ArticleThe Journal of biological chemistry2014
Response gene to complement 32 protein promotes macrophage phagocytosis via activation of protein kinase C pathway.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Local administration of regulatory T cells promotes tissue healing.Nature communications · 2024Article
- Novel Candidate Genes Involved in an Initial Stage of White Striping Development in Broiler Chickens.Animals : an open access journal from MDPI · 2024Article
- Diclofenac Disrupts the Circadian Clock and through Complex Cross-Talks Aggravates Immune-Mediated Liver Injury-A Repeated Dose Study in Minipigs for 28 Days.International journal of molecular sciences · 2023Article
- Regulator of Cell Cycle Protein (RGCC/RGC-32) Protects against Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Role of RGC-32 in multiple sclerosis and neuroinflammation - few answers and many questions.Frontiers in immunology · 2022Review
- Dendritic Cells and Macrophages in the Pathogenesis of Psoriasis.Frontiers in immunology · 2022Review
- RGCC balances self-renewal and neuronal differentiation of neural stem cells in the developing mammalian neocortex.EMBO reports · 2021Article
- Article
- Protective Effect of Piplartine against LPS-Induced Sepsis through Attenuating the MAPKs/NF-κB Signaling Pathway and NLRP3 Inflammasome Activation.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Surfactant Protein A, a Novel Regulator for Smooth Muscle Phenotypic Modulation and Vascular Remodeling-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Zerumbone Suppresses the LPS-Induced Inflammatory Response and Represses Activation of the NLRP3 Inflammasome in Macrophages.Frontiers in pharmacology · 2021Article
- Response gene to complement 32 expression in macrophages augments paracrine stimulation-mediated colon cancer progression.Cell death & disease · 2019Article
- RGC-32 and diseases: the first 20 years.Immunologic research · 2019Review
- Response Gene to Complement 32 Maintains Blood Pressure Homeostasis by Regulating α-Adrenergic Receptor Expression.Circulation research · 2018Article
- New insights into the roles of RGC-32.Cellular & molecular immunology · 2018Article
- Response by Cui et al to Letter Regarding Article, "RGC-32 (Response Gene to Complement 32) Deficiency Protects Endothelial Cells From Inflammation and Attenuates Atherosclerosis".Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Pumilio directs deadenylation-associated translational repression of the cyclin-dependent kinase 1 activator RGC-32.Nucleic acids research · 2018Article
- RGC32 Promotes Bleomycin-Induced Systemic Sclerosis in a Murine Disease Model by Modulating Classically Activated Macrophage Function.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- RGC-32 (Response Gene to Complement 32) Deficiency Protects Endothelial Cells From Inflammation and Attenuates Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Response Gene to Complement 32 in Vascular Diseases.Frontiers in cardiovascular medicine · 2018Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Macrophage phagocytosis plays an important role in host defense. The molecular mechanism, especially factors regulating the phagocytosis, however, is not completely understood. In the present study, we found that response gene to complement 32 (RGC-32) is an important regulator of phagocytosis. Although RGC-32 is induced and abundantly expressed in macrophage during monocyte-macrophage differentiation, RGC-32 appears not to be important for this process because RGC-32-deficient bone marrow progenitor can normally differentiate to macrophage. However, both peritoneal macrophages and bone marrow-derived macrophages with RGC-32 deficiency exhibit significant defects in phagocytosis, whereas RGC-32-overexpressed macrophages show increased phagocytosis. Mechanistically, RGC-32 is recruited to macrophage membrane where it promotes F-actin assembly and the formation of phagocytic cups. RGC-32 knock-out impairs F-actin assembly. RGC-32 appears to interact with PKC to regulate PKC-induced phosphorylation of F-actin cross-linking protein myristoylated alanine-rich protein kinase C substrate. Taken together, our results demonstrate for the first time that RGC-32 is a novel membrane regulator for macrophage phagocytosis.
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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.