PLA1A Participates in the Antiviral Innate Immune Response by Facilitating the Recruitment of TANK-Binding Kinase 1 to Mitochondria

Gao, Xiaoxiao; Chen, Dan; Zhou, Yuan; Wang, Yun; Wu, Chunchen; Chen, Jizheng; Wang, Yanyi; Pei, Rongjuan; Chen, Xinwen

doi:10.1159/000489832

Cited by 16 publications

(7 citation statements)

References 39 publications

(59 reference statements)

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“…As a result, TRIM26 bridges interaction between TBK1 with NEMO and facilitates the activation of the antiviral immune response [68]. In addition, varieties of molecules facilitate the formation of TBK1-containing complexes to enhance antiviral responses by directly binding to TBK1, such as ArfGAP domain-containing protein 2 (ADAP2) [69], muscle segment homeobox1 (MSX1) [70], ERassociated protein ZDHHC1 [71], downstream of kinase 3 (DOK3) [72], translocases of outer membrane 70 (Tom70) heat-shock protein of 90 KDa (HSP90) complex [73], IFNinduced TPR protein IFIT3 [74] and phosphatidylserinespecific phospholipase PLA1A [75].…”

Section: Formation Of Functional Tbk1-containing Complexesmentioning

confidence: 99%

TANK-binding kinase 1 as a novel therapeutic target for viral diseases

Zhao

2019

Expert Opinion on Therapeutic Targets

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Introduction: TANK-binding kinase 1 (TBK1) is vital for the induction of antiviral innate immune responses. Both RNA and DNA viral infection induces TBK1 activation, triggers phosphorylation of interferon regulatory factor (IRF) 3 and subsequent expression of type I interferons (IFNs; IFN-α/β). Type I IFNs can induce the expression of numerous antiviral genes called interferon-stimulated genes (ISGs) to build a remarkable antiviral state and limit viral replication. Thus, optimal TBK1 activity is crucial for IRF3-induced type I IFNs expression and ISGs-mediated viral elimination. Areas covered: This review provides an overview of the diverse roles of TBK1 in antiviral innate immune responses, the regulatory mechanisms of TBK1 activity and the implication in antiviral development. Expert opinion: TBK1 is a key kinase against antiviral infection via inducing type I IFNs expression. Multiple types of post-translational modifications of TBK1 tightly regulate TBK1 activity and subsequent TBK1-dependent antiviral responses. The identified regulators of TBK1 unveil regulatory mechanisms of host antiviral innate immunity and immuno-escape mechanism of virus provide strategies to control viral diseases by modulating TBK1 activity.

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Section: Formation Of Functional Tbk1-containing Complexesmentioning

confidence: 99%

TANK-binding kinase 1 as a novel therapeutic target for viral diseases

Zhao

2019

Expert Opinion on Therapeutic Targets

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“…Moreover, two genes, the inflammatory cytokine, CCL5 and the phospholipase, PLA1A that are normally induced by viral infection were downregulated in SARS but not DHOV-infected cells. Because CCL5 is involved in activation of the innate immune response [ 39 ] and knockdown of PLA1A expression suppresses the innate immune signaling induced by RNA viruses [ 40 ], this suggests that SARS-CoV-1 rapidly inhibits the innate antiviral immune response. One possible mechanism of this inhibition was suggested by a study showing that SARS-CoV-1 appears to manipulate host mitochondrial function to evade host innate immune responses [ 41 ]; mitochondrial signaling has been shown to control innate and adaptive immune responses [ 42 ].…”

Section: Resultsmentioning

confidence: 99%

Leveraging publicly available coronavirus data to identify new therapeutic targets for COVID-19

et al. 2021

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Many important questions remain regarding severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the viral pathogen responsible for COVID-19. These questions include the mechanisms explaining the high percentage of asymptomatic but highly infectious individuals, the wide variability in disease susceptibility, and the mechanisms of long-lasting debilitating effects. Bioinformatic analysis of four coronavirus datasets representing previous outbreaks (SARS-CoV-1 and MERS-CoV), as well as SARS-CoV-2, revealed evidence of diverse host factors that appear to be coopted to facilitate virus-induced suppression of interferon-induced innate immunity, promotion of viral replication and subversion and/or evasion of antiviral immune surveillance. These host factors merit further study given their postulated roles in COVID-19-induced loss of smell and brain, heart, vascular, lung, liver, and gut dysfunction.

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“…In this context, however, the responsible LysoPS receptors remain to be elucidated in Table 1. The same group also demonstrated the role of PS-PLA 1 in anti-viral cellular responses [30]. Overexpression of PS-PLA 1 enhances the anti-viral type-I interferon response, which is induced by the infectious Sendai virus, while PS-PLA 1 knockdown reduces the response.…”

Section: Phosphatidylserine-specific Pla1 (Ps-pla1)mentioning

confidence: 89%

Current Knowledge on the Biology of Lysophosphatidylserine as an Emerging Bioactive Lipid

Omi

Kano

Aoki

2021

Cell Biochem Biophys

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Lysophosphatidylserine (LysoPS) is an emerging lysophospholipid (LPL) mediator, which acts through G protein-coupled receptors, like lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P). LysoPS is detected in various tissues and cells and thought to be produced mainly by the deacylation of phosphatidylserine. LysoPS has been known to stimulate degranulation of mast cells. Recently, four LysoPS-specific G protein-coupled receptors (GPCRs) were identified. These GPCRs belong to the P2Y family which covers receptors for nucleotides and LPLs and are predominantly expressed in immune cells such as lymphocytes and macrophages. Studies on knockout mice of these GPCRs have revealed that LysoPS has immune-modulatory functions. Up-regulation of a LysoPS-producing enzyme, PS-specific phospholipase A1, was frequently observed in situations where the immune system is activated including autoimmune diseases and organ transplantations. Therefore, modulation of LysoPS signaling appears to be a promising method for providing therapies for the treatment of immune diseases. In this review, we summarize the biology of LysoPS-producing enzymes and receptors, recent developments in LysoPS signal modulators, and prospects for future therapeutic applications.

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PLA1A Participates in the Antiviral Innate Immune Response by Facilitating the Recruitment of TANK-Binding Kinase 1 to Mitochondria

Cited by 16 publications

References 39 publications

TANK-binding kinase 1 as a novel therapeutic target for viral diseases

TANK-binding kinase 1 as a novel therapeutic target for viral diseases

Leveraging publicly available coronavirus data to identify new therapeutic targets for COVID-19

Current Knowledge on the Biology of Lysophosphatidylserine as an Emerging Bioactive Lipid

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