Signaling pathways involved in regulating apoptosis induction in host cells upon PRRSV infection
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Summary
The potential signaling pathways that contribute to PRRSV-induced apoptosis are summarized, and the issues that need to be addressed in future studies are proposed for a better understanding of the molecular basis underlying the pathogenesis of PRRS.
- Type
- review
- Published
- 2019-04-19
- Cited by
- 13
- References
- 73
- OpenAlex
- https://openalex.org/W2936331370
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:123174651
Keywords
Biology, Porcine reproductive and respiratory syndrome virus, Pathogenesis, Apoptosis, Signal transduction
References
- Ultrastructural pathogenesis of the PRRS virus.
- Direct Activation of Bax by p53 Mediates Mitochondrial Membrane Permeabilization and Apoptosis
- Induction of ROS generation and NF-κB activation in MARC-145 cells by a novel porcine reproductive and respiratory syndrome virus in Southwest of China isolate
- p53 in survival, death and metabolic health: a lifeguard with a licence to kill
- JNK and p38 Mitogen-Activated Protein Kinase Pathways Contribute to Porcine Circovirus Type 2 Infection
- Autophagy sustains the replication of porcine reproductive and respiratory virus in host cells
- Involvement of unfolded protein response, p53 and Akt in modulation of porcine reproductive and respiratory syndrome virus-mediated JNK activation.
- Autophagic cell death: the story of a misnomer
- Coupling endoplasmic reticulum stress to the cell death program
- Induction of autophagy enhances porcine reproductive and respiratory syndrome virus replication
- Activation of c-Jun NH(2)-terminal kinase is required for porcine reproductive and respiratory syndrome virus-induced apoptosis but not for virus replication.
- From acute ER stress to physiological roles of the Unfolded Protein Response
- Porcine reproductive and respiratory syndrome virus infection activates NOD2-RIP2 signal pathway in MARC-145 cells.
- Control of the PI3K/Akt pathway by porcine reproductive and respiratory syndrome virus
- Porcine reproductive and respiratory syndrome virus induces autophagy to promote virus replication
- Role of phosphatidylinositol 3-kinase (PI3K) and Akt1 kinase in porcine reproductive and respiratory syndrome virus (PRRSV) replication
- Cell death modalities: classification and pathophysiological implications
- Protective mechanisms of p53-p21-pRb proteins against DNA damage-induced cell death
- Viral Control of Mitochondrial Apoptosis
- Porcine reproductive and respiratory syndrome virus (PRRSV) causes apoptosis during its replication in fetal implantation sites.
Cited by
- Molecular and Cellular Mechanisms for PRRSV Pathogenesis and Host Response to Infection
- TREM2 suppresses the proinflammatory response to facilitate PRRSV infection via PI3K/NF-κB signaling
- Distinctive Cellular and Metabolic Reprogramming in Porcine Lung Mononuclear Phagocytes Infected With Type 1 PRRSV Strains
- Antiviral Mechanism of Tea Polyphenols against Porcine Reproductive and Respiratory Syndrome Virus
- Regulation of antiviral immune response by African swine fever virus (ASFV)
- Systematic Identification and Comparison of the Expressed Profiles of Exosomal MiRNAs in Pigs Infected with NADC30-like PRRSV Strain
- Pathological observation and transcriptomic analysis of thymus injury in PRRSV-infected piglets
- Histopathological Pulmonary Lesions in 1st-Day Newborn Piglets Derived from PRRSV-1 MLV Vaccinated Sows at the Last Stage of Gestation
- African swine fever virus proteins against host antiviral innate immunity and their implications for vaccine development
- A Comprehensive Review on Porcine Reproductive and Respiratory Syndrome Virus with Emphasis on Immunity
- Mitochondrial dysfunction in PRRSV-2-infected macrophages
- Single-cell RNA sequencing reveals immune response dynamics and infection mechanisms in PRRSV-infected porcine alveolar macrophages.
- Development and validation of a dual-fluorescent isothermal enzymatic recombinase amplification assay for the rapid differentiation of porcine reproductive and respiratory syndrome virus-1 and porcine reproductive and respiratory syndrome virus-2.
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