ArticleCancer science2022
Complement C1q binding protein regulates T cells' mitochondrial fitness to affect their survival, proliferation, and anti-tumor immune function.
Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- T Cell Exhaustion in Cancer Immunotherapy: Heterogeneity, Mechanisms, and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Unveiling the mysteries of C1QBP in gynecological tumors (Review).Molecular and clinical oncology · 2026Review
- Reprogramming myeloid cells and restoring T cell fitness in checkpoint inhibitor resistant melanoma patients.Biomarker research · 2026Article
- Construction of circadian clock signature for tumor microenvironment in predicting survival of esophageal squamous cell carcinoma.Frontiers in immunology · 2026Article
- C1QBP Associated With Immune Infiltration Predicts Poor Prognosis in Lung Adenocarcinoma.Cancer informatics · 2026Article
- αPD-1-conjugated acid-cleavable nanodrugs overcomes cellular immunotherapy barriers in pancreatic tumors.Nature communications · 2025Article
- TIPE2 Protects Bronchial Epithelial Cells From Pyroptosis and Oxidative Stress by Interacting With the E3 Ubiquitin Ligase FBW1A in Asthmatic Mice.Journal of biochemical and molecular toxicology · 2025Article
- Proteomic Profiling of EUS-FNA Samples Differentiates Pancreatic Adenocarcinoma from Mass-Forming Chronic Pancreatitis.Biomedicines · 2025Article
- Mitochondrial Metabolism in T-Cell Exhaustion.International journal of molecular sciences · 2025Review
- C1QBP Modulates DNA Damage Response and Radiosensitivity in Hepatocellular Carcinoma by Regulating NF-κB Activity.International journal of molecular sciences · 2025Article
- Genome-wide association studies of dairy cattle resistance to digital dermatitis recorded at four distinct lactation stages.Scientific reports · 2025Article
- C1QBP promotes apoptosis of goat fetal turbinate cells via inhibiting the expression of TRIM5 or TNFSF10.Frontiers in veterinary science · 2025Article
- A Machine-Learning Prognostic Model for Colorectal Cancer Using a Complement-Related Risk Signature.Oncology research · 2025Article
- Endogenous complement 1q binding protein (C1qbp) regulates mitochondrial permeability transition and post-myocardial infarction remodeling and dysfunction.Journal of molecular and cellular cardiology · 2024Article
- Monocyte Production of C1q Potentiates CD8American journal of respiratory cell and molecular biology · 2024Article
- Polygenic risk associated with Alzheimer's disease and other traits influences genes involved in T cell signaling and activation.Frontiers in immunology · 2024Article
- Mitochondrial C1QBP is essential for T cell antitumor function by maintaining mitochondrial plasticity and metabolic fitness.Cancer immunology, immunotherapy : CII · 2023Article
- Sertoli Cells Express Accommodation, Survival, and Immunoregulatory Factors When Exposed to Normal Human Serum.Biomedicines · 2023Article
- gC1qR: A New Target for Cancer Immunotherapy.Frontiers in immunology · 2023Review
- Complement C1q binding protein regulates T cells' mitochondrial fitness to affect their survival, proliferation, and anti-tumor immune function.Cancer science · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
T cells survival, proliferation, and anti-tumor response are closely linked to their mitochondrial health. Complement C1q binding protein (C1QBP) promotes mitochondrial fitness through regulation of mitochondrial metabolism and morphology. However, whether C1QBP regulates T cell survival, proliferation, and anti-tumor immune function remains unclear. Our data demonstrated that C1QBP knockdown induced the accumulation of reactive oxygen species (ROS) and the loss of mitochondrial membrane potential to impair T cell mitochondrial fitness. At the same time, C1QBP insufficiency reduced the recruitment of the anti-apoptotic proteins, including Bcl-2 and Bcl-XL, and repressed caspase-3 activation and poly (ADP-ribose) polymerase cleavage, which consequently accelerated the T cell apoptotic process. In contrast, C1QBP knockdown rendered T cells with relatively weaker proliferation due to the inhibition of AKT/mTOR signaling pathway. To investigate the exact role of C1QBP in anti-tumor response, C1QBP
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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.