ArticleThe Journal of biological chemistry2014
NF-κB and enhancer-binding CREB protein scaffolded by CREB-binding protein (CBP)/p300 proteins regulate CD59 protein expression to protect cells from complement attack.
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 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Molecular characterization ofOpen veterinary journal · 2026Article
- Exploring the role of glucocorticoid receptors and co-chaperones in Pemphigus foliaceus stratification.Archives of dermatological research · 2025Article
- Pre-existing cell subpopulations in primary prostate cancer tumors display surface fingerprints of docetaxel-resistant cells.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Expression of CREBBP and EP300 Associated With Tumor Volume in Patients With Grade-3 Glioma: A Retrospective Analysis.Clinical Medicine Insights. Oncology · 2024Article
- Article
- Complement and complement regulatory proteins are upregulated in lungs of COVID-19 patients.Pathology, research and practice · 2023Article
- Near-Death Cells Cause Chemotherapy-Induced Metastasis via ATF4-Mediated NF-κB Signaling Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Sulforaphene suppresses oesophageal cancer growth through mitogen- and stress-activated kinase 2 in a PDX mouse model.American journal of cancer research · 2023Article
- Potentiating effect of reovirus on immune checkpoint inhibition in microsatellite stable colorectal cancer.Frontiers in oncology · 2022Article
- PHLPP Signaling in Immune Cells.Current topics in microbiology and immunology · 2022Review
- Abiraterone Acetate Induces CREB1 Phosphorylation and Enhances the Function of the CBP-p300 Complex, Leading to Resistance in Prostate Cancer Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Herbal NF-κB Inhibitors Sensitize Rituximab-Resistant B Lymphoma Cells to Complement-Mediated Cytolysis.Frontiers in oncology · 2021Article
- Novel genetic variants in HDAC2 and PPARGC1A of the CREB-binding protein pathway predict survival of non-small-cell lung cancer.Molecular carcinogenesis · 2020Article
- SIK1 Regulates CRTC2-Mediated Gluconeogenesis Signaling Pathway in Human and Mouse Liver Cells.Frontiers in endocrinology · 2020Article
- Effects of the Bone/Bone Marrow Microenvironments on Prostate Cancer Cells and CD59 Expression.BioMed research international · 2020Article
- Inhibition of CREB-mediated ZO-1 and activation of NF-κB-induced IL-6 by colonic epithelial MCT4 destroys intestinal barrier function.Cell proliferation · 2019Article
- Overexpression of CD59 inhibits apoptosis of T-acute lymphoblastic leukemia via AKT/Notch1 signaling pathway.Cancer cell international · 2019Article
- CapG promotes resistance to paclitaxel in breast cancer through transactivation of PIK3R1/P50.Theranostics · 2019Article
- Quetiapine ameliorates collagen-induced arthritis in mice via the suppression of the AKT and ERK signaling pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Article
- Stability and bioactivity of chitosan as a transfection agent in primary human cell cultures: A case for chitosan-only controls.Carbohydrate polymers · 2018Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement system can be activated spontaneously for immune surveillance or induced to clear invading pathogens, in which the membrane attack complex (MAC, C5b-9) plays a critical role. CD59 is the sole membrane complement regulatory protein (mCRP) that restricts MAC assembly. CD59, therefore, protects innocent host cells from attacks by the complement system, and host cells require the constitutive and inducible expression of CD59 to protect themselves from deleterious destruction by complement. However, the mechanisms that underlie CD59 regulation remain largely unknown. In this study we demonstrate that the widely expressed transcription factor Sp1 may regulate the constitutive expression of CD59, whereas CREB-binding protein (CBP)/p300 bridge NF-κB and CREB, which surprisingly functions as an enhancer-binding protein to induce the up-regulation of CD59 during in lipopolysaccharide (LPS)-triggered complement activation, thus conferring host defense against further MAC-mediated destruction. Moreover, individual treatment with LPS, TNF-α, and the complement activation products (sublytic MAC (SC5b-9) and C5a) could increase the expression of CD59 mainly by activating NF-κB and CREB signaling pathways. Together, our findings identify a novel gene regulation mechanism involving CBP/p300, NF-κB, and CREB; this mechanism suggests potential drug targets for controlling various complement-related human diseases.
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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.