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E, Chaloin L, Fenard D, Devaux C, Chazal N, Briant L: VSV-G pseudotyping rescues HIV-1 CA mutations that impair core assembly or stability. Retrovirology 2008,5(57):1–15. Go6983 Competing interests The authors declare that they have no competing interests. Authors’ contributions AG, GC, and J-BP designed the research; AG, CH, TB, EB, DC, DG, and J-BP carried out the experiment; AG and J-BP analyzed the data; and AG, MR, and ABT 737 J-BP wrote the find more paper. All authors read and approved the final manuscript.”
“Background Chlamydia pneumoniae is a gram negative, obligate intracellular pathogen that has been associated with community-acquired pneumonia , atherosclerosis
, arthritis , and Alzheimer’s disease . C. pneumoniae is characterized by a unique, biphasic life cycle beginning with an infectious, metabolically attenuated elementary body (EB). Chlamydial invasion is initiated by attachment of the EB to the host eukaryotic cell membrane and recruitment of actin to the site of attachment. This Arachidonate 15-lipoxygenase remodeling of the actin cytoskeleton is thought to be mediated by the type III secretion (T3S) effector
protein, the translocated actin recruitment protein (TARP), which facilitates chlamydial entry into the host cell [5, 6]. Bacterial uptake involves modulation of the host MEK-ERK pathway and PI 3-kinase, possibly through the action of T3S effectors [7, 8]. Once internalized, the remainder of the chlamydial life cycle takes place within a parasitophorous membrane-bound vesicle known as an inclusion, where EBs differentiate into the non-infectious, metabolically active form, termed a reticulate body (RB). Within the inclusion, RBs acquire amino acids, nucleotides, lipids and cholesterol from the host cell, events possibly orchestrated via T3S across the inclusion membrane, while at the same time inhibiting apoptosis to ensure survival [9–11]. Golgi fragmentation appears to be a crucial step in intercepting host pathways to obtain these nutrients and compounds, as well as in the maturation of the chlamydiae sps. within the inclusion . The RB interacts with the inclusion membrane until such time as inclusion membrane RB docking sites are no longer available and an unknown signal triggers detachment of the RB from the inclusion membrane followed by asynchronous differentiation into EBs [13, 14]. The newly formed EBs then exit the cell by either cellular lysis or a packaged release mechanism termed extrusion . C.