induce the symmetric expansion of satellite stem cells. Newly activated satellite cells dynamically remodel their niche via transient high-level expression of FN. Knockdown of FN in prospectively isolated satellite cells severely impaired their ability to repopulate the satellite cell niche. Conversely, in vivo overexpression of FN with Wnt7a dramatically stimulated the expansion of satellite stem cells in regenerating muscle. Therefore, activating satellite cells remodel their niche through autologous expression of FN that provides feedback to stimulate Wnt7a signaling through the Fzd7/Sdc4 coreceptor complex. Thus, FN and Wnt7a together regulate the homeostatic levels of satellite stem cells and satellite myogenic cells during regenerative myogenesis. The data set contains one microarray of pooled quiescent skeletal muscle satellite cells

2014-07-11 | E-GEOD-59272 | biostudies-arrayexpress

Medication for acromegaly reduces expression of MUC16, MACC1 and GRHL2 in pituitary neuroendocrine tumour tissue

Project description:Acromegaly is a disease mainly caused by pituitary neuroendocrine tumours (PitNETs) overproducing growth hormone. First-line medication for this condition is the use of somatostatin analogues (SSAs), that decrease tumour mass and induce antiproliferative effects on PitNET cells. Dopamine agonists (DAs) can also be used, if SSA treatment is not effective. This study aimed to determine differences in transcriptome signatures induced by SSA/DA therapy in PitNET tissue. We selected tumour tissue from twelve patients with somatotrophinomas, with half of the patients receiving SSA/DA treatment before surgery, and the other half treatment naive. Transcriptome sequencing was then carried out to identify differentially expressed genes (DEGs) and their protein-protein interactions, using pathway analyses. We found 34 upregulated and six downregulated DEGs in patients with SSA/DA treatment. Three tumour development promoting factors MUC16, MACC1 and GRHL2, were significantly downregulated in therapy administered PitNET tissue. Protein-protein interactions and pathway analyses revealed extracellular matrix involvement in the antiproliferative effects of this type of the drug treatment, with pronounced alterations in collagen regulation. Here, we have demonstrated that somatotrophinomas can be distinguished based on their transcriptional profiles following SSA/DA therapy, and SSA/DA treatment does indeed cause changes in gene expression. Treatment with SSA/DA, significantly downregulated several factors involved in tumourigenesis, including MUC16, MACC1 and GRHL2. Genes that were upregulated, however, did not have a direct influence on antiproliferative function in the PitNET cells. These findings suggested that SSA/DA treatment acted in a tumour suppressive manner and furthermore, collagen related interactions and pathways were enriched, implicating extracellular matrix involvement in this anti-tumour effect of drug treatment.

2020-10-28 | GSE160195 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data