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BAG3 protein regulates caspase‐3 activation in HIV‐1‐infected human primary microglial cells
Author(s) -
Rosati Alessandra,
Khalili Kamel,
Deshmane Satish L.,
Radhakrishnan Sujatha,
Pascale Maria,
Turco M. Caterina,
Marzullo Liberato
Publication year - 2009
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21604
Subject(s) - apoptosis , heat shock protein , bag3 , biology , microbiology and biotechnology , programmed cell death , necroptosis , cytoplasm , cell , cancer research , gene , genetics
Abstract BAG3, a member of the BAG co‐chaperones family, is expressed in several cell types subjected to stressful conditions, such as exposure to high temperature, heavy metals, drugs. Furthermore, it is constitutively expressed in some tumors. Among the biological activities of the protein, there is apoptosis downmodulation; this appears to be exerted through BAG3 interaction with the heat shock protein (Hsp) 70, that influences cell apoptosis at several levels. We recently reported that BAG3 protein was detectable in the cytoplasm of reactive astrocytes in HIV‐1‐associated encephalopathy biopsies. Here we report that downmodulation of BAG3 protein levels allows caspase‐3 activation by HIV‐1 infection in human primary microglial cells. This is the first reported evidence of a role for BAG3 in the balance of death versus survival during viral infection. J. Cell. Physiol. 218: 264–267, 2009. © 2008 Wiley‐Liss, Inc.