p32: A new player in autophagy

Jiao, Haifeng; You, Han

doi:10.1080/23723556.2015.1061097

Cited by 7 publications

(9 citation statements)

References 13 publications

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“…Meanwhile, this study showed that PCV2 Cap act as a predominant regulator to promote porcine cGAS phosphorylation and HDAC6 activation through mediating PI3K/AKT and PKCδ signaling activation. Importantly, PCV2 Cap-binding protein gC1qR (also known as C1QBP/gC1qR/HABP1/p32), a multiligand-binding and multifunctional protein [ 56 , 57 ], is also a crucial regulator for the activation of HDAC6 and HDAC6/autophagy-mediated cGAS degradation in PCV2-infected cells. Taken together, these data demonstrated that PCV2 infection activates the gC1qR/HDAC6/autophagy regulator axis to promote cGAS degradation.…”

Section: Discussionmentioning

confidence: 99%

PCV2 targets cGAS to inhibit type I interferon induction to promote other DNA virus infection

Wang

Chen

et al. 2021

PLoS Pathog

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Viruses use diverse strategies to impair the antiviral immunity of host in order to promote infection and pathogenesis. Herein, we found that PCV2 infection promotes the infection of DNA viruses through inhibiting IFN-β induction in vivo and in vitro. In the early phase of infection, PCV2 promotes the phosphorylation of cGAS at S278 via activation of PI3K/Akt signaling, which directly silences the catalytic activity of cGAS. Subsequently, phosphorylation of cGAS at S278 can facilitate the K48-linked poly-ubiquitination of cGAS at K389, which can been served as a signal for recognizing by the ubiquitin-binding domain of histone deacetylase 6 (HDAC6), to promote the translocation of K48-ubiquitinated-cGAS from cytosol to autolysosome depending on the deacetylase activity of HDAC6, thereby eventually resulting in a markedly increased cGAS degradation in PCV2 infection-induced autophagic cells relative to Earle’s Balanced Salt Solution (EBSS)-induced autophagic cells (a typical starving autophagy). Importantly, we found that PCV2 Cap and its binding protein gC1qR act as predominant regulators to promote porcine cGAS phosphorylation and HDAC6 activation through mediating PI3K/AKT signaling and PKCδ signaling activation. Based on this finding, gC1qR-binding activity deficient PCV2 mutant (PCV2RmA) indeed show a weakened inhibitory effect on IFN-β induction and a weaker boost effect for other DNA viruses infection compared to wild-type PCV2. Collectively, our findings illuminate a systematic regulation mechanism by which porcine circovirus counteracts the cGAS-STING signaling pathway to inhibit the type I interferon induction and promote DNA virus infection, and identify gC1qR as an important regulator for the immunosuppression induced by PCV2.

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Section: Discussionmentioning

confidence: 99%

PCV2 targets cGAS to inhibit type I interferon induction to promote other DNA virus infection

Wang

Chen

et al. 2021

PLoS Pathog

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“…Thus, understanding how C1QBP orchestrates mitophagy to maintain mitochondrial homeostasis could provide critical insights. Jiao et al (2015) reported that C1QBP controlled mitochondrial autophagy to help cells adapt better to the challenging microenvironment (Jiao and You, 2016). Serine/ threonine kinase Unc-51-like kinase-1 (ULK1) is crucial in inducing mitophagy.…”

Section: Complement C1q Binding Protein Is Responsible For Mitochondr...mentioning

confidence: 99%

“… Jiao et al (2015) reported that C1QBP controlled mitochondrial autophagy to help cells adapt better to the challenging microenvironment ( Jiao and You, 2016 ). Serine/threonine kinase Unc-51-like kinase-1 (ULK1) is crucial in inducing mitophagy.…”

Section: Complement C1q Binding Protein Modulation Of Mitochondrial P...mentioning

confidence: 99%

“…The association of C1QBP with mitochondrial RNA and mitochondrial ribosomes is required for some mitochondrial protein translation. Besides, C1QBP is also involved in mitochondrial autophagy to remove the dysfunctional mitochondria to maintain healthy cellular homeostasis ( Jiao et al, 2015 ; Jiao and You, 2016 ). Consequently, C1QBP is integral to mitochondrial fitness, cell metabolism, and survival.…”

Section: Introductionmentioning

confidence: 99%

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C1QBP regulates mitochondrial plasticity to impact tumor progression and antitumor immune response

et al. 2022

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Mitochondrial plasticity including mitochondrial dynamics, metabolic flexibility, and mitochondrial quality control, impact tumor cells’ progression and determine immune cells’ fate. Complement C1q binding protein (C1QBP) plays an indispensable role through regulating mitochondrial morphology, metabolism, and autophagy. C1QBP promotes mitochondrial plasticity to impact tumor metastasis and their therapeutic response. At the same time, C1QBP is involved in regulating immune cells’ maturation, differentiation, and effector function through the enhancement of mitochondrial function. In this regard, manipulation of C1QBP has been shown to adjust the competitive balance between tumor cells and immune cells. In the course of evolution, mitochondrial plasticity has endowed numerous advantages against the relentless microenvironment of tumors. In this current review, we summarize the current knowledge of the mechanism of C1QBP regulation of cancer and immunity. We explain this process in vision of potentially new anticancer therapies.

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“…Complement C11 binding protein (C1QBP, also named p32 and HABP1) is a multifunctional protein which plays a pivotal role in diverse cellular processes such autophagy and cell apoptosis 7 , 8 . It has been reported that C1QBP is mainly localized in the mitochondrial matrix and is less expressed in the cytoplasm, nucleus and on the cell surface 9 - 11 .…”

Section: Introductionmentioning

confidence: 99%

The Mitochondrial Protein C1QBP Promotes Hepatocellular Carcinoma Progression by Enhancing Cell Survival, Migration and Invasion

Hou¹,

Lu²,

Wang³

et al. 2022

J. Cancer

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Backgrounds: Hepatocellular carcinoma (HCC) is a major type of death-causing cancer whose pathological mechanisms are not fully understood. In addition, the identification of effective biomarkers for HCC prognosis is in emergency. Although a variety of studies have shown that Complement C11 binding protein (C1QBP) may play a tumor-promoting or tumor-suppressive role in cancer, the functions and mechanisms of C1QBP in HCC progression are under-investigating. Methods and results: Bioinformatic approaches were employed for checking the expression of C1QBP in HCC patient samples and the association between C1QBP mRNA expression and survival rates of patients with HCC or the promoter methylation of C1QBP . MTT analysis, PI/Annexin V staining, transwell and metabolic flux assays were performed to examine the effects of C1QBP on proliferation, apoptosis, migration, invasion, and oxidative phosphorylation of HCC cells. In the present study, we observed that C1QBP is lower expressed in HCC samples and cell lines. Moreover, high levels of C1QBP were associated with unfavorable outcomes of HCC patients. Loss-of-function assays showed that proliferation, migration and invasion of HCC cells were mitigated while cell apoptosis was augmented upon the loos of C1QBP. Moreover, the oxidative phosphorylation was moderately decreased when C1QBP was depleted. Furthermore, we also investigated the methylation status and copy number variation of C1QBP and analyzed their correlation with its mRNA expression in HCC patients. Finally, we suggested that C1QBP is correlated with genes encoding ribosome RPL-related proteins and mitochondrial MRPL-related proteins in HCC patients. Conclusions: C1QBP is correlated with a poor prognosis of HCC patients and promotes the survival, migration and invasion of HCC cells.

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p32: A new player in autophagy

Cited by 7 publications

References 13 publications

PCV2 targets cGAS to inhibit type I interferon induction to promote other DNA virus infection

PCV2 targets cGAS to inhibit type I interferon induction to promote other DNA virus infection

C1QBP regulates mitochondrial plasticity to impact tumor progression and antitumor immune response

The Mitochondrial Protein C1QBP Promotes Hepatocellular Carcinoma Progression by Enhancing Cell Survival, Migration and Invasion

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