| Mitochondrial C1QBP is essential for T cell antitumor function by maintaining mitochondrial plasticity and metabolic fitness. | Mitochondrial C1QBP is essential for T cell antitumor function by maintaining mitochondrial plasticity and metabolic fitness.
Tian H, Chai D, Wang G, Wang Q, Sun N, Jiang G, Li H, Song J, Fang L, Wang M, Guo Z, Zheng J. | 06/15/2023 |
| Complement C1q binding protein regulates T cells' mitochondrial fitness to affect their survival, proliferation, and anti-tumor immune function. | Complement C1q binding protein regulates T cells' mitochondrial fitness to affect their survival, proliferation, and anti-tumor immune function.
Tian H, Wang G, Wang Q, Zhang B, Jiang G, Li H, Chai D, Fang L, Wang M, Zheng J., Free PMC Article | 03/12/2022 |
| Mitochondrial translation deficiency impairs NAD(+) -mediated lysosomal acidification. | Mitochondrial translation deficiency impairs NAD(+) -mediated lysosomal acidification.
Yagi M, Toshima T, Amamoto R, Do Y, Hirai H, Setoyama D, Kang D, Uchiumi T., Free PMC Article | 10/23/2021 |
| Protective immune response against P32 oncogenic peptide-pulsed PBMCs in mouse models of breast cancer. | Protective immune response against P32 oncogenic peptide-pulsed PBMCs in mouse models of breast cancer.
Dehghan-Manshadi M, Nikpoor AR, Hadinedoushan H, Zare F, Sankian M, Fesahat F, Rafatpanah H. | 05/29/2021 |
| p32/C1QBP regulates OMA1-dependent proteolytic processing of OPA1 to maintain mitochondrial connectivity related to mitochondrial dysfunction and apoptosis. | p32/C1QBP regulates OMA1-dependent proteolytic processing of OPA1 to maintain mitochondrial connectivity related to mitochondrial dysfunction and apoptosis.
Noh S, Phorl S, Naskar R, Oeum K, Seo Y, Kim E, Kweon HS, Lee JY., Free PMC Article | 12/19/2020 |
| Arginase II activity-dependent production of spermine augments Ca(2+) transition from the cytosol to the mitochondria in a mitochondrial p32 protein -dependent manner and regulates CaMKII-dependent constriction in vascular smooth muscle cells. | Arginase II activity regulates cytosolic Ca(2+) level in a p32-dependent manner that contributes to Ca(2+)-dependent vasoconstriction in native low-density lipoprotein-stimulated vascular smooth muscle cells.
Koo BH, Hong D, Hong HD, Lim HK, Hoe KL, Won MH, Kim YM, Berkowitz DE, Ryoo S., Free PMC Article | 06/27/2020 |
| Dendritic cell maturation is regulated by citrate production via p32-dependent pyruvate dehydrogenase [PDH] complex activity. | Mitochondrial p32/C1qbp Is a Critical Regulator of Dendritic Cell Metabolism and Maturation.
Gotoh K, Morisaki T, Setoyama D, Sasaki K, Yagi M, Igami K, Mizuguchi S, Uchiumi T, Fukui Y, Kang D. | 12/14/2019 |
| Here, we found that mice lacking p32 in the central nervous system (p32cKO mice) showed white matter degeneration accompanied by progressive oligodendrocyte loss, axon degeneration and vacuolation in the mid brain and brain stem regions. Furthermore, p32cKO mice died within 8 weeks of birth. | Neural-specific deletion of mitochondrial p32/C1qbp leads to leukoencephalopathy due to undifferentiated oligodendrocyte and axon degeneration.
Yagi M, Uchiumi T, Sagata N, Setoyama D, Amamoto R, Matsushima Y, Kang D., Free PMC Article | 07/13/2019 |
| Data show that p32 (C1QBP) plays a critical role in energy homeostasis and represents a potential target for the development of anti-obesity drugs | p32 heterozygosity protects against age- and diet-induced obesity by increasing energy expenditure.
Liu Y, Leslie PL, Jin A, Itahana K, Graves LM, Zhang Y., Free PMC Article | 02/23/2019 |
| p32 promotes lipid biosynthesis by modulating fatty acid-induced ER stress. p32 interacts with GCS1 and reduces GCS1 in a lysosome-dependent manner. | p32 regulates ER stress and lipid homeostasis by down-regulating GCS1 expression.
Liu Y, Leslie PL, Jin A, Itahana K, Graves LM, Zhang Y., Free PMC Article | 02/16/2019 |
| these results demonstrate that host-derived p32 has an important immunomodulating function that helps to counterbalance an overwhelming danger-associated molecular patterns response | Immunoregulation of Neutrophil Extracellular Trap Formation by Endothelial-Derived p33 (gC1q Receptor).
Neumann A, Papareddy P, Westman J, Hyldegaard O, Snäll J, Norrby-Teglund A, Herwald H., Free PMC Article | 12/22/2018 |
| Cardiomyocyte-specific loss of mitochondrial p32/C1qbp causes cardiomyopathy and activates stress responses, leading to heart failure. | Cardiomyocyte-specific loss of mitochondrial p32/C1qbp causes cardiomyopathy and activates stress responses.
Saito T, Uchiumi T, Yagi M, Amamoto R, Setoyama D, Matsushima Y, Kang D. | 05/26/2018 |
| macrophage/neutrophil-specific p32 conditional knockout mice showed exacerbated inflammation and reduced survival in response to LPS. Based on these findings, p32 is an important regulator of inflammatory signaling and is a potential drug candidate for treatment of sepsis in mammals. | p32 is Required for Appropriate Interleukin-6 Production Upon LPS Stimulation and Protects Mice from Endotoxin Shock.
Sasaki K, Gotoh K, Miake S, Setoyama D, Yagi M, Igami K, Uchiumi T, Kang D., Free PMC Article | 03/31/2018 |
| Hepatitis C virus core protein ligates gC1qR to induce A20 expression in macrophages via P38, JNK and NF-kappaB signaling pathways, which leads to a low-grade chronic inflammation during HCV infection. | HCV core protein binds to gC1qR to induce A20 expression and inhibit cytokine production through MAPKs and NF-κB signaling pathways.
Song X, Yao Z, Yang J, Zhang Z, Deng Y, Li M, Ma C, Yang L, Gao X, Li W, Liu J, Wei L., Free PMC Article | 12/23/2017 |
| application of p33 significantly improved survival in mice receiving an otherwise lethal dose of histones. | Treatment with p33 curtails morbidity and mortality in a histone-induced murine shock model.
Westman J, Smeds E, Johansson L, Mörgelin M, Olin AI, Malmström E, Linder A, Herwald H., Free PMC Article | 07/4/2015 |
| Authors propose that p32 is required for functional mitoribosome formation to synthesize proteins within mitochondria. | p32/gC1qR is indispensable for fetal development and mitochondrial translation: importance of its RNA-binding ability.
Yagi M, Uchiumi T, Takazaki S, Okuno B, Nomura M, Yoshida S, Kanki T, Kang D., Free PMC Article | 01/26/2013 |
| we have identified a mitochondrial protein p32 as a novel interactor of parkin in the brain | p32 regulates mitochondrial morphology and dynamics through parkin.
Li Y, Wan OW, Xie W, Chung KK. | 04/7/2012 |
| C1qbp could directly bind to CypD. Therefore C1qbp appears to act as an endogenous inhibitor of the MPT pore, most likely through binding to CypD, and thus protects cells against oxidative stress. | Complement 1q-binding protein inhibits the mitochondrial permeability transition pore and protects against oxidative stress-induced death.
McGee AM, Baines CP., Free PMC Article | 02/26/2011 |
| Intracellular localization and further functional studies suggested that CHCHD2 and HABP1 may mutually regulate each other to balance cell migration. | Identification of novel cell migration-promoting genes by a functional genetic screen.
Seo M, Lee WH, Suk K. | 03/1/2010 |
| p32 phosphorylation by ATM might be a new transcriptional regulatory pathway for specific DNA damage responses in heart. | Identification of p32 as a novel substrate for ATM in heart.
Kato H, Takashima S, Asano Y, Shintani Y, Yamazaki S, Seguchi O, Yamamoto H, Nakano A, Higo S, Ogai A, Minamino T, Kitakaze M, Hori M. | 01/21/2010 |
| Differential isoform expression and interaction with the P32 regulatory protein controls the subcellular localization of the splicing factor U2AF26 | Differential isoform expression and interaction with the P32 regulatory protein controls the subcellular localization of the splicing factor U2AF26.
Heyd F, Carmo-Fonseca M, Möröy T. | 01/21/2010 |
| Mitochondrial p32/C1QBP is a critical mediator of p14ARF-induced apoptosis. | Mitochondrial p32 is a critical mediator of ARF-induced apoptosis.
Itahana K, Zhang Y., Free PMC Article | 01/21/2010 |
| The reduction in oxidant generation and drop in apoptotic cell population caused by disruption of HABP1, corroborating the fact that excess ROS generation in HABP1 overexpressing cells leading to apoptosis was due to mitochondrial HABP1 accumulation. | Excessive reactive oxygen species induces apoptosis in fibroblasts: role of mitochondrially accumulated hyaluronic acid binding protein 1 (HABP1/p32/gC1qR).
Chowdhury AR, Ghosh I, Datta K. | 01/21/2010 |
| Rat and mouse homologs of the HABP1 pseudogene also contain multiple mutations, leading to the insertion of premature stop codons confirming the identity of a processed pseudogene. | Evidence for the presence of HABP1 pseudogene in multiple locations of mammalian genome.
Majumdar M, Bharadwaj A, Ghosh I, Ramachandran S, Datta K. | 01/21/2010 |
| Study demonstrates the differential expression of HABP1 during progression of epidermal carcinoma. | Differential expression of Hyaluronic Acid Binding Protein 1 (HABP1)/P32/C1QBP during progression of epidermal carcinoma.
Ghosh I, Chowdhury AR, Rajeswari MR, Datta K. | 01/21/2010 |