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Liceaga / Aguilar-Toala chia seed protein hydrolysate antimicrobial peptides

ABSTRACT: Aguilar-Toala 2019: Investigators under Andrea Liceaga at Department of Food Science at Purdue University examined the proteomes of chia seeds for their anti-microbial properties and enzyme inhibition [doi:10.1007/s00726-020-02879-4 and doi:10.1007/s12602-020-09653-8]. They followed activity for different size exclusion chromatography fractions of peptides generated through alcalase and flavourzyme digestion. Tandem mass spectra were generated on a Q Exactive Plus by Emma Doud in the Proteomics Core at the Indiana University School of Medicine. The LC-MS/MS experiment representing proteins below 3 kDa was emphasized because it represented the biological activity they sought; the instrument produced 44,208 tandem mass spectra at a rate peaking near 11 Hz. When sequence availability for chia proved to be problematic, Doud made use of PEAKS Studio to infer sequences directly from the fragment ions.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Salvia Hispanica (ncbitaxon:49212)

SUBMITTER: Andrea M. Liceaga

PROVIDER: MSV000086856 | MassIVE | Fri Feb 12 06:18:00 GMT 2021

SECONDARY ACCESSION(S): PXD024163

REPOSITORIES: MassIVE

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Project description:A functional genetic screen to identify genes causing tamoxifen resistance in an estrogen-dependent human breast cancer cell model was performed. By insertion of defective retrovirus into the genome, individual genetic changes were introduced at random in ZR-75-1 cells. Subsequently, infected cells were selected for their ability to proliferate while being exposed to tamoxifen, and from these cultures stable cell lines were established. The retrovirus insertion sites were mapped enabling the identification of several candidate breast cancer anti-estrogen resistance (BCAR) genes. By cDNA transfection of estrogen-dependent cells resulting in their transformation into a tamoxifen-resistant phenotype, proof was provided for the causative role of BCAR genes.A functional genetic screen to identify genes causing tamoxifen resistance in an estrogen-dependent human breast cancer cell model was performed. By insertion of defective retrovirus into the genome, individual genetic changes were introduced at random in ZR-75-1 cells. Subsequently, infected cells were selected for their ability to proliferate while being exposed to tamoxifen, and from these cultures stable cell lines were established. The retrovirus insertion sites were mapped enabling the identification of several candidate breast cancer anti-estrogen resistance (BCAR) genes identified. By cDNA transfection of estrogen-dependent cells resulting in their transformation into a tamoxifen-resistant phenotype, proof was provided for the causative role of BCAR genes (Van Agthoven et al, Breast Cancer Res Treat DOI:10.1007/s10549-008-9969-5, 2008). To elucidate the mechanisms how these individual BCAR genes induce cell proliferation in growth-arrested ZR-75-1 cells, we assessed the gene expression patterns between the different groups of cell lines. Keywords: Expression profiling, reference design RNA was isolated from two independent cultures of 69 tamoxifen-resistant cell lines. Detailed information regarding these cell lines with respect to the viral integration sites, was described previously (Van Agthoven et al, Breast Cancer Res Treat DOI:10.1007/s10549-008-9969-5, 2008). Each sample was hybridized in duplicate/triplicate and once in a dye-swap. The mixture of cell lines used as a reference was detailed previously (Jansen et al, J Clin Oncol 23, 732, 2005).

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Liceaga / Aguilar-Toala chia seed protein hydrolysate antimicrobial peptides

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