Literature DB >> 17825295

Toxoplasma gondii: effect of infection on expression of 14-3-3 proteins in human epithelial cells.

Fernando P Monroy1.   

Abstract

14-3-3 Proteins are expressed in most eukaryotes organisms and play varied and crucial roles in a wide range of regulatory processes. In mammalian cells, seven 14-3-3 isoforms have been identified. However, it is not known what effect infection has on 14-3-3 isoform expression. In this study human colonic carcinoma cell lines were infected with Toxoplasma gondii for 24h and expression of 14-3-3 proteins was determined by RT-PCR. HT-29 cells only expressed 3 out of the 7 isoforms while 5 and all 7 isoforms were found in HCT-116 and Caco-2 cells, respectively. Infection had little or no effect in the expression of 14-3-3gamma, epsilon, sigma, and xi; but in HCT-116 cells induced expression of 14-3-3eta and sigma, while 14-3-3beta, eta, and xi were induced in HT-29 cells. If 14-3-3 proteins are involved in cell survival and/or prevention of parasite replication, longer incubation times may be required as no differences in percentage of infection were found among the cell lines at 24h post-infection.

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Year:  2007        PMID: 17825295      PMCID: PMC2244797          DOI: 10.1016/j.exppara.2007.07.008

Source DB:  PubMed          Journal:  Exp Parasitol        ISSN: 0014-4894            Impact factor:   2.011


  34 in total

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Journal:  Vaccine       Date:  2001-12-12       Impact factor: 3.641

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Journal:  Int J Parasitol       Date:  2000-08       Impact factor: 3.981

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Authors:  C B Umbricht; E Evron; E Gabrielson; A Ferguson; J Marks; S Sukumar
Journal:  Oncogene       Date:  2001-06-07       Impact factor: 9.867

10.  A 14-3-3 protein homologue is expressed in feline enteroepithelial-stages of Toxoplasma gondii.

Authors:  T Koyama; T Ohsawa; S Shimada; Y Omata; X Xuan; N Inoue; R Maeda; T Mikami; A Saito
Journal:  Vet Parasitol       Date:  2001-03-05       Impact factor: 2.738

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Journal:  PLoS One       Date:  2009-03-11       Impact factor: 3.240

3.  Glucocorticoids and myosin5b loss of function induce heightened PKA signaling in addition to membrane traffic defects.

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