HRES-1/Rab4-mediated depletion of Drp1 impairs mitochondrial homeostasis and represents a target for treatment in SLE

Tiffany N. Caza, David R. Fernandez, Gergely Talaber, Zachary Oaks, Mark Haas, Michael P. Madaio, Zhi Wei Lai, Gabriella Miklossy, Ram R. Singh, Dmitriy M. Chudakov, Walter Malorni, Frank Middleton, Katalin Banki, Andras Perl

Research output: Contribution to journalArticle

61 Scopus citations

Abstract

Objective: Accumulation of mitochondria underlies T-cell dysfunction in systemic lupus erythematosus (SLE). Mitochondrial turnover involves endosomal traffic regulated by HRES-1/Rab4, a small GTPase that is overexpressed in lupus T cells. Therefore, we investigated whether (1) HRES-1/Rab4 impacts mitochondrial homeostasis and (2) Rab geranylgeranyl transferase inhibitor 3-PEHPC blocks mitochondrial accumulation in T cells, autoimmunity and disease development in lupusprone mice.

Original languageEnglish (US)
Pages (from-to)1888-1897
Number of pages10
JournalAnnals of the rheumatic diseases
Volume73
Issue number10
DOIs
StatePublished - Jan 1 2014

ASJC Scopus subject areas

  • Immunology and Allergy
  • Rheumatology
  • Immunology
  • Biochemistry, Genetics and Molecular Biology(all)

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    Caza, T. N., Fernandez, D. R., Talaber, G., Oaks, Z., Haas, M., Madaio, M. P., Lai, Z. W., Miklossy, G., Singh, R. R., Chudakov, D. M., Malorni, W., Middleton, F., Banki, K., & Perl, A. (2014). HRES-1/Rab4-mediated depletion of Drp1 impairs mitochondrial homeostasis and represents a target for treatment in SLE. Annals of the rheumatic diseases, 73(10), 1888-1897. https://doi.org/10.1136/annrheumdis-2013-203794