<?xml version="1.0" encoding="ASCII"?>
<biogps><data><item key="owner">ArrayExpress Uploader</item><item key="ownerprofile_id">arrayexpress_sid</item><item key="species">human</item><item key="factors"><item><item key="GSM587958 1"/></item><item><item key="GSM587959 1"/></item><item><item key="GSM587960 1"/></item><item><item key="GSM587961 1"/></item><item><item key="GSM587962 1"/></item><item><item key="GSM587963 1"/></item><item><item key="GSM587964 1"/></item><item><item key="GSM587965 1"/></item></item><item key="id">3792</item><item key="pop_total">0</item><item key="platform">4</item><item key="summary_wrapped">Protein homeostasis in the endoplasmic reticulum (ER) has recently emerged as a therapeutic target for cancer treatment. Disruption of ER...</item><item key="geo_gse_id">E-GEOD-23849</item><item key="owner_profile">/profile/8773/arrayexpressuploader</item><item key="factor_count">0</item><item key="sample_count">8</item><item key="tags"><item>cancer</item><item>cell</item><item>class</item><item>endoplasmic reticulum</item><item>lymphoma</item><item>mantle cell lymphoma</item><item>membrane</item><item>multiple myeloma</item><item>myeloma</item><item>protein</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_id_plat">E-GEOD-23849_A-AFFY-44</item><item key="slug">the-erad-inhibitor-eeyarestatin-i-is-a-bifunctiona</item><item key="geo_gds_id"/><item key="name">The ERAD inhibitor Eeyarestatin I is a bifunctional compound with an ER localizing domain and a p97/VCP inhibitory group</item><item key="created">Sep.15, 2014</item><item key="summary">Protein homeostasis in the endoplasmic reticulum (ER) has recently emerged as a therapeutic target for cancer treatment. Disruption of ER homeostasis results in ER stress, which is a major cause of cell death for cells exposed to the proteasome inhibitor Bortezomib, an anti-cancer drug approved for treatment of multiple myeloma and Mantle cell lymphoma. We recently reported that the ERAD inhibitor Eeyarestatin I (EerI) also disturbs ER homeostasis and has anti-cancer activities resembling that of Bortezomib. Our findings reveal a class of bifunctional chemical agents that can preferentially inhibit membrane-bound p97 to disrupt ER homeostasis and induce tumor cell death. These results also suggest that the AAA ATPase p97 may be a potential drug target for cancer therapy. Cells were treated with EerI, CBU-028, or 5-NA each at 10uM in duplicates for 10h</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-23849</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-23849/samples/</item></data></biogps>
