Refine
Has Fulltext
- yes (16)
Is part of the Bibliography
- yes (16)
Year of publication
Document Type
- Journal article (16)
Language
- English (16)
Keywords
- breast cancer (4)
- CD39 (2)
- CD73 (2)
- Parkinson’s disease (2)
- adenosine (2)
- expression (2)
- immune escape (2)
- immune response (2)
- neurodegeneration (2)
- ovarian cancer (2)
Institute
- Frauenklinik und Poliklinik (12)
- Institut für Virologie und Immunbiologie (3)
- Klinik und Poliklinik für Anästhesiologie (ab 2004) (3)
- Kinderklinik und Poliklinik (2)
- Neurologische Klinik und Poliklinik (2)
- Pathologisches Institut (2)
- Theodor-Boveri-Institut für Biowissenschaften (2)
- Institut für Hygiene und Mikrobiologie (1)
- Institut für Klinische Neurobiologie (1)
- Institut für Medizinische Strahlenkunde und Zellforschung (1)
Obligate intracellular bacteria depend entirely on nutrients from the host cell for their reproduction. Here, we show that obligate intracellular Chlamydia downregulate the central tumor suppressor p53 in human cells. This reduction of p53 levels is mediated by the PI3K-Akt signaling pathway, activation of HDM2, and subsequent proteasomal degradation of p53. The stabilization of p53 in human cells severely impaired chlamydial development and caused the loss of infectious particle formation. DNA-damage-induced p53 interfered with chlamydial development through downregulation of the pentose phosphate pathway (PPP). Increased expression of the PPP key enzyme glucose-6-phosphate dehydrogenase rescued the inhibition of chlamydial growth induced by DNA damage or stabilized p53. Thus, downregulation of p53 is a key event in the chlamydial life cycle that reprograms the host cell to create a metabolic environment supportive of chlamydial growth.