Affinage

C1QBP

Complement component 1 Q subcomponent-binding protein, mitochondrial · UniProt Q07021

Length
282 aa
Mass
31.4 kDa
Annotated
2026-04-28
100 papers in source corpus 46 papers cited in narrative 46 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

C1QBP/p32/gC1qR is a multifunctional homotrimeric protein that serves as a central regulator of mitochondrial oxidative phosphorylation, a multiligand cell-surface receptor in innate immunity and coagulation, and a participant in DNA damage repair. Within the mitochondrial matrix, C1QBP functions as an RNA/protein chaperone essential for mitochondrial translation and maintenance of respiratory chain complexes I, III, and IV; its loss shifts cellular metabolism from OXPHOS to glycolysis, activates OMA1-dependent OPA1 cleavage causing mitochondrial fragmentation, and impairs mitophagy through ULK1 destabilization (PMID:20100866, PMID:32606429, PMID:25909887, PMID:28942965). Biallelic loss-of-function mutations in C1QBP cause combined mitochondrial respiratory chain deficiency presenting as cardiomyopathy and myopathy (PMID:28942965). At the cell surface, C1QBP assembles Factor XII and high-molecular-weight kininogen into a Zn²⁺-dependent ternary complex that initiates the contact activation/kinin-forming cascade for bradykinin generation, and serves as a receptor for pathogen ligands including Listeria InlB, HCV core protein, and HIV-1 gp41, transducing signals through PI3K, Lck/ZAP-70, and RhoGAP pathways to modulate immune cell function and microbial entry (PMID:32559765, PMID:10747014, PMID:15163734, PMID:20617170). In the nucleus, C1QBP forms a complex with MRE11 and RAD50 that sequesters MRE11 nuclease activity until ATM-mediated phosphorylation releases MRE11 for recruitment to DNA double-strand breaks, enabling homologous recombination repair (PMID:31353207).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1998 Low

    Identifying viral protein interactions with p32 revealed it as a host factor co-opted by multiple viruses, beginning with the demonstration that EBV EBNA-1 binds p32 at regions critical for viral replication and transactivation.

    Evidence Co-immunoprecipitation with deletion mutant mapping of EBNA-1 interaction domains

    PMID:9678487

    Open questions at the time
    • Functional consequence of EBNA-1/p32 interaction on viral replication not directly demonstrated
    • No reciprocal validation or in vitro reconstitution
  2. 1999 Medium

    Establishing that gC1qR assembles the plasma contact activation system began with the discovery that it mediates Zn²⁺-dependent binding of high-molecular-weight kininogen to endothelial cells, identifying gC1qR as a key surface receptor for the kinin-forming cascade.

    Evidence Affinity chromatography, inhibitory antibody experiments blocking 72–86% of HK binding to endothelial cells

    PMID:10479529

    Open questions at the time
    • Structural basis of Zn²⁺-dependent HK binding unknown at this point
    • Physiological role in bradykinin generation in vivo not yet shown
  3. 2000 Medium

    Defining the multicompartmental distribution of p32 resolved the paradox of a predominantly mitochondrial matrix protein functioning at the cell surface; immunogold EM confirmed mitochondrial matrix as the major location with secondary presence at the cell surface, nucleus, and secretory granules.

    Evidence Immunogold electron microscopy across multiple cell lines and rat tissues

    PMID:11083468 PMID:11243856

    Open questions at the time
    • Mechanism of cell-surface translocation without transmembrane domain unresolved
    • Relative abundance at surface versus mitochondria not quantified
  4. 2000 High

    Demonstrating that gC1qR serves as a pathogen receptor for Listeria InlB established a direct functional role for surface C1QBP in bacterial invasion, showing that InlB binding activates PI3-kinase and Gab1 phosphorylation to enable bacterial entry.

    Evidence Affinity chromatography, transfection of non-permissive cells, soluble C1q blocking, Co-IP of Gab1

    PMID:10747014

    Open questions at the time
    • Whether C1QBP is sufficient or requires co-receptors (e.g., Met) for InlB entry unclear
    • Structural basis of InlB-gC1qR interaction unknown
  5. 2001 High

    Reconstituting the endothelial contact activation cascade showed that gC1qR and cytokeratin 1 together catalyze Factor XII-dependent prekallikrein-to-kallikrein conversion, establishing gC1qR as an initiating surface for bradykinin generation.

    Evidence Purified protein reconstitution, chromogenic substrate assays, inhibitory antibodies, factor-deficient plasma controls

    PMID:11204562

    Open questions at the time
    • In vivo significance for bradykinin-mediated vascular permeability not tested
    • Relative contributions of gC1qR versus cytokeratin 1 not delineated
  6. 2002 Medium

    Solving the crystal structure revealed the homotrimeric doughnut-shaped architecture of gC1qR with unique charged surface loops, explaining its capacity for multiligand binding and confirming the absence of a classical membrane anchor.

    Evidence X-ray crystallography and structure-function analysis

    PMID:11784324 PMID:12396004

    Open questions at the time
    • No co-crystal structures with ligands at this stage
    • Mechanism of membrane association still undefined
  7. 2004 High

    Demonstrating that HCV core protein suppresses T-cell receptor signaling through surface gC1qR established a viral immune evasion mechanism, with quantitative SPR showing direct binding and functional knockdown/rescue confirming signaling through Lck/ZAP-70/Akt.

    Evidence SPR binding kinetics, siRNA knockdown, gain-of-function transfection, kinase activation Western blots

    PMID:14517080 PMID:15163734 PMID:16306613

    Open questions at the time
    • Whether gC1qR-mediated immune suppression is sufficient for HCV persistence in vivo not established
    • Downstream mechanism linking gC1qR engagement to Lck inhibition not defined
  8. 2005 High

    Identifying C1QBP as a host adaptor exploited by herpesviruses for nuclear egress showed that p32 recruits CMV kinase pUL97 to the nuclear lamina for lamin phosphorylation and capsid release, establishing a mechanistic role in nuclear envelope dissolution during viral egress.

    Evidence Co-IP, catalytically inactive kinase mutant, GFP-lamin imaging, viral replication quantification

    PMID:15975922 PMID:25355318 PMID:26085152

    Open questions at the time
    • Whether p32 nuclear lamina role is conserved across all herpesviruses not fully tested
    • Mechanism of p32 recruitment to nuclear membrane unknown
  9. 2009 High

    Discovering that C1QBP translocates to the mitochondrial outer membrane upon viral infection to inhibit RIG-I/MDA5 signaling via MAVS interaction revealed an innate immune regulatory function, explaining how C1QBP dampens antiviral interferon responses.

    Evidence Reciprocal Co-IP, subcellular fractionation, siRNA knockdown with virus replication assays

    PMID:19164550

    Open questions at the time
    • Signal that triggers C1QBP translocation from matrix to outer membrane unresolved
    • Whether this represents immune evasion or physiological immune homeostasis unclear
  10. 2010 High

    Establishing that p32 loss shifts cancer cell metabolism from OXPHOS to glycolysis and reduces tumorigenicity demonstrated that p32 is a critical determinant of the OXPHOS/glycolysis balance, with rescue by re-expression confirming specificity.

    Evidence siRNA knockdown, metabolic flux assays, rescue by exogenous expression, in vivo tumor formation in multiple cell lines

    PMID:20100866

    Open questions at the time
    • Which mitochondrial translation products are most affected not delineated
    • Relationship between metabolic shift and tumorigenicity mechanism unclear
  11. 2013 High

    Identifying the p32–RNase H1 complex as essential for mitochondrial pre-rRNA processing placed p32 in a specific step of mitochondrial ribosome biogenesis: p32 enhances RNase H1 turnover to process 12S/16S pre-rRNA.

    Evidence Co-IP, in vitro kinetic cleavage assays, siRNA co-depletion with mitochondrial pre-rRNA quantification

    PMID:23990920

    Open questions at the time
    • Whether p32 participates in additional mitochondrial RNA processing steps unknown
    • Structural basis of p32-RNase H1 interaction not determined
  12. 2015 High

    Demonstrating that p32 stabilizes ULK1 by preventing K48-linked polyubiquitination connected mitochondrial p32 to autophagy and mitophagy regulation, with rescue experiments confirming ULK1 as the critical downstream effector.

    Evidence Co-IP, K48/K63-linkage-specific ubiquitination assays, autophagy flux assays, rescue by ULK1 re-expression

    PMID:25909887

    Open questions at the time
    • Identity of the E3 ligase mediating ULK1 K48-ubiquitination in absence of p32 unknown
    • How p32 selectively modulates ubiquitin chain linkage type unresolved
  13. 2017 High

    Human genetics established that biallelic C1QBP loss-of-function mutations cause combined respiratory chain deficiency with cardiomyopathy/myopathy, and tissue-specific KO models confirmed that p32 acts as an RNA/protein chaperone essential for mitochondrial translation in heart and brain.

    Evidence Patient genetics with complementation rescue in C1qbp−/− MEFs, cardiac-specific and neural-specific Cre-loxP KO mice with echocardiography, EM, metabolic assays, and differentiation assays

    PMID:28498888 PMID:28942965 PMID:29123152

    Open questions at the time
    • Precise RNA substrates chaperoned by p32 beyond pre-rRNA not catalogued
    • Whether all patient phenotypes are explained by mitochondrial translation defects alone unclear
  14. 2019 High

    Discovering the MRC complex (MRE11–RAD50–C1QBP) and its ATM-dependent dissolution extended p32 function to DNA double-strand break repair, showing that C1QBP sequesters MRE11 nuclease activity until DSB-triggered phosphorylation releases MRE11 for chromatin recruitment.

    Evidence Reconstituted complex, in vitro nuclease assays, phospho-site mutagenesis, ATM kinase assays, ChIP, knockdown/rescue

    PMID:31353207

    Open questions at the time
    • How MRC complex forms and is maintained in unchallenged cells not structurally resolved
    • Whether C1QBP also participates in NHEJ or other repair pathways untested
  15. 2020 High

    Defining the p32–OMA1–OPA1 axis showed that p32 prevents OMA1-dependent OPA1 cleavage; its loss causes mitochondrial fragmentation and swelling, linking p32 to mitochondrial dynamics beyond metabolism.

    Evidence Genetic KO, OPA1 processing Western blots, OMA1 activity assays, oxygen consumption measurements

    PMID:32606429

    Open questions at the time
    • Whether p32 directly inhibits OMA1 or acts indirectly through membrane potential unknown
    • Relationship between OPA1 processing defect and respiratory chain deficiency not dissected
  16. 2020 High

    Crystal structures of FXII and HK domains bound to gC1qR resolved the molecular basis of contact activation assembly: Zn²⁺ coordination by gC1qR Asp185/His187 allosterically modulates FXII binding, and asymmetric occupancy of the trimer produces a ~500 kDa ternary complex that stimulates coagulation.

    Evidence X-ray crystallography of FXIIFnII–gC1qR and HKD5–gC1qR complexes, SPR with mutagenesis, gel filtration, plasma coagulation assays

    PMID:32559765

    Open questions at the time
    • Full-length FXII/HK complex structure on cell surface not available
    • In vivo significance for contact activation-driven thromboinflammation not validated
  17. 2024 Medium

    Linking p32 copper-binding capacity to DLAT oligomerization and PDHc activation revealed a metal-dependent mechanism for TCA cycle regulation, connecting p32 to copper-dependent metabolic control in cancer.

    Evidence Co-IP, copper binding assays, DLAT oligomerization assays, PDHc activity, in vivo tumor models

    PMID:38169635

    Open questions at the time
    • Structural basis of p32 copper binding not determined
    • Physiological copper concentrations required for DLAT oligomerization in vivo unknown
    • Independent replication awaited

Open questions

Synthesis pass · forward-looking unresolved questions
  • The mechanism by which C1QBP, a protein lacking a transmembrane domain or GPI anchor, reaches the cell surface and is retained there remains unresolved, as does the regulatory logic that determines the partitioning of p32 among mitochondrial, nuclear, and surface pools.
  • No trafficking mechanism for cell-surface translocation defined
  • No quantitative model of compartmental partitioning
  • No structure of full-length p32 in a membrane-associated state

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3 GO:0003723 RNA binding 2 GO:0044183 protein folding chaperone 2
Localization
GO:0005739 mitochondrion 6 GO:0005886 plasma membrane 6 GO:0005634 nucleus 2 GO:0005635 nuclear envelope 2
Pathway
R-HSA-1430728 Metabolism 5 R-HSA-109582 Hemostasis 4 R-HSA-168256 Immune System 4 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-9612973 Autophagy 2 R-HSA-73894 DNA Repair 1 R-HSA-8953854 Metabolism of RNA 1
Partners
CD44DLATMAVSMRE11OPA1RAD50RNASEH1ULK1
Complex memberships
MRC complex (MRE11-RAD50-C1QBP)gC1qR-FXII-HK ternary complexp32-RNase H1 complex

Evidence

Reading pass · 46 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 C1QBP/p32 knockdown in human cancer cells strongly shifts metabolism from oxidative phosphorylation (OXPHOS) to glycolysis, with reduced synthesis of mitochondrial-DNA-encoded OXPHOS polypeptides and reduced tumorigenicity in vivo; restoration of p32 rescues wild-type phenotype, establishing p32 as a critical regulator of the OXPHOS/glycolysis balance. siRNA knockdown, metabolic flux assays (glucose consumption, lactate production), rescue by exogenous expression, in vivo tumor formation assay Molecular and cellular biology High 20100866
2000 gC1qR/C1QBP serves as a direct cell-surface receptor for Listeria monocytogenes InlB invasion protein; this interaction promotes PI3-kinase activation and tyrosine phosphorylation of adaptor protein Gab1, enabling bacterial entry into mammalian cells. Affinity chromatography, ELISA, transient transfection of non-permissive cells, soluble C1q/antibody blocking, Co-IP of Gab1 The EMBO journal High 10747014
2009 gC1qR inhibits RIG-I and MDA5-dependent antiviral signaling by translocating to the mitochondrial outer membrane upon dsRNA/virus stimulation and interacting with the adaptor VISA/MAVS/IPS-1, thereby disrupting antiviral signaling and promoting virus replication; gC1qR knockdown enhances RIG-I-dependent antiviral responses. Co-immunoprecipitation, subcellular fractionation, siRNA knockdown, virus replication assays Proceedings of the National Academy of Sciences of the United States of America High 19164550
2005 Cellular p32/C1QBP recruits cytomegalovirus kinase pUL97 to the nuclear membrane by interacting with the lamin B receptor, leading to phosphorylation of lamins A/C and lamin B receptor by pUL97, redistribution of nuclear lamina components, and enhanced viral capsid egress; catalytically inactive pUL97 fails to induce lamina redistribution. Co-IP, transfection of active vs. catalytically inactive kinase mutant, GFP-tagged lamin imaging, phosphorylation assays, viral replication quantification The Journal of biological chemistry High 15975922
2019 C1QBP forms a complex (MRC) with MRE11 and RAD50, stabilizing MRE11/RAD50 while inhibiting MRE11 nuclease activity by preventing DNA/chromatin binding; upon DNA double-strand breaks, ATM phosphorylates MRE11-S676/S678 to dissociate the MRC complex, allowing MRE11 recruitment to DSBs and proper homologous recombination repair. Co-IP, in vitro nuclease assays, phospho-site mutagenesis (S676/S678), ATM kinase assays, ChIP, knockdown/rescue experiments Molecular cell High 31353207
2020 p32/C1QBP regulates mitochondrial morphology by controlling OMA1-dependent proteolytic cleavage of OPA1; genetic ablation of p32/C1QBP activates OMA1, promotes OPA1 cleavage to short forms, and causes mitochondrial fragmentation and swelling, decreased mitochondrial respiration, and a metabolic shift from OXPHOS to glycolysis. Genetic KO, Western blot for OPA1 processing, OMA1 activity assays, oxygen consumption measurements, metabolic assays Scientific reports High 32606429
2017 Biallelic loss-of-function mutations in C1QBP cause combined respiratory-chain enzyme deficiency of complexes I, III, and IV, associated with cardiomyopathy and myopathy; C1qbp-/- mouse embryonic fibroblasts show multiple OXPHOS defects, rescued by wild-type but not mutated C1qbp complementation. Patient genetics, steady-state protein analysis, respiratory chain enzyme assays, C1qbp-/- MEF complementation with wild-type vs. mutant American journal of human genetics High 28942965
2017 Cardiomyocyte-specific deletion of p32/C1qbp causes cardiac mitochondrial dysfunction (decreased COX1 expression, reduced oxygen consumption, increased oxidative stress), contractile dysfunction, and impairs mammalian target of rapamycin signaling (constitutive AMPK phosphorylation, reduced 4EBP-1/S6K phosphorylation); p32 functions as an RNA and protein chaperone required for mitochondrial translation in cardiomyocytes. Cre-loxP cardiac-specific deletion, echocardiography, mitochondrial electron microscopy, oxygen consumption assays, metabolic analysis Cardiovascular research High 28498888
2013 Human RNase H1 binds specifically to p32/C1QBP via its hybrid-binding domain at approximately 1:1 stoichiometry; p32 enhances RNase H1 cleavage activity by reducing substrate affinity and enhancing enzyme turnover; co-depletion of either protein accumulates mitochondrial pre-ribosomal RNA (12S/16S), placing the p32-RNase H1 complex in mitochondrial pre-rRNA processing. Co-IP, domain mapping, in vitro cleavage assays with kinetic analysis, siRNA knockdown, mitochondrial pre-rRNA quantification by qPCR PloS one High 23990920
2015 p32/C1QBP stabilizes ULK1 by forming a complex with it, preventing K48-linked polyubiquitination and proteasomal degradation; p32 depletion potentiates K48-linked ubiquitination and impairs K63-linked ubiquitination of ULK1, leading to ULK1 degradation, impaired autophagic flux, and defective mitophagy; restoring ULK1 in p32-depleted cells rescues autophagy and mitophagy. Co-IP, ubiquitination assays (K48- vs K63-linkage specific), siRNA knockdown, autophagy flux assays, rescue experiments Cell death and differentiation High 25909887
2004 Direct binding of HCV core protein to gC1qR/C1QBP on T cells impairs Lck/ZAP-70 kinase activation and Akt phosphorylation; gC1qR-silencing reduces core binding, and transfection of human gC1qR into non-expressing cells enhances core binding, demonstrating that HCV core suppresses early T-cell activation via gC1qR. BIAcore surface plasmon resonance (Kd determination), siRNA knockdown, transfection of gC1qR into non-expressing cells, kinase activation assays (Western blot) Journal of virology High 15163734
2020 The fibronectin type II domain of Factor XII binds gC1qR in a Zn2+-dependent manner; crystal structure of the FXIIFnII-gC1qR complex shows asymmetric binding with Arg36 and Arg65 contacting two negatively charged pockets on gC1qR, and Zn2+ coordination by gC1qR Asp185/His187 allosterically modulates FXII binding; high-molecular-weight kininogen domain 5 binds asymmetrically with only one high-affinity site per trimer via the central G3-loop; gC1qR clusters FXII and HK into a ~500 kDa ternary complex and stimulates coagulation in a FXII-dependent manner. X-ray crystallography, surface plasmon resonance with mutagenesis, gel filtration, plasma-based coagulation assays Blood High 32559765
2002 gC1q-R/p33 crystal structure reveals a homotrimeric doughnut-shaped assembly; the structure identifies unique charged loops that explain its multiligand binding capacity and provides evidence that membrane anchoring is not via a classical transmembrane domain or GPI anchor. X-ray crystallography, structure-function analysis Immunobiology Medium 12396004
2001 p32/C1QBP is predominantly localized to the mitochondrial matrix in vivo but also accumulates in the nucleus upon leptomycin B or actinomycin D treatment; deletion analysis identified regions of p32 involved in nuclear import and export, indicating CRM1-dependent nuclear export. EGFP-p32 fusion constructs, pharmacological inhibitors (leptomycin B, actinomycin D), deletion mutant analysis, confocal microscopy Biochemical and biophysical research communications Medium 11243856
2000 p32/gC1qR is localized primarily to the mitochondrial matrix in multiple cell lines and rat tissues by immunogold electron microscopy, but also localizes to the cell surface of microvascular endothelial cells, zymogen granules, acrosome of spermatids, and nuclei of splenic lymphocytes under normal physiological conditions. Immunogold electron microscopy, Western blot of subcellular fractions Histochemistry and cell biology Medium 11083468
2005 Rubella virus capsid protein requires two clusters of arginine residues for stable binding to p32; mutation of these arginine clusters abrogates p32 binding, reduces mitochondrial clustering, and results in decreased subgenomic RNA production and lower viral titers, establishing that capsid-p32 interaction is required for viral RNA replication regulation. Mutagenesis of arginine clusters, pulldown assays, viral replication assays, subgenomic RNA quantification, plaque assays Journal of virology High 16051872
2015 p32 is a direct transcriptional target of c-Myc; in Myc-expressing glioma cells, p32 is required to maintain respiratory capacity to sustain glutamine metabolism; p32 knockdown impairs tumor formation and induces resistance to glutamine deprivation while sensitizing cells to glucose withdrawal. ChIP, siRNA knockdown, metabolic assays, in vivo tumor formation, glutamine/glucose withdrawal experiments Oncotarget Medium 25528767
2007 p32/C1QBP physically interacts with the mitochondrial smARF (short isoform of ARF) and co-localizes with it at mitochondria; p32 knockdown reduces smARF steady-state levels by increasing its turnover, thereby reducing smARF-induced autophagy and mitochondrial membrane dissipation; this stabilization is selective for mitochondrial smARF and does not affect nucleolar p19ARF. Co-IP, co-localization imaging, siRNA knockdown, autophagy assays, mitochondrial membrane potential assays Oncogene Medium 17486078
2014 In HSV-1-infected cells, viral ICP34.5 associates with p32 and recruits it to the inner nuclear membrane, paralleling phosphorylation and rearrangement of nuclear lamina; p32 knockdown significantly reduces production of cell-free virus, identifying p32 as a mediator of HSV-1 nuclear egress. Mass spectrometry identification, Co-IP, confocal imaging of nuclear lamina phosphorylation, siRNA knockdown with viral titer assay The Journal of biological chemistry Medium 25355318
2015 In HSV-1-infected cells, host p32 accumulates at the nuclear rim in a UL47-dependent manner; p32 forms a complex with HSV-1 nuclear egress complex components UL31, UL34, Us3, UL47, and ICP22; p32 knockdown induces membranous invaginations containing primary enveloped virions and impairs ULK31/UL34 localization, establishing p32 as a component of the herpesvirus nuclear egress complex regulating de-envelopment. Tandem affinity purification/mass spectrometry, Co-IP, confocal imaging, siRNA knockdown, electron microscopy Journal of virology Medium 26085152
2001 gC1qR and cytokeratin 1 on endothelial cell surfaces catalyze zinc-dependent, Factor XII-dependent conversion of prekallikrein to kallikrein; antibodies to gC1qR and cytokeratin 1 inhibit normal plasma activation on endothelial cells, establishing gC1qR as an initiating surface for the plasma kinin-forming cascade. Purified protein incubation assays, chromogenic substrate assays, inhibitory antibodies, plasma activation assays with factor-deficient plasma Thrombosis and haemostasis High 11204562
1999 gC1qR mediates zinc-dependent binding of high-molecular-weight kininogen (HK) light chain to endothelial cells; anti-gC1qR antibody inhibits HK binding by 72%, and together with anti-cytokeratin 1 antibody inhibits binding by 86%; gC1qR and cytokeratin 1 form a binary complex independently of kininogen. Affinity chromatography, dot blot, SDS-PAGE/Western blot, inhibitory antibody experiments, amino acid sequencing Clinical immunology (Orlando, Fla.) Medium 10479529
2014 C1QBP interacts with YBX1 and negatively regulates its phosphorylation and nuclear translocation in renal cell carcinoma; C1QBP knockdown enhances YBX1 phosphorylation and nuclear localization, placing C1QBP as a negative regulator of YBX1 oncogenic activation. Co-IP, mass spectrometry interactome, Western blot for phospho-YBX1, subcellular fractionation, siRNA knockdown Journal of proteome research Medium 25497084
2016 C1QBP interacts with dihydrolipoyllysine-residue acetyltransferase (DLAT), a component of the pyruvate dehydrogenase complex (PDHc), in the mitochondria; C1QBP expression level affects PDH enzymatic activity, placing C1QBP as a regulator of cellular energy metabolism through the PDHc. Subcellular fractionation coupled with Co-IP/mass spectrometry, validation by Co-IP, PDH activity assays Analytical and bioanalytical chemistry Medium 26753982
2024 p32/C1QBP interacts with DLAT and regulates PDHc activation to control the TCA cycle; p32 has direct binding affinity for copper and facilitates copper-induced oligomerization of lipoylated DLAT (lipo-DLAT) specifically in ccRCC cells, linking the p32/DLAT/copper complex to regulation of glycometabolism and the TCA cycle. Co-IP, PDHc activity assays, copper binding assays, DLAT oligomerization assays, OXPHOS measurements, in vivo tumor models International journal of biological sciences Medium 38169635
2014 RECQ4 forms a complex with mitochondrial p32 in the mitochondria; p32 interaction negatively controls transport of RECQ4 and its replication factor MCM10 from nucleus to mitochondria; a cancer-associated RECQ4 deletion mutant no longer interacts with p32 and is enriched in mitochondria, leading to abnormally high mtDNA synthesis via interaction with PEO1 helicase. Co-IP in different cellular compartments, subcellular fractionation, mtDNA copy number analysis, interaction domain mapping Cell reports Medium 24746816
2002 HABP1/p32 exists as a noncovalently associated trimer and a covalently linked dimer-of-trimers (hexamer) through Cys186-mediated disulfide bonds; the hexameric form shows enhanced affinity for hyaluronan, gC1q, and mannosylated BSA compared to the trimeric form, demonstrating that oligomerization state regulates ligand binding. Size-exclusion chromatography, glutaraldehyde cross-linking, Cys186 modification, fluorescence spectroscopy, ligand binding assays European journal of biochemistry Medium 11784324
2010 HIV-1 gp41 3S motif binds to gC1qR on CD4+ T cells, triggering a signaling cascade involving sequential activation of PI3K, NADPH oxidase, p190 RhoGAP, and inactivation of TC10, leading to surface translocation of NKp44L, rendering T cells susceptible to NK cell killing. Immunoprecipitation, ELISA, blocking antibodies, 2D-PAGE, PIP3/H2O2 treatment, small molecule inhibitors, wild-type vs. mutant p190 RhoGAP plasmids, RNAi of TC10 PLoS pathogens Medium 20617170
2003 HCV core protein interaction with gC1qR on T cells causes G0/G1 cell cycle arrest by stabilizing the CDK inhibitor p27Kip1, preventing its degradation upon mitogenic stimulation, and reducing Cdk2/4, cyclin E/D expression and pRb phosphorylation; this effect is reversible by anti-gC1qR antibody. T cell stimulation assays, Western blot for CDK/cyclin/p27 levels, antibody blocking, cell cycle analysis Virology Medium 14517080
2005 HCV core from chronically infected patients binds gC1qR more efficiently than core from resolved infections and induces SOCS1 and SOCS3 to disrupt STAT phosphorylation and suppress T cell IFN-γ production; silencing SOCS1 or SOCS3 reverses the core-induced inhibition, placing gC1qR-mediated SOCS induction as the mechanism of HCV immune persistence. Binding competition assays, siRNA silencing of SOCS1/SOCS3, STAT phosphorylation Western blot, IFN-γ ELISA Journal of virology Medium 16306613
2000 Staphylococcus aureus protein A directly binds platelet gC1qR/p33; the interaction is mediated by the same protein A tyrosil residues required for IgG Fc binding; a truncated gC1qR mutant lacking amino acids 74-95 retains protein A binding, mapping the protein A binding domain outside the C1q-binding N-terminal alpha helix. Affinity pulldown, ELISA, solid-phase binding assays, chemical inactivation of protein A, truncation mutant binding Infection and immunity Medium 10722602
2003 gC1qR interacts specifically with the C-terminal tails of alpha1B- and alpha1D-adrenoceptors but not alpha1A-adrenoceptors through arginine-rich C-tail motifs; C-terminal truncation of the receptors abolishes interaction with gC1qR. Co-immunoprecipitation in HEK293 cells, C-terminal truncation mutants, reciprocal immunoprecipitation Journal of receptor and signal transduction research Low 14626446
2018 p32/C1QBP interacts with ER-anchored glucosidase GCS1 and reduces GCS1 protein levels in a lysosome-dependent manner; p32 depletion increases GCS1 expression, alleviates fatty acid-induced ER stress, and reduces lipid accumulation by downregulating Srebp1, Fasn, and Acc, placing p32 as a regulator of ER homeostasis and lipid biosynthesis. Co-IP, lysosome inhibitor experiments, siRNA knockdown, lipid accumulation assays, qPCR for lipogenic genes FASEB journal Medium 29465311
2017 Neural-specific deletion of p32/C1qbp in mice causes white matter degeneration with oligodendrocyte loss, axon degeneration, and activation of the integrated stress response; p32-deficient oligodendrocytes show reduced differentiation and impaired myelination in primary culture, establishing mitochondrial p32 as essential for oligodendrocyte differentiation and axon maintenance. Cre-loxP neural-specific KO, electron microscopy, primary cell culture differentiation assays, immunofluorescence, ISR marker analysis Scientific reports Medium 29123152
1998 EBNA-1 of Epstein-Barr virus co-immunoprecipitates with the 32-kDa p32/C1QBP protein; the interaction maps to EBNA-1 residues 1-102 and 325-357, a region previously shown to have dominant-negative effects on viral DNA replication and transactivation. Co-immunoprecipitation, deletion mutant mapping Journal of biomedical science Low 9678487
2022 circMTCL1 directly binds C1QBP protein via a specific sequence (+159 to +210), inhibiting its ubiquitin-proteasome-mediated degradation; stabilized C1QBP protein then directly interacts with β-catenin to suppress its phosphorylation and accelerate β-catenin cytoplasmic and nuclear accumulation, activating Wnt/β-catenin signaling. RNA pulldown, RIP, Co-IP, ubiquitination assay, rescue experiments, in vitro/in vivo tumor models Molecular cancer Medium 35366893
2015 ZNF32 transcriptionally activates C1QBP expression; C1QBP is a direct downstream target of ZNF32 that inactivates the p38 MAPK pathway to protect cells from oxidative stress-induced apoptosis; ZNF32 maintains mitochondrial membrane potential and antioxidant capacity through C1QBP. ChIP, promoter reporter assays, siRNA knockdown, rescue experiments, p38 MAPK pathway analysis Oncotarget Medium 26497555
2017 C1QBP regulates RCC cell adhesion and metastasis through the GSK3/β-catenin/L1CAM signaling pathway; C1QBP knockdown increases L1CAM expression, enhances cell adhesion and invasion in vitro, and promotes metastasis to lung and liver in vivo. siRNA knockdown, gene expression profiling, Western blot for pathway components, in vivo metastasis models Scientific reports Medium 28428626
2013 Calreticulin and gC1qR form a cytoplasmic complex in response to viral infection; this complex prevents gC1qR translocation to mitochondria and suppresses apoptosis; disruption of complex formation by overexpression of complex-domain peptides induces cancer cell apoptosis, establishing CRT/gC1qR interaction as a conserved anti-apoptotic mechanism. Co-IP, subcellular fractionation, apoptosis assays, peptide overexpression, conservation analysis across species Journal of molecular cell biology Medium 23378602
2007 HABP1/p32 overexpression in mitochondria causes inhibition of respiratory chain complex I, increased ROS generation, Ca2+ influx into mitochondria, drop in mitochondrial membrane potential, and eventually apoptosis with cytochrome c release; disruption of HABP1 expression reduces ROS generation and apoptosis. Respiratory chain complex activity assays, ROS measurement, Ca2+ imaging, mitochondrial membrane potential assays, electron microscopy, cytochrome c release assay, siRNA Experimental cell research Medium 18166172
2021 p32/C1QBP loss impairs goblet cell differentiation in ulcerative colitis by shifting colonic epithelial cells from mitochondrial oxidative phosphorylation to glycolysis; p32 silencing in HT29-MTX cells abolishes butyrate-induced goblet cell differentiation, establishing p32 as required for the metabolic switch that drives goblet cell commitment. Patient biopsies, siRNA knockdown in cell lines, differentiation assays, metabolic flux measurements, ATP8 mutant mouse model, nutritional intervention Cellular and molecular gastroenterology and hepatology Medium 33515804
2021 The exosomal CD44v6/C1QBP complex is delivered to the plasma membrane of hepatic stellate cells, where it promotes phosphorylation of IGF-1 signaling molecules, leading to HSC activation and liver fibrosis; C1QBP knockdown or CD44v6 knockdown suppresses this pro-metastatic fibrotic program. Exosome isolation, lentiviral knockdown/overexpression, tail vein injection models, intrasplenic injection liver metastasis models, signaling Western blots Gut Medium 33827783
2017 C1QBP in lipid rafts forms a complex with CD44v6 upon IGF-1 stimulation and drives IGF-1R phosphorylation and activation of downstream PI3K and MAPK signaling to promote pancreatic cancer hepatic metastasis; C1QBP knockdown suppresses hepatic metastasis in nude mice. Lipid raft fractionation, Co-IP, phospho-IGF1R/PI3K/MAPK Western blots, siRNA knockdown, nude mouse metastasis model International journal of cancer Medium 28608366
2011 Deletion mutant analysis of gC1qR identifies residues 154-162 and Trp233 as critical for bradykinin generation; additional HK binding sites are located at residues 144-162 and 190-202 (in addition to the known 204-218 site); soluble gC1qR enhances both intrinsic and extrinsic coagulation pathways in a dose-dependent manner. Deletion mutants, BK immunoassay, HK binding assays with synthetic peptides, coagulation time assays Frontiers in immunology Medium 22282702
2013 Soluble gC1qR binds to endothelial cell surface-bound fibrinogen via a conserved domain consisting of residues 174-180, and this binding induces B1R (bradykinin receptor 1) expression on endothelial cells; gC1qR lacking residues 174-180 shows diminished binding and B1R induction. Solid-phase binding assay, deconvolution fluorescence microscopy, ELISA, deletion mutants, Western blot for B1R Journal of immunology Medium 24319267
2003 gC1qR on platelet surface is upregulated upon platelet activation with TRAP, epinephrine, or ADP, as detected by antibody 74.5.2 (recognizing C-terminal residues 204-218); surface expression is sustained after activation; gC1qR surface expression is antibody-epitope dependent. Flow cytometry, confocal microscopy, platelet activation with different agonists, PGE1 reversal experiments Thrombosis and haemostasis Medium 12574814

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2010 Mitochondrial p32 protein is a critical regulator of tumor metabolism via maintenance of oxidative phosphorylation. Molecular and cellular biology 276 20100866
2000 gC1q-R/p32, a C1q-binding protein, is a receptor for the InlB invasion protein of Listeria monocytogenes. The EMBO journal 229 10747014
2021 Exosome-delivered CD44v6/C1QBP complex drives pancreatic cancer liver metastasis by promoting fibrotic liver microenvironment. Gut 157 33827783
2005 Cellular p32 recruits cytomegalovirus kinase pUL97 to redistribute the nuclear lamina. The Journal of biological chemistry 157 15975922
2001 gC1q-R/p33, a member of a new class of multifunctional and multicompartmental cellular proteins, is involved in inflammation and infection. Immunological reviews 150 11414365
2000 Staphylococcus aureus protein A recognizes platelet gC1qR/p33: a novel mechanism for staphylococcal interactions with platelets. Infection and immunity 142 10722602
2004 cC1q-R (calreticulin) and gC1q-R/p33: ubiquitously expressed multi-ligand binding cellular proteins involved in inflammation and infection. Molecular immunology 124 15159063
2009 Inhibition of RIG-I and MDA5-dependent antiviral response by gC1qR at mitochondria. Proceedings of the National Academy of Sciences of the United States of America 112 19164550
2000 Localization of P32 protein (gC1q-R) in mitochondria and at specific extramitochondrial locations in normal tissues. Histochemistry and cell biology 109 11083468
2004 Direct binding of hepatitis C virus core to gC1qR on CD4+ and CD8+ T cells leads to impaired activation of Lck and Akt. Journal of virology 86 15163734
2004 Receptor for the globular heads of C1q (gC1q-R, p33, hyaluronan-binding protein) is preferentially expressed by adenocarcinoma cells. International journal of cancer 77 15146564
2010 HIV gp41 engages gC1qR on CD4+ T cells to induce the expression of an NK ligand through the PIP3/H2O2 pathway. PLoS pathogens 72 20617170
1999 Cytokeratin 1 and gC1qR mediate high molecular weight kininogen binding to endothelial cells. Clinical immunology (Orlando, Fla.) 72 10479529
2022 Circular RNA MTCL1 promotes advanced laryngeal squamous cell carcinoma progression by inhibiting C1QBP ubiquitin degradation and mediating beta-catenin activation. Molecular cancer 71 35366893
2006 High-molecular-weight kininogen fragments stimulate the secretion of cytokines and chemokines through uPAR, Mac-1, and gC1qR in monocytes. Arteriosclerosis, thrombosis, and vascular biology 70 16902163
1998 Structure and function of gC1q-R: a multiligand binding cellular protein. Immunobiology 70 9777408
2019 The C1q Receptors: Focus on gC1qR/p33 (C1qBP, p32, HABP-1)1. Seminars in immunology 67 31744753
2007 The contribution of gC1qR/p33 in infection and inflammation. Immunobiology 65 17544818
2016 New p32/gC1qR Ligands for Targeted Tumor Drug Delivery. Chembiochem : a European journal of chemical biology 64 26895508
2019 C1QBP Promotes Homologous Recombination by Stabilizing MRE11 and Controlling the Assembly and Activation of MRE11/RAD50/NBS1 Complex. Molecular cell 59 31353207
2015 Role of Host Cell p32 in Herpes Simplex Virus 1 De-Envelopment during Viral Nuclear Egress. Journal of virology 58 26085152
2007 Excessive reactive oxygen species induces apoptosis in fibroblasts: role of mitochondrially accumulated hyaluronic acid binding protein 1 (HABP1/p32/gC1qR). Experimental cell research 58 18166172
2017 Biallelic C1QBP Mutations Cause Severe Neonatal-, Childhood-, or Later-Onset Cardiomyopathy Associated with Combined Respiratory-Chain Deficiencies. American journal of human genetics 55 28942965
2005 Chemotaxis of human monocyte-derived dendritic cells to complement component C1q is mediated by the receptors gC1qR and cC1qR. Molecular immunology 55 16140380
2003 Constitutive expression of hyaluronan binding protein 1 (HABP1/p32/gC1qR) in normal fibroblast cells perturbs its growth characteristics and induces apoptosis. Biochemical and biophysical research communications 53 12507504
2017 Targeting of p32 in peritoneal carcinomatosis with intraperitoneal linTT1 peptide-guided pro-apoptotic nanoparticles. Journal of controlled release : official journal of the Controlled Release Society 52 28603028
2014 cC1qR/CR and gC1qR/p33: observations in cancer. Molecular immunology 52 25044096
2011 Mitochondrial p32/C1QBP is highly expressed in prostate cancer and is associated with shorter prostate-specific antigen relapse time after radical prostatectomy. Cancer science 52 21205079
2004 Expression of gC1q-R/p33 and its major ligands in human atherosclerotic lesions. Molecular immunology 52 15234555
2001 Mitochondrial protein p32 can accumulate in the nucleus. Biochemical and biophysical research communications 52 11243856
2012 DC-SIGN, C1q, and gC1qR form a trimolecular receptor complex on the surface of monocyte-derived immature dendritic cells. Blood 49 22700724
2007 The autophagic inducer smARF interacts with and is stabilized by the mitochondrial p32 protein. Oncogene 49 17486078
2017 Cardiomyocyte-specific loss of mitochondrial p32/C1qbp causes cardiomyopathy and activates stress responses. Cardiovascular research 48 28498888
2002 gC1q-R/p33: structure-function predictions from the crystal structure. Immunobiology 48 12396004
2003 Activation-dependent surface expression of gC1qR/p33 on human blood platelets. Thrombosis and haemostasis 47 12574814
2014 p32 is a novel target for viral protein ICP34.5 of herpes simplex virus type 1 and facilitates viral nuclear egress. The Journal of biological chemistry 46 25355318
2013 Human RNase H1 is associated with protein P32 and is involved in mitochondrial pre-rRNA processing. PloS one 45 23990920
2003 HCV core/gC1qR interaction arrests T cell cycle progression through stabilization of the cell cycle inhibitor p27Kip1. Virology 45 14517080
1966 Normal serum cytotoxicity for P32-labeled smooth Enterobacteriaceae. I. Loss of label, death, and ultrastructural damage. Journal of bacteriology 45 5323295
2015 Chaperone-like protein p32 regulates ULK1 stability and autophagy. Cell death and differentiation 44 25909887
2005 Interactions between rubella virus capsid and host protein p32 are important for virus replication. Journal of virology 44 16051872
2001 Factor XII-dependent contact activation on endothelial cells and binding proteins gC1qR and cytokeratin 1. Thrombosis and haemostasis 44 11204562
2021 Loss of Mucosal p32/gC1qR/HABP1 Triggers Energy Deficiency and Impairs Goblet Cell Differentiation in Ulcerative Colitis. Cellular and molecular gastroenterology and hepatology 42 33515804
2010 The multicompartmental p32/gClqR as a new target for antibody-based tumor targeting strategies. The Journal of biological chemistry 40 21156793
2018 Multi-functional, multicompartmental hyaluronan-binding protein 1 (HABP1/p32/gC1qR): implication in cancer progression and metastasis. Oncotarget 39 29535843
2006 Upregulation of hyaluronan binding protein 1 (HABP1/p32/gC1qR) is associated with Cisplatin induced apoptosis. Apoptosis : an international journal on programmed cell death 39 16544101
2006 gC1qR/p33 serves as a molecular bridge between the complement and contact activation systems and is an important catalyst in inflammation. Advances in experimental medicine and biology 39 16893067
2017 Complement component 1, q subcomponent binding protein (C1QBP) in lipid rafts mediates hepatic metastasis of pancreatic cancer by regulating IGF-1/IGF-1R signaling. International journal of cancer 38 28608366
2015 Mitochondrial p32 is upregulated in Myc expressing brain cancers and mediates glutamine addiction. Oncotarget 37 25528767
2004 Differential expression of Hyaluronic Acid Binding Protein 1 (HABP1)/P32/C1QBP during progression of epidermal carcinoma. Molecular and cellular biochemistry 37 15663194
2021 P32-specific CAR T cells with dual antitumor and antiangiogenic therapeutic potential in gliomas. Nature communications 35 34127674
2016 Cytoadhesion to gC1qR through Plasmodium falciparum Erythrocyte Membrane Protein 1 in Severe Malaria. PLoS pathogens 34 27835682
2015 λ-Carrageenan P32 Is a Potent Inhibitor of Rabies Virus Infection. PloS one 34 26465753
2015 ZNF32 protects against oxidative stress-induced apoptosis by modulating C1QBP transcription. Oncotarget 34 26497555
2001 Human blood platelet gC1qR/p33. Immunological reviews 34 11414364
2016 Incidence and molecular characterisation of lumpy skin disease virus in Zimbabwe using the P32 gene. Tropical animal health and production 33 27671793
2011 Interaction of high-molecular-weight kininogen with endothelial cell binding proteins suPAR, gC1qR and cytokeratin 1 determined by surface plasmon resonance (BiaCore). Thrombosis and haemostasis 33 21544310
2020 p32/C1QBP regulates OMA1-dependent proteolytic processing of OPA1 to maintain mitochondrial connectivity related to mitochondrial dysfunction and apoptosis. Scientific reports 32 32606429
2005 SOCS1 and SOCS3 are targeted by hepatitis C virus core/gC1qR ligation to inhibit T-cell function. Journal of virology 32 16306613
1999 Interaction of factor XII and high molecular weight kininogen with cytokeratin 1 and gC1qR of vascular endothelial cells and with aggregated Abeta protein of Alzheimer's disease. Immunopharmacology 32 10596854
2013 Soluble gC1qR is an autocrine signal that induces B1R expression on endothelial cells. Journal of immunology (Baltimore, Md. : 1950) 31 24319267
2014 C1QBP negatively regulates the activation of oncoprotein YBX1 in the renal cell carcinoma as revealed by interactomics analysis. Journal of proteome research 30 25497084
2011 Involvement of p32 and microtubules in alteration of mitochondrial functions by rubella virus. Journal of virology 29 21248045
2018 Porcine Circovirus Type 2 Suppresses IL-12p40 Induction via Capsid/gC1qR-Mediated MicroRNAs and Signalings. Journal of immunology (Baltimore, Md. : 1950) 27 29858268
2016 Identification of a novel mitochondrial interacting protein of C1QBP using subcellular fractionation coupled with CoIP-MS. Analytical and bioanalytical chemistry 27 26753982
2020 Factor XII and kininogen asymmetric assembly with gC1qR/C1QBP/P32 is governed by allostery. Blood 26 32559765
2013 A calreticulin/gC1qR complex prevents cells from dying: a conserved mechanism from arthropods to humans. Journal of molecular cell biology 26 23378602
1986 Varicella-zoster virus p32/p36 complex is present in both the viral capsid and the nuclear matrix of the infected cell. Journal of virology 26 3001341
2014 Impaired p32 regulation caused by the lymphoma-prone RECQ4 mutation drives mitochondrial dysfunction. Cell reports 25 24746816
2019 Systematic Multiomics Analysis of Alterations in C1QBP mRNA Expression and Relevance for Clinical Outcomes in Cancers. Journal of clinical medicine 24 30991713
2017 C1QBP suppresses cell adhesion and metastasis of renal carcinoma cells. Scientific reports 24 28428626
2011 A novel pathogen-binding gC1qR homolog, FcgC1qR, in the Chinese white shrimp, Fenneropenaeus chinensis. Developmental and comparative immunology 24 21893092
2004 Coordinated regulation of replication protein A activities by its subunits p14 and p32. The Journal of biological chemistry 24 15205463
2024 p32 regulates glycometabolism and TCA cycle to inhibit ccRCC progression via copper-induced DLAT lipoylation oligomerization. International journal of biological sciences 23 38169635
2017 Mitochondrial protein p32/HAPB1/gC1qR/C1qbp is required for efficient respiratory syncytial virus production. Biochemical and biophysical research communications 23 28576489
2017 A novel small molecule inhibitor of p32 mitochondrial protein overexpressed in glioma. Journal of translational medicine 23 29047383
2017 Neural-specific deletion of mitochondrial p32/C1qbp leads to leukoencephalopathy due to undifferentiated oligodendrocyte and axon degeneration. Scientific reports 22 29123152
2022 Complement C1q Binding Protein (C1QBP): Physiological Functions, Mutation-Associated Mitochondrial Cardiomyopathy and Current Disease Models. Frontiers in cardiovascular medicine 21 35310974
2002 Disulfide bond formation through Cys186 facilitates functionally relevant dimerization of trimeric hyaluronan-binding protein 1 (HABP1)/p32/gC1qR. European journal of biochemistry 21 11784324
2017 C1QBP Regulates YBX1 to Suppress the Androgen Receptor (AR)-Enhanced RCC Cell Invasion. Neoplasia (New York, N.Y.) 20 28107702
2014 Characterization of a gC1qR from the giant freshwater prawn, Macrobrachium rosenbergii. Fish & shellfish immunology 20 25555810
2011 Structure-function studies using deletion mutants identify domains of gC1qR/p33 as potential therapeutic targets for vascular permeability and inflammation. Frontiers in immunology 20 22282702
2002 Reduction in the level of hyaluronan binding protein 1 (HABP1) is associated with loss of sperm motility. Journal of reproductive immunology 20 11730903
1998 Physical association between the EBV protein EBNA-1 and P32/TAP/hyaluronectin. Journal of biomedical science 20 9678487
2020 gC1qR/HABP1/p32 Is a Potential New Therapeutic Target Against Mesothelioma. Frontiers in oncology 19 32903438
2017 C1QBP is upregulated in colon cancer and binds to apolipoprotein A-I. Experimental and therapeutic medicine 19 28565870
2016 Antibody neutralization of cell-surface gC1qR/HABP1/SF2-p32 prevents lamellipodia formation and tumorigenesis. Oncotarget 19 27363031
2016 Analysis of the Interaction between Globular Head Modules of Human C1q and Its Candidate Receptor gC1qR. Frontiers in immunology 19 28018340
2015 Soluble gC1qR in Blood and Body Fluids: Examination in a Pancreatic Cancer Patient Cohort. International journal of cancer research and molecular mechanisms 19 26973884
2011 The role of gC1qR in regulating survival of human papillomavirus 16 oncogene-transfected cervical cancer cells. International journal of oncology 19 21725590
2013 Autophagic vacuolation induced by excess ROS generation in HABP1/p32/gC1qR overexpressing fibroblasts and its reversal by polymeric hyaluronan. PloS one 18 24205125
2012 Interaction of HmC1q with leech microglial cells: involvement of C1qBP-related molecule in the induction of cell chemotaxis. Journal of neuroinflammation 18 22356764
2007 The exosporium of B. cereus contains a binding site for gC1qR/p33: implication in spore attachment and/or entry. Advances in experimental medicine and biology 18 17892212
2003 Sperm surface hyaluronan binding protein (HABP1) interacts with zona pellucida of water buffalo (Bubalus bubalis) through its clustered mannose residues. Molecular reproduction and development 18 12506357
1998 The soluble recombinant form of a binding protein/receptor for the globular domain of C1q (gC1qR) enhances blood coagulation. Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis 18 9607116
2022 An approach to p32/gC1qR/HABP1: a multifunctional protein with an essential role in cancer. Journal of cancer research and clinical oncology 17 35441886
2018 p32 regulates ER stress and lipid homeostasis by down-regulating GCS1 expression. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 17 29465311
2013 Targeting gC1qR domains for therapy against infection and inflammation. Advances in experimental medicine and biology 17 23402021
2003 Specific interactions between gC1qR and alpha1-adrenoceptor subtypes. Journal of receptor and signal transduction research 17 14626446
2002 Stage-specific expression of proprotein form of hyaluronan binding protein 1 (HABP1) during spermatogenesis in rat. Molecular reproduction and development 17 11984833