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The MAPK pathway. Model representing the MAPK pathway, which starts with RTKs being activated by extracellular ligands, thus leading to tyrosine autophosphorylation of the receptor's cytoplasmic domain. Adaptor proteins like SHC1 bind to phosphorylated RTKs via SH2 interactions, recruiting other docking proteins such as GRB2. GRB2 activates the guanine nucleotide exchange factor SOS, which then drives the switch of inactive, GDP-bound RAS to active, GTPbound RAS. Activated RAS promotes recruitment, heterodimerization, and activation of RAF, a kinase that phosphorylates and activates MEK. The kinase MEK then activates ERK, which controls gene transcription by regulating several transcription factors through phosphorylation. Figure was modified from Cell Signaling Technology, 2010. 

The MAPK pathway. Model representing the MAPK pathway, which starts with RTKs being activated by extracellular ligands, thus leading to tyrosine autophosphorylation of the receptor's cytoplasmic domain. Adaptor proteins like SHC1 bind to phosphorylated RTKs via SH2 interactions, recruiting other docking proteins such as GRB2. GRB2 activates the guanine nucleotide exchange factor SOS, which then drives the switch of inactive, GDP-bound RAS to active, GTPbound RAS. Activated RAS promotes recruitment, heterodimerization, and activation of RAF, a kinase that phosphorylates and activates MEK. The kinase MEK then activates ERK, which controls gene transcription by regulating several transcription factors through phosphorylation. Figure was modified from Cell Signaling Technology, 2010. 

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Figure 1-2. Developmental cycle of Chlamydia. The chlamydial...
Figure 1-4. The MAPK pathway. Model representing the MAPK pathway,...
Figure 3-1. Graphical representation of Tarp. Tarp amino acid sequences...
Figure 3-2. Multiple alignment of Tarp sequences. Multiple sequence...
+45 Figure 3-3. Quantitative protein interaction mapping. Quantitative data...
Exploitation of host cellular pathways by Chlamydia trachomatis
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  • Jan 2012
Like many bacterial pathogens, C. trachomatis translocates effector proteins into the host cell to manipulate host cell functions. The early phase effector protein Tarp harbors N-terminal SH2 binding sites and a C-terminal SH3 binding site for the interaction with host cell proteins. To assess these interactions, protein microarrays comprising virt...
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... that endogenous levels of RAS are not sufficient to recruit detectable amounts of the GFP reporter ( Bivona et al., 2006). Therefore, cells were cotransfected with mCherry-tagged H-RAS for the overexpression of RAS. HeLa cells were infected with C. trachomatis L2 (phase contrast, MOI 100). RAS activation at the plasma membrane could be detected from 2 min after addition of infectious particles to the cells, decreasing to basal levels after 12 min (Figure 3-14). Further downstream RAS activation, both MEK and ERK phosphorylation increased sharply 5-10 min p.i. in HeLa (Figure 3-15) and End1/E6E7 cells (primary immortalized endocervical cells; data not shown), then decreased to ~20 % and ~10 % above basal levels for MEK and ERK, respectively, after 1 h. MEK/ERK activation was dependent on MOI (data not shown). A similar degree of reduction occurred after stimulation of uninfected SHC1 knockdown cells with inducers of MEK/ERK phosphorylation such as TNFα and EGF (Figure 3-17, A and B). These results show that SHC1 phosphorylation during early infection is ...