Identification of compounds that enhance the anti-lymphoma activity of rituximab using flow cytometric high-content screening

Gasparetto, Maura; Gentry, Tracy; Sebti, Saı̈d M.; O'Bryan, Erica; Nimmanapalli, Ramadevi; Blaskovich, Michelle A.; Bhalla, Kapil N.; Rizzieri, David A.; Haaland, Perry D.; Dunne, John F.; Smith, Clay

doi:10.1016/j.jim.2004.06.003

Cited by 34 publications

(46 citation statements)

References 28 publications

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“…In 2003, Paschen et al [44] reported that 10 and 70 µM of salubrinal efficiently protect rat pheochromocytoma cell line PC-12 against death induced by tunicamycin-mediated ER stress [44]. Moreover, Gasparetto et al [45] demonstrated that salubrinal reduced nephrotoxicity induced by cyclosporine mediated ER stress in rat. Recently Liu et al [28] found that salubrinal protects cardomyocyte from tunicamycin and hypoxia-induced apoptosis via PERKeIF2α signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Salubrinal protects against toxin B-induced CT26 cell death

Chen

Sun

et al. 2017

ABBS

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Clostridium difficile (C. difficile) is considered to be the major cause of the antibiotic-associated diarrhea and pseudomembranous colitis in animals and humans. The prevalence of C. difficile infections (CDI) has been increasing since 2000. Two exotoxins of C. difficile, Toxin A (TcdA) and Toxin B (TcdB), are the main virulence factors of CDI, which can induce glucosylation of Rho GTPases in host cytosol, leading to cell morphological changes, cell apoptosis, and cell death. The mechanism of TcdB-induced cell death has been investigated for decades, but it is still not completely understood. It has been reported that TcdB induces endoplasmic reticulum stress via PERK-eIF2α signaling pathway in CT26 cell line (BALB/C mouse colon tumor cells). In this study, we found that salubrinal, a selective inhibitor of eIF2α dephosphorylation, efficiently protects CT26 cell line against TcdB-induced cell death and tried to explore the mechanism underlying in this protective effect. Our results demonstrated that salubrinal protects CT26 cells from TcdB-mediated cytotoxic and cytopathic effect, inhibits apoptosis and death of the toxin-exposed cells via caspase-9-dependent pathway, eIF2α signaling pathway, and autophagy. These findings will be helpful for the development of CDI therapies.

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Section: Discussionmentioning

confidence: 99%

Salubrinal protects against toxin B-induced CT26 cell death

Chen

Sun

et al. 2017

ABBS

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“…This so-named Diversity Set has been offered as a discovery tool by the DTP to the scientific community, and it has been used repeatedly in assay development and validation. [17][18][19][20][21] All compounds in the DTP repository are identified by a National Service Center (NSC) number, with the name, structure, and chemical and physical properties found at http://www. dtp.nci.nih.gov/branches/dscb/diversity_explanation.html.…”

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confidence: 99%

Overcoming Problems of Compound Storage in DMSO: Solvent and Process Alternatives

2009

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“…A further study determined the potency of salubrinal in ameliorating neurotoxicity produced by cyclosporine-induced endoplasmic reticulum stress response in rats (Gasparetto et al, 2004). Furthermore, salubrinal has been used in the treatment of patients with urinary disease (Katsoulieris et al, 2009) and diabetes (Cnop et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Role of salubrinal in protecting cardiomyocytes from doxorubicin-induced apoptosis

Gong¹,

Wu²,

Liang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. We determined whether salubrinal can protect cardiomyocytes from doxorubicin-induced apoptosis and explored the related mechanisms to provide experimental evidence for exploring novel drug candidates to decrease cardiac toxicity. Neonatal rat cardiomyocytes were isolated, cultured in vitro, and pretreated with salubrinal (10, 20, or 40 μM) to observe their response to doxorubicin-induced cell apoptosis. Lactate dehydrogenase assay, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling staining, and flow cytometry were used to assess the extent of cardiomyocyte apoptosis. Fluorescent probes conjugated with 2',7'-dichlorofluorescein diacetate and a chemiluminescence assay were used to detect the production of reactive oxygen species. Western blotting was employed to quantify expression levels of cleaved caspase-3, cytosolic cytochrome c, and B-cell lymphoma-extra large (Bcl-xL). The mechanisms of salubrinal-related functions were also explored. Salubrinal effectively inhibited doxorubicin-induced reactive oxygen species production and N. Gong et al.

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Identification of compounds that enhance the anti-lymphoma activity of rituximab using flow cytometric high-content screening

Cited by 34 publications

References 28 publications

Salubrinal protects against toxin B-induced CT26 cell death

Salubrinal protects against toxin B-induced CT26 cell death

Overcoming Problems of Compound Storage in DMSO: Solvent and Process Alternatives

Role of salubrinal in protecting cardiomyocytes from doxorubicin-induced apoptosis

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