ArticleJournal of bacteriology2010
A systemic network for Chlamydia pneumoniae entry into human cells.
Article in Journal of bacteriology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- 3-O Sulfated Heparan Sulfate (G2) Peptide Ligand Impairs the Infectivity ofBiomolecules · 2025Article
- ITRAQ-based quantitative proteomics analysis of forest musk deer with pneumonia.Frontiers in veterinary science · 2022Article
- Zika virus genome biology and molecular pathogenesis.Emerging microbes & infections · 2017Review
- Lead Discovery Strategies for Identification of Chlamydia pneumoniae Inhibitors.Microorganisms · 2016Review
- Systematically dissecting the global mechanism of miRNA functions in mouse pluripotent stem cells.BMC genomics · 2015Article
- The Chlamydia effector TarP mimics the mammalian leucine-aspartic acid motif of paxillin to subvert the focal adhesion kinase during invasion.The Journal of biological chemistry · 2014Article
- Construction and application of a protein interaction map for white spot syndrome virus (WSSV).Molecular & cellular proteomics : MCP · 2014Article
- Transcription factor complex AP-1 mediates inflammation initiated by Chlamydia pneumoniae infection.Cellular microbiology · 2013Article
- Article
- Chlamydia pneumoniae binds to the lectin-like oxidized LDL receptor for infection of endothelial cells.Microbes and infection · 2012Article
- Functional modules distinguish human induced pluripotent stem cells from embryonic stem cells.Stem cells and development · 2011Article
- Systems biology approaches to new vaccine development.Current opinion in immunology · 2011Review
- Alzheimer's Disease: APP, Gamma Secretase, APOE, CLU, CR1, PICALM, ABCA7, BIN1, CD2AP, CD33, EPHA1, and MS4A2, and Their Relationships with Herpes Simplex, C. Pneumoniae, Other Suspect Pathogens, and the Immune System.International journal of Alzheimer's disease · 2011Article
- A systemic network triggered by human cytomegalovirus entry.Advances in virology · 2011Article
- Integrated microRNA-mRNA-analysis of human monocyte derived macrophages upon Mycobacterium avium subsp. hominissuis infection.PloS one · 2011Article
- Systems biology approaches to understanding mycobacterial survival mechanisms.Drug discovery today. Disease mechanisms · 2010Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial entry is a multistep process triggering a complex network, yet the molecular complexity of this network remains largely unsolved. By employing a systems biology approach, we reveal a systemic bacterial-entry network initiated by Chlamydia pneumoniae, a widespread opportunistic pathogen. The network consists of nine functional modules (i.e., groups of proteins) associated with various cellular functions, including receptor systems, cell adhesion, transcription, and endocytosis. The peak levels of gene expression for these modules change rapidly during C. pneumoniae entry, with cell adhesion occurring at 5 min postinfection, receptor and actin activity at 25 min, and endocytosis at 2 h. A total of six membrane proteins (chemokine C-X-C motif receptor 7 [CXCR7], integrin beta 2 [ITGB2], platelet-derived growth factor beta polypeptide [PDGFB], vascular endothelial growth factor [VEGF], vascular cell adhesion molecule 1 [VCAM1], and GTP binding protein overexpressed in skeletal muscle [GEM]) play a key role during C. pneumoniae entry, but none alone is essential to prevent entry. The combination knockdown of three genes (coding for CXCR7, ITGB2, and PDGFB) significantly inhibits C. pneumoniae entry, but the entire network is resistant to the six-gene depletion, indicating a resilient network. Our results reveal a complex network for C. pneumoniae entry involving at least six key proteins.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.