Proteomics

Dataset Information

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Helicobacter pylori infection dysregulates gastric proteome

ABSTRACT: The purpose of the study was to define gastric cell-specific proteomic changes, induced by H. pylori oncogenic strains, that are critical for initiation of the gastric carcinogenic cascade. Gastric cell scrapings were harvested from H. pylori-infected and uninfected animals for quantitative proteomic analyses using isobaric tags for relative and absolute quantitation (iTRAQ). Canonical and disease pathway mapping using Ingenuity Pathway Analysis (IPA) identified significantly altered inflammatory and cancer-signaling pathways that included Rab/Ras signaling proteins.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Meriones Unguiculatus

TISSUE(S): Gastric Epithelium, Epithelial Cell

DISEASE(S): Gastric Adenocarcinoma

SUBMITTER: Kristie Lindsey Rose  

LAB HEAD: Kristie Lindsey Rose

PROVIDER: PXD009583 | Pride | 2018-11-23

REPOSITORIES: Pride

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BioRep1_4588_QuantProtein_suppdataTable1_04_2018.xlsx Xlsx
BioRep2_4671_QuantProtein_suppdataTable2_04_2018.xlsx Xlsx
Rep1_tagSummary.1.tsv Tabular
Rep2_tagSummary.1.tsv Tabular
ah_4671_JN_120716_UN1B_115_Inf2B_117_0mM.raw Raw
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Publications

Carcinogenic <i>Helicobacter pylori</i> Strains Selectively Dysregulate the <i>In Vivo</i> Gastric Proteome, Which May Be Associated with Stomach Cancer Progression.

Noto Jennifer M JM   Rose Kristie L KL   Hachey Amanda J AJ   Delgado Alberto G AG   Romero-Gallo Judith J   Wroblewski Lydia E LE   Schneider Barbara G BG   Shah Shailja C SC   Cover Timothy L TL   Wilson Keith T KT   Israel Dawn A DA   Roa Juan Carlos JC   Schey Kevin L KL   Zavros Yana Y   Piazuelo M Blanca MB   Peek Richard M RM  

Molecular & cellular proteomics : MCP 20181119 2

<i>Helicobacter pylori</i> is the strongest risk factor for gastric cancer. Initial interactions between <i>H. pylori</i> and its host originate at the microbial-gastric epithelial cell interface, and contact between <i>H. pylori</i> and gastric epithelium activates signaling pathways that drive oncogenesis. One microbial constituent that increases gastric cancer risk is the <i>cag</i> pathogenicity island, which encodes a type IV secretion system that translocates the effector protein, CagA, in  ...[more]

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