Hijacking of GPCRs and RTKs by pathogens
1Biology Department, College of Arts and Sciences, Khalifa University, PO Box 127788, Abu Dhabi, United Arab Emirates.
Cellular Signalling
|July 12, 2023
Summary
Pathogens hijack host cell surface receptors like G protein-coupled receptors (GPCRs) and receptor tyrosine kinases (RTKs) to infect organisms. Understanding these interactions can lead to new treatments for infectious diseases.
Area of Science:
- Molecular biology
- Cell biology
- Infectious diseases
Background:
- Pathogens utilize host cellular and molecular pathways for survival and spread.
- Cell surface receptors, including GPCRs and RTKs, are common pathogen targets due to their widespread expression and critical cellular roles.
- Pathogen interactions with these receptors disrupt normal host cell signaling.
Purpose of the Study:
- To review major examples of pathogen infections targeting GPCRs and RTKs.
- To elucidate the molecular mechanisms of pathogen-induced hijacking of host signaling pathways.
- To provide a foundation for developing novel anti-infective strategies.
Main Methods:
- Literature review of pathogen-host interactions.
- Analysis of molecular mechanisms involving pathogen effectors/toxins and host receptors.
- Compilation of case studies on GPCR/RTK targeted infections.
Main Results:
- Pathogens directly or indirectly interact with GPCRs and RTKs.
- These interactions interfere with receptor activation and downstream signaling.
- Pathogens manipulate host signaling pathways for their own benefit, enhancing virulence.
Conclusions:
- Pathogen hijacking of GPCR and RTK signaling is a key virulence mechanism.
- Understanding these molecular interactions is crucial for combating infections.
- Pharmacological targeting of GPCRs and RTKs presents a promising therapeutic avenue.
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