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| Author(s): |
Camila Bonin Pinto
Total Authors: 1
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| Document type: | Master's Dissertation |
| Press: | São Paulo. |
| Institution: | Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI) |
| Defense date: | 2012-10-11 |
| Examining board members: |
Maristela Martins de Camargo;
Hugo Aguirre Armelin;
Jose Alexandre Marzagao Barbuto
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| Advisor: | Maristela Martins de Camargo |
| Abstract | |
The unfolded protein response (UPR) is a signaling pathway activated by endoplasmic reticulum (ER) stress. Previously we described a patient (Patient P) with Common Variable Immunodeficiency (CVID) whose delayed activation of the UPR associates with accumulation of immunoglobulins and slower rate of proliferation. Our results showed that chronic UPR stress interrupted cell cycling of EBV-B cells through dysruption of the cyclic nature of cyclin A1. This interrption is depend of the cell type and drug. Furthermore, chronic ER stress triggered early apoptosis through activation of the PERK branch of the UPR. EBV-B and ex vivo cells from patient presented low metabolic rate and a high apoptosis rate even in the absence of ER stressors.. We noted that the deficiency of UPR pathway activation by Patient P apears to be on the recognition of unfolded proteins. Our results support the hypothesis that deficient proliferation observed in some CVID patients might be the result of deficient UPR activation. (AU) | |
| FAPESP's process: | 10/04244-3 - Effects of UPR pathways disregulation on cyclin A1 expression by human B lymphocyts |
| Grantee: | Camila Bonin Pinto |
| Support Opportunities: | Scholarships in Brazil - Master |