Affinage

C1QBP

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

Length
282 aa
Mass
31.4 kDa
Annotated
2026-06-09
100 papers in source corpus 42 papers cited in narrative 42 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

C1QBP (p32/gC1qR/HABP1) is a homotrimeric multifunctional protein whose primary residence is the mitochondrial matrix, where it supports mitochondrial gene expression and energy metabolism, but which also operates as a multiligand docking platform across the cell surface, cytoplasm, and nucleus (PMID:9531316, PMID:22904065, PMID:32559765). An N-terminal presequence directs import into the mitochondrial matrix, where the mature protein binds mitochondrial mRNAs and associates with the mitoribosome to drive mitochondrial translation; loss of C1QBP causes mid-gestation lethality and severe respiratory-chain dysfunction in mice, and biallelic loss-of-function mutations in humans cause combined deficiency of OXPHOS complexes I, III, and IV (PMID:9531316, PMID:22904065, PMID:28942965). Within the matrix it binds the PDH E2 subunit DLAT and positively regulates pyruvate dehydrogenase activity, linking it to acetyl-CoA supply, and tissue-specific deletion produces cardiac contractile failure with AMPK activation and integrated stress responses while CD8+ T-cell-specific loss impairs effector differentiation through metabolite-driven histone hypoacetylation and hypermethylation (PMID:30428349, PMID:26753982, PMID:28498888, PMID:34860557). The protein assembles as a trimer in equilibrium with a disulfide-linked hexamer, and a crystal structure of the FXII fibronectin type II domain bound to the gC1qR trimer defines the zinc-dependent, asymmetric binding chemistry by which it clusters FXII and high-molecular-weight kininogen into a procoagulant ternary complex on endothelial cells together with uPAR and cytokeratin 1 (PMID:11784324, PMID:32559765, PMID:11986212, PMID:8710908). Through spatially distinct binding sites it engages an extensive ligand repertoire — C1q, vitronectin, fibrinogen, and microbial proteins including Listeria InlB, HCV core, and S. aureus protein A — to modulate complement, kinin, coagulation, and host-pathogen interactions (PMID:8900153, PMID:8710908, PMID:10747014, PMID:11086025, PMID:10722602, PMID:10075865, PMID:28018340). C1QBP additionally restrains innate antiviral signaling by translocating to the mitochondrial outer membrane and binding MAVS to suppress RIG-I/MDA5 responses, forms a nuclear complex with MRE11/RAD50 (the MRC) that is dissociated by ATM-mediated MRE11 phosphorylation to license homologous-recombination repair, and acts as an ERK substrate that relocates to the nucleus upon mitogenic stimulation (PMID:19164550, PMID:31353207, PMID:11866440). In cancer it interacts with YBX1 to suppress oncogenic invasion signaling, and caspase-1 cleavage prevents its mitochondrial import to redirect metabolism toward aerobic glycolysis (PMID:25497084, PMID:28107702, PMID:33102234).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1996 High

    Established that gC1qR is a cell-surface receptor whose ligand-binding repertoire extends beyond C1q, defining anatomically distinct binding sites for vitronectin and for the contact-system proteins HK and factor XII.

    Evidence Affinity chromatography of endothelial membranes and recombinant protein binding assays with truncation/inhibition mapping

    PMID:8710908 PMID:8900153

    Open questions at the time
    • Structural basis of distinct ligand sites not resolved
    • Physiological relevance of cell-surface display from a mitochondrial protein not addressed
  2. 1997 Medium

    Demonstrated that gC1qR physically associates with calreticulin (cC1qR), an early hint that it acts as a scaffold forming multiprotein receptor complexes rather than a lone receptor.

    Evidence Solid-phase ELISA, domain mapping, and Co-IP from cell membranes

    PMID:9233640

    Open questions at the time
    • Functional consequence of the cC1qR/gC1qR complex unclear
    • Single lab
  3. 1998 High

    Defined the dual localization paradox by identifying an N-terminal mitochondrial targeting presequence directing the protein to the matrix, while also showing soluble recombinant protein has procoagulant activity in plasma.

    Evidence GFP-presequence fusion, mitoplast fractionation, and plasma coagulation assays

    PMID:9531316 PMID:9607116

    Open questions at the time
    • Mechanism by which a matrix protein reaches the cell surface unexplained
    • Molecular basis of procoagulant activity not defined
  4. 1999 Medium

    Extended the coagulation/kinin role by mapping gC1qR binding to the HK light chain and to the fibrinogen D domain, where it inhibits fibrin polymerization, positioning the protein at multiple nodes of the contact and clotting systems.

    Evidence Affinity chromatography with domain peptides, fibrin turbidity assays, and antibody inhibition

    PMID:10075865 PMID:10479529

    Open questions at the time
    • In vivo relevance of fibrin inhibition versus procoagulant activity unreconciled
    • Single lab
  5. 2000 High

    Revealed gC1qR as a hijacked microbial receptor, serving as the direct entry receptor for Listeria InlB (recruiting Gab1/PI3K), binding HCV core to suppress T cells, and binding S. aureus protein A.

    Evidence Yeast two-hybrid, affinity chromatography, gain-of-function transfection entry assays, and Co-IP

    PMID:10722602 PMID:10747014 PMID:11086025

    Open questions at the time
    • How surface gC1qR transduces signals lacking a transmembrane domain unresolved
    • Receptor partners required for signaling incompletely defined
  6. 2001 High

    Defined the endothelial contact-system receptor complex (gC1qR/uPAR/cytokeratin 1) that binds and activates factor XII/prekallikrein zinc-dependently, and identified gC1qR as an ERK substrate that translocates to the nucleus, linking it to mitogenic signaling and to GABA(A) receptor beta subunits in brain.

    Evidence Flow cytometry/EM co-localization, purified-protein activation assays, in vitro kinase assay with PD98059, and reciprocal Co-IP from brain

    PMID:11204562 PMID:11350968 PMID:11866440 PMID:11986212

    Open questions at the time
    • Functional role of nuclear translocation not defined
    • GABA(A) interaction physiology unexplored
  7. 2002 Medium

    Characterized the quaternary structure, showing the protein equilibrates between a noncovalent trimer and a disulfide-linked hexamer (via Cys186) with the hexamer exhibiting enhanced ligand affinity.

    Evidence Size-exclusion chromatography, cross-linking, Cys186 modification, and comparative ligand binding

    PMID:11784324

    Open questions at the time
    • In vivo prevalence of hexamer not established
    • Single lab
  8. 2009 High

    Identified an immunoregulatory mechanism whereby gC1qR translocates to the mitochondrial outer membrane and binds MAVS to dampen RIG-I/MDA5 antiviral signaling, promoting viral replication.

    Evidence Co-IP with MAVS, siRNA knockdown with antiviral readouts, and fractionation showing translocation

    PMID:19164550

    Open questions at the time
    • Stimulus-driven trafficking mechanism to outer membrane unresolved
    • Single lab
  9. 2012 High

    Established the core mitochondrial function: C1QBP binds mitochondrial mRNAs and the mitoribosome and is essential for mitochondrial translation, with knockout causing embryonic lethality and respiratory-chain failure.

    Evidence p32-knockout mouse, in vitro RNA-binding assays, and mitoribosome Co-IP

    PMID:22904065

    Open questions at the time
    • Specificity/mechanism of mRNA binding not structurally defined
    • Role at the mitoribosome step not resolved
  10. 2017 High

    Cemented C1QBP as essential for human and tissue energy metabolism through disease genetics, complementation rescue, and a cardiomyocyte knockout linking its loss to OXPHOS failure, AMPK activation, and integrated stress responses.

    Evidence Patient genetics with C1qbp-/- MEF complementation (WT vs mutant), enzyme assays, and Cre-loxP cardiac knockout with respirometry

    PMID:28498888 PMID:28942965

    Open questions at the time
    • Genotype-phenotype spectrum of human mutations incompletely mapped
    • Tissue-specific vulnerability determinants unclear
  11. 2016 High

    Connected C1QBP directly to central carbon metabolism by identifying the PDH E2 subunit DLAT as a mitochondrial partner and showing C1QBP positively regulates PDH activity.

    Evidence Subcellular fractionation Co-IP-MS with PDH activity validation, later extended with dendritic-cell knockout and PDH-inhibitor phenocopy

    PMID:26753982 PMID:30428349

    Open questions at the time
    • Whether C1QBP regulates PDH directly or via translation of components unresolved
    • Stoichiometry of DLAT interaction undefined
  12. 2019 High

    Defined a nuclear genome-stability role: C1QBP forms the MRC complex with MRE11/RAD50 that holds MRE11 nuclease inactive until ATM phosphorylates MRE11 to dissociate the complex and license MRN-mediated DSB repair.

    Evidence Co-IP, nuclease activity assays, ATM kinase assay, phospho-site mutagenesis, and chromatin recruitment with genetic perturbation

    PMID:31353207

    Open questions at the time
    • How nuclear C1QBP pool is established relative to mitochondrial pool unclear
    • Dosage-sensitivity mechanism not fully defined
  13. 2021 High

    Demonstrated that C1QBP-dependent mitochondrial metabolism drives epigenetic programming of immune cell fate, with CD8+ T-cell loss causing metabolite imbalances that silence effector genes via histone modification changes.

    Evidence Conditional knockout with metabolomics, ChIP histone-modification analysis, respirometry, and pharmacological rescue

    PMID:34860557

    Open questions at the time
    • Generality across other immune lineages unestablished
    • Direct chromatin targets of the metabolite shift not enumerated
  14. 2020 High

    Provided the structural mechanism for contact-system clustering, showing zinc-dependent asymmetric binding of FXII and HK on the gC1qR trimer to form a procoagulant ~500 kDa ternary complex.

    Evidence Crystal structure of FXIIFnII-gC1qR, SPR with mutagenesis, gel filtration, and plasma coagulation assay

    PMID:32559765

    Open questions at the time
    • Structural basis of other ligand interactions still lacking
    • Physiological control of surface clustering in vivo unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How C1QBP partitions between mitochondrial, surface, cytoplasmic, and nuclear pools — and what governs the trafficking decisions that switch it between metabolic, signaling, repair, and receptor functions — remains the central unresolved question.
  • No unifying model for trafficking of a presequence-bearing matrix protein to the cell surface
  • Regulatory logic selecting among its functions per compartment unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0001618 virus receptor activity 3 GO:0098772 molecular function regulator activity 3 GO:0003723 RNA binding 1
Localization
GO:0005739 mitochondrion 4 GO:0005886 plasma membrane 4 GO:0005634 nucleus 2 GO:0005829 cytosol 2
Pathway
R-HSA-109582 Hemostasis 4 R-HSA-1430728 Metabolism 4 R-HSA-168256 Immune System 3 R-HSA-392499 Metabolism of proteins 1 R-HSA-73894 DNA Repair 1
Partners
C1QCD44DLATF12MAVSMRE11RAD50YBX1
Complex memberships
DC-SIGN/C1q/gC1qRMRE11/RAD50 (MRC)gC1qR/uPAR/cytokeratin 1 contact-system receptormitoribosome

Evidence

Reading pass · 42 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 p32/gC1qR contains a 33-amino acid N-terminal presequence that functions as a mitochondrial targeting sequence; a fusion protein of this presequence with GFP translocated to mitochondria of transfected COS-7 cells with proteolytic removal of ~6 kDa, and the mature protein resides in the mitochondrial matrix and/or inner membrane. Confocal laser-scanning microscopy, GFP fusion protein transfection, mitoplast fractionation, immunocytochemistry Journal of immunology High 9531316
1996 Recombinant gC1qR binds the heparin-binding multimeric form of vitronectin (but not the plasma form) with saturable, high-affinity interaction (KD ~20 nM) inhibitable by glycosaminoglycans; this binding site is distinct from the C1q-binding site, as a truncated gC1qR lacking the N-terminal 22 amino acids lost vitronectin binding but retained C1q binding. Recombinant protein expression, affinity chromatography with plasma/serum, solid-phase binding assay, inhibition studies with truncation mutants The Journal of biological chemistry High 8900153
1996 gC1qR is a zinc-dependent endothelial cell binding protein for high molecular weight kininogen (HK) and factor XII; these proteins bind to a site on gC1qR distinct from the C1q-binding site, as C1q did not inhibit HK binding and anti-C1q-blocking mAbs did not block HK binding. HK-affinity chromatography of HUVEC membrane proteins in presence/absence of ZnCl2, SDS-PAGE, Western blot with anti-gC1qR mAbs, ligand blot, 125I-HK binding inhibition assay Proceedings of the National Academy of Sciences High 8710908
2000 gC1q-R/p33 is a direct cellular receptor for InlB, the Listeria monocytogenes invasion protein; InlB binds gC1qR directly (shown by affinity chromatography and ELISA), and transfection of non-permissive cells with human gC1qR promotes entry of InlB-coated beads. gC1qR associates with the adaptor Gab1 upon InlB stimulation and mediates InlB-dependent PI3-kinase membrane recruitment and activation. Affinity chromatography, ELISA, transfection of non-permissive GPC16 cells, entry assay with InlB-coated beads, co-immunoprecipitation (gC1qR with Gab1), antibody/C1q inhibition of entry The EMBO journal High 10747014
2000 HCV core protein binds gC1qR (identified by yeast two-hybrid screen) and inhibits T-cell proliferation via gC1qR; the core binds the region spanning amino acids 188–259 of gC1qR (distinct from C1q-binding site), and anti-gC1qR antibody reverses core-induced T-cell proliferation inhibition. Yeast two-hybrid screen of human T-cell library, biochemical binding analysis with deletion mutants, T-cell proliferation assay with antibody reversal The Journal of clinical investigation High 11086025
2000 Staphylococcus aureus protein A directly binds platelet gC1qR/p33; the protein A-binding domain on gC1qR lies outside the N-terminal alpha helix (residues 74–95), distinct from the C1q-binding site. gC1qR capture of S. aureus was inhibited by soluble rgC1qR, anti-gC1qR F(ab')2, and rabbit IgG, and tyrosine inactivation of protein A abrogated gC1qR binding. Affinity capture with fixed S. aureus/protein A-agarose, solid-phase ELISA with biotinylated gC1qR, inhibition studies, truncated gC1qR mutant lacking residues 74–95 Infection and immunity Medium 10722602
2001 Factor XII binds to a multiprotein receptor complex on endothelial cell membranes comprising gC1qR, urokinase plasminogen activator receptor (uPAR), and cytokeratin 1; antibodies to gC1qR, uPAR, and CK1 each block FXII binding. FXII binds via a region in its fibronectin type II domain (peptide YHK9 from residues 39–47). Flow cytometry binding assays with FITC/biotin-FXII, confocal and electron microscopy co-localization, antibody blocking assays, recombinant receptor inhibition Blood High 11986212
2001 Factor XII, prekallikrein, and HK activation (conversion of prekallikrein to kallikrein) is catalyzed by gC1qR and cytokeratin 1 in a zinc-dependent, Factor XII-dependent manner; normal plasma activation on endothelial cells is inhibited by antibodies to gC1qR and cytokeratin 1. Purified protein contact activation assay, plasma activation assay on endothelial cells, antibody inhibition Thrombosis and haemostasis Medium 11204562
1999 gC1qR binds the light chain of HK (zinc-dependent) while cytokeratin 1 binds the heavy-chain domain 3 of HK; anti-gC1qR antibody inhibits HK binding to endothelial cells by 72% and combined anti-gC1qR + anti-CK1 inhibits by 86%. Affinity chromatography of HUVEC membranes with HK or domain 3 peptide columns, zinc-dependent elution, Western blot, antibody inhibition of 125I-HK binding Clinical immunology Medium 10479529
1997 cC1qR (calreticulin) and gC1qR form a complex; biotinylated cC1qR binds recombinant and native gC1qR with binding sites at N-terminal residues 76–93 and 204–218. Anti-gC1qR mAbs 60.11, 46.23, and 74.5.2 inhibit this interaction, and co-immunoprecipitation of Raji cell membranes with anti-gC1qR mAbs co-precipitates cC1qR. Solid-phase ELISA with biotinylated cC1qR and recombinant gC1qR, antibody inhibition, co-immunoprecipitation from cell membranes Journal of immunology Medium 9233640
1999 gC1qR binds the C-terminal cytoplasmic domain of the alpha1B-adrenergic receptor (residues 344–516, specifically the arginine-rich residues 369–378) as identified by yeast two-hybrid; co-expression of gC1qR with the receptor causes redistribution of the receptor from plasma membrane to intracellular locations and receptor downregulation. Yeast two-hybrid screen of rat liver cDNA library, co-immunoprecipitation from COS-7 cells, confocal co-localization, deletion mutant mapping The Journal of biological chemistry Medium 10409668
2002 HABP1/C1QBP is an endogenous substrate for MAP kinase (ERK); in vitro kinase assay demonstrates ERK phosphorylates HABP1, and HABP1 co-immunoprecipitates with activated ERK in cells. Upon PMA stimulation, HABP1 translocates from cytoplasm to nucleus in an ERK-dependent manner (blocked by PD98059). In vitro kinase assay, co-immunoprecipitation with activated ERK, subcellular fractionation/immunofluorescence after PMA treatment, ERK inhibitor PD98059 Biochemical and biophysical research communications Medium 11866440
2004 Direct binding of HCV core protein to gC1qR on T cells impairs Lck and Akt activation; this binding is inhibitable by anti-gC1qR antibody or soluble gC1qR, is reduced by gC1qR siRNA knockdown, and enhanced by gC1qR transfection. BIAcore analysis gives binding affinity constant of 3.8×10−7 M. BIAcore surface plasmon resonance, flow cytometry binding, siRNA knockdown of gC1qR, transfection of guinea pig cells with human gC1qR, Western blot for Lck/ZAP-70/Akt phosphorylation Journal of virology High 15163734
2003 HCV core binding to gC1qR on T cells induces G0/G1 cell cycle arrest by stabilizing the CDK inhibitor p27Kip1, thereby preventing CDK2/4 and cyclin E/D expression, pRb phosphorylation, and G1→S transition; arrest is reversible by anti-gC1qR antibody. T-cell proliferation assay, flow cytometry cell cycle analysis, Western blot for CDK2/4, cyclin E/D, pRb, p27Kip1, antibody rescue experiment Virology Medium 14517080
2005 HCV core/gC1qR ligation on T cells induces SOCS1 and SOCS3 expression, which disrupts STAT phosphorylation and inhibits IFN-γ production; siRNA silencing of either SOCS1 or SOCS3 abrogates the inhibitory effect of core on T-cell IFN-γ production. T-cell functional assay, Western blot for SOCS1/3 and p-STAT, siRNA knockdown of SOCS1 and SOCS3, IFN-γ ELISA Journal of virology Medium 16306613
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/Cardif, thereby disrupting RIG-I/MDA5 signaling and promoting virus replication. Knockdown of gC1qR enhances RIG-I-dependent antiviral signaling. Co-immunoprecipitation (gC1qR with MAVS), siRNA knockdown, subcellular fractionation showing translocation, viral replication assays Proceedings of the National Academy of Sciences High 19164550
2001 MT1-MMP cleaves gC1qR proteolytically at Gly79↓Gln80 in vitro and in cell culture; the hemopexin-like domain of MT1-MMP is required for proteolysis. A catalytically inactive MT1-MMP retains gC1qR binding ability and acts as a cell-surface receptor for gC1qR. In vitro proteolysis assay with recombinant proteins, cell culture experiments, MT1-MMP domain deletion constructs, hydroxamate inhibitor studies, co-precipitation The Journal of biological chemistry Medium 11773076
2012 p32/gC1qR is required for mitochondrial translation; p32-knockout mice show mid-gestation lethality and severe respiratory chain dysfunction. Recombinant p32 binds mitochondrial mRNA (not DNA), endogenous p32 associates with all mitochondrial mRNA species in vivo, and co-immunoprecipitation shows p32 associates with the mitoribosome. p32-knockout mouse generation, primary embryonic fibroblast analysis, in vitro RNA-binding assay, co-immunoprecipitation with mitoribosome, mitochondrial respiratory chain assays Nucleic acids research High 22904065
2007 Plasmodium falciparum-infected red blood cells use gC1qR/HABP1/p32 as a receptor to bind to human brain microvascular endothelial cells and to platelets for clumping, as demonstrated by in vitro cytoadherence assays. In vitro cytoadherence assay on cells expressing gC1qR, blocking with anti-gC1qR antibodies and recombinant gC1qR PLoS pathogens Medium 17907801
2011 Cell-surface gC1qR is required for growth factor-induced lamellipodia formation and cell migration; gC1qR is concentrated in lamellipodia with CD44, monosialoganglioside, actin, and phospho-FAK, and gC1qR depletion reduces FAK activation, receptor tyrosine kinase activation, lamellipodia formation, cell migration, and in vivo metastasis. siRNA knockdown, immunofluorescence co-localization in lamellipodia, Western blot for FAK/RTK phosphorylation, migration assay, xenograft mouse model The Journal of biological chemistry Medium 21536672
2013 Soluble gC1qR binds to endothelial cells via residues 174–180, with binding mediated through surface-bound fibrinogen; this binding induces upregulation of bradykinin receptor B1R expression, an effect diminished by gC1qR lacking residues 174–180 and 154–162 and inhibited by anti-fibrinogen antibody. Solid-phase binding assay, deconvolution fluorescence microscopy, flow cytometry for B1R expression, deletion mutant analysis, antibody inhibition Journal of immunology Medium 24319267
2001 gC1q-R/GABA(A) receptor beta subunit interaction: gC1qR co-purifies with immunopurified GABA(A) receptors and exhibits reciprocal co-immunoprecipitation from rat brain membranes. Yeast two-hybrid showed all beta subunits (but not alpha1 or gamma2) interact with gC1qR via a 15-amino-acid stretch (residues 399–413) containing 7 positively charged residues. Immunopurification from bovine brain, mass spectrometric identification, reciprocal Co-IP from rat brain membranes, yeast two-hybrid with deletion mutants The Journal of biological chemistry Medium 11350968
2017 Biallelic loss-of-function mutations in C1QBP cause combined respiratory-chain enzyme deficiency of complexes I, III, and IV; complementation of C1qbp−/− MEFs with wild-type but not mutagenized C1qbp restores OXPHOS protein levels and mitochondrial enzyme activities, establishing C1QBP as essential for mitochondrial energy metabolism. Patient genetics, C1qbp−/− MEF complementation assay (wild-type vs. mutant), respiratory chain enzyme activity assays, OXPHOS complex protein levels American journal of human genetics High 28942965
2017 Cardiomyocyte-specific deletion of p32/C1qbp causes contractile dysfunction, cardiac dilatation, fibrosis, decreased COX1 expression, reduced oxygen consumption, and increased oxidative stress. p32-deficient hearts show constitutive AMPK phosphorylation, reduced mTOR signaling, increased FGF21/integrated stress response, and impaired urea cycle, with median lifespan ~14 months. Cre-loxP cardiac-specific knockout, echocardiography, electron microscopy of mitochondria, Western blot for AMPK/mTOR/signaling proteins, metabolic analysis, Seahorse respirometry Cardiovascular research High 28498888
2018 p32/C1qbp interacts with the E2 component of the pyruvate dehydrogenase (PDH) complex (dihydrolipoamide S-acetyltransferase, DLAT) and positively regulates PDH activity; p32-deficient DCs show impaired LPS-induced citrate increase, and PDH inhibitor reproduces the p32-null phenotype of decreased DC maturation in vivo. Co-immunoprecipitation of p32 with DLAT, PDH activity assay in p32-deficient DCs, metabolic analysis, PDH inhibitor in vivo study in p32-null mice Cell reports High 30428349
2016 Subcellular fractionation combined with Co-IP-MS identified DLAT (dihydrolipoyllysine-residue acetyltransferase, E2 subunit of PDH complex) as a novel mitochondrial interacting partner of C1QBP; PDH activity is affected by C1QBP expression level. Subcellular fractionation coupled with Co-IP and mass spectrometry, validation by Co-IP/Western blot, PDH activity assay Analytical and bioanalytical chemistry Medium 26753982
2019 C1QBP forms a complex (MRC) with MRE11 and RAD50 that stabilizes MRE11/RAD50 but inhibits MRE11 nuclease activity by preventing DNA/chromatin binding. Upon DNA double-strand breaks, ATM phosphorylates MRE11 at S676/S678, dissociating the MRC and allowing MRN complex assembly and recruitment to DSBs; either excess or insufficient C1QBP impairs DSB repair. Co-immunoprecipitation, MRE11 nuclease activity assay, chromatin fractionation, ATM kinase assay, phosphorylation site mutagenesis, C1QBP knockdown/overexpression with DSB response readouts Molecular cell High 31353207
2014 C1QBP interacts with YBX1 and negatively regulates YBX1 activation; C1QBP knockdown enhances YBX1 phosphorylation and nuclear translocation in renal cell carcinoma. Co-immunoprecipitation followed by mass spectrometry, validation by IP/Western blot, siRNA knockdown of C1QBP, nuclear fractionation Journal of proteome research Medium 25497084
2017 C1QBP interacts with YBX1 and suppresses YBX1 activation by altering YBX1 phosphorylation and nuclear translocation in RCC cells; this suppresses AR-modulated MMP9 signaling to inhibit cell invasion, confirmed in orthotopic in vivo mouse model. Co-immunoprecipitation, Western blot for YBX1 phosphorylation and nuclear translocation, siRNA/overexpression functional assays, orthotopic mouse model Neoplasia Medium 28107702
2015 ZNF32 transcriptionally activates C1QBP expression; C1QBP is a direct target gene of ZNF32 that inactivates the p38 MAPK pathway to protect against oxidative stress-induced apoptosis. ZNF32-deficient cells show reduced C1QBP and increased p38 MAPK activation. Chromatin immunoprecipitation (ZNF32 binding to C1QBP promoter), ZNF32 knockdown/overexpression with C1QBP and p38 MAPK readouts, luciferase promoter assay Oncotarget Medium 26497555
2020 The FXII fibronectin type II (FnII) domain binds gC1qR in a Zn2+-dependent, asymmetric fashion on the gC1qR trimer; crystal structure of the FXIIFnII–gC1qR complex reveals Arg36 and Arg65 of FXII contact two distinct negatively charged pockets of gC1qR. gC1qR residues Asp185 and His187 coordinate Zn2+ adjacent to the FXII-binding site; binding induces allosteric ordering of the anionic G1-loop. HK domain 5 (HKD5) binds only one high-affinity site per gC1qR trimer via a central G3-loop (steric occlusion mechanism). gC1qR clusters FXII and HK into a ~500 kDa ternary complex and stimulates coagulation in a FXII-dependent manner. Crystal structure determination, SPR with mutagenesis, gel filtration for ternary complex, plasma-based FXII-dependent coagulation assay Blood High 32559765
2021 C1qbp is intrinsically required for effector CD8+ T cell differentiation; C1qbp-deficient CD8+ T cells fail to increase mitochondrial respiratory capacity upon activation, resulting in diminished acetyl-CoA and elevated fumarate and 2-hydroxyglutarate, leading to H3K27 hypoacetylation and hypermethylation and transcriptional silencing of effector genes. Fumarate supplementation or HDAC inhibitor + acetate reversed the differentiation defect. Conditional C1qbp knockout in CD8+ T cells, metabolomics, histone modification analysis (ChIP), Seahorse respirometry, viral infection models, pharmacological rescue Science advances High 34860557
2020 Active caspase-1 cleaves gC1qR at two caspase-1 cleavage sites, preventing mitochondrial import of gC1qR; this results in aerobic glycolysis (Warburg effect) and enhanced cell proliferation. Non-mitochondrial gC1qR localization correlated with caspase-1 activation and tumor grade in colorectal carcinoma patients. Caspase-1 cleavage assay in vitro, mitochondrial import assay, metabolic profiling of glycolysis/OXPHOS, cell proliferation assay, immunohistochemistry correlation in patient tumors Frontiers in oncology Medium 33102234
1999 gC1qR binds directly to the D domain of fibrinogen/fibrin (specifically the C-terminal segment of the fibrinogen gamma chain in fragment D-100, lost upon further plasmin digestion to D-60) and inhibits fibrin polymerization in a dose-dependent manner; at 2:1 molar ratio (gC1qR:fibrinogen), fibrin clot formation is completely inhibited. Solid-phase ELISA with biotinylated gC1qR, fibrin polymerization turbidity assay, binding to fibrinogen degradation fragments Clinical immunology Medium 10075865
1998 Soluble recombinant gC1qR (rgC1qR) enhances blood coagulation: it dose-dependently shortens prothrombin time and plasma recalcification time, with procoagulant activity measurable in factor XII- or factor XI-deficient plasma, suggesting activity not exclusively through the contact system. Prothrombin time assay in human plasma, plasma recalcification time assay, factor-deficient plasma studies, chromogenic substrate assays for thrombin and factor Xa Blood coagulation & fibrinolysis Medium 9607116
2021 Exosomal CD44v6/C1QBP complex from pancreatic cancer cells is delivered to the plasma membrane of hepatic stellate cells (HSCs), leading to phosphorylation of IGF-1 signaling molecules, HSC activation, and liver fibrosis promoting metastasis. C1QBP knockdown suppresses this effect in vitro and in vivo. Exosome isolation, stable lentiviral knockdown/overexpression, mouse liver metastasis models, Western blot for IGF-1R phosphorylation, HSC activation markers Gut Medium 33827783
2017 C1QBP in lipid rafts is required for IGF-1-induced hepatic metastasis of pancreatic cancer; IGF-1 triggers translocation of C1QBP from cytoplasm to lipid rafts and formation of a CD44v6/C1QBP complex, which promotes IGF-1R phosphorylation and downstream PI3K/MAPK signaling. C1QBP knockdown suppresses hepatic metastasis in nude mice. Lipid raft fractionation, Co-IP of CD44v6 and C1QBP, Western blot for IGF-1R/PI3K/MAPK phosphorylation, siRNA knockdown, hepatic metastasis mouse model International journal of cancer Medium 28608366
2002 HABP1/gC1qR forms a noncovalently associated homotrimer in equilibrium with a covalently linked hexamer (dimer of trimers) through disulfide bonds at Cys186; the hexameric form shows enhanced affinity for hyaluronan, gC1q, and mannosylated BSA compared with the trimer. Size-exclusion chromatography, glutaraldehyde cross-linking, fluorescence spectroscopy with Hg2+, Cys186 chemical modification, ligand-binding assays comparing trimer vs. hexamer European journal of biochemistry Medium 11784324
2012 DC-SIGN, C1q, and gC1qR form a trimolecular receptor complex on immature dendritic cells; DC-SIGN binds directly to C1q (and its globular domain) in a Ca2+-dependent manner at its mannose-binding pocket, and C1q/gC1qR associate with DC-SIGN on blood DC precursors and immature DCs by immunofluorescence and antigen-capture ELISA. ELISA, flow cytometry, immunoprecipitation, surface plasmon resonance, immunofluorescence microscopy, mannan competition, calcium chelation Blood Medium 22700724
2022 C1QBP directly interacts with the C9-ALS-associated proline-arginine dipeptide repeat protein (PR50); C1QBP knockdown in HMC3 microglial cells induces NLRP3 inflammasome activation similar to PR50 expression. The compound syringin blocks the PR50-C1QBP interaction and reduces PR50-induced NLRP3 inflammasome activation. Co-immunoprecipitation, siRNA knockdown of C1QBP, NLRP3 inflammasome activity assay, syringin treatment/competitive inhibition Cells Low 36231090
2005 HABP1/gC1qR localizes to the Golgi apparatus and disperses throughout the cell during mitosis, resembling the distribution dynamics of its ligand hyaluronan. Indirect immunofluorescence with Golgi and mitochondrial markers across cell cycle stages Cell research Low 15780180
2016 Mutational analysis of C1q globular head modules revealed that Arg162 of the ghA module is central to C1q-gC1qR interaction, while an Arg114Glu substitution in ghB enhanced binding; ghA, ghB, and ghC each independently bind gC1qR and attenuate PHA-stimulated PBMC proliferation. Recombinant globular head module expression, substitution mutagenesis, ELISA binding assays, cell proliferation assay Frontiers in immunology Medium 28018340

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 Mitochondrial/cell-surface protein p32/gC1qR as a molecular target in tumor cells and tumor stroma. Cancer research 278 18757437
2000 Interaction between complement receptor gC1qR and hepatitis C virus core protein inhibits T-lymphocyte proliferation. The Journal of clinical investigation 257 11086025
2000 gC1q-R/p32, a C1q-binding protein, is a receptor for the InlB invasion protein of Listeria monocytogenes. The EMBO journal 230 10747014
1996 Identification of the zinc-dependent endothelial cell binding protein for high molecular weight kininogen and factor XII: identity with the receptor that binds to the globular "heads" of C1q (gC1q-R). Proceedings of the National Academy of Sciences of the United States of America 202 8710908
2021 Exosome-delivered CD44v6/C1QBP complex drives pancreatic cancer liver metastasis by promoting fibrotic liver microenvironment. Gut 165 33827783
2001 gC1q-R/p33, a member of a new class of multifunctional and multicompartmental cellular proteins, is involved in inflammation and infection. Immunological reviews 151 11414365
1998 The multiligand-binding protein gC1qR, putative C1q receptor, is a mitochondrial protein. Journal of immunology (Baltimore, Md. : 1950) 147 9531316
2002 Factor XII interacts with the multiprotein assembly of urokinase plasminogen activator receptor, gC1qR, and cytokeratin 1 on endothelial cell membranes. Blood 145 11986212
2000 Staphylococcus aureus protein A recognizes platelet gC1qR/p33: a novel mechanism for staphylococcal interactions with platelets. Infection and immunity 142 10722602
2012 p32/gC1qR is indispensable for fetal development and mitochondrial translation: importance of its RNA-binding ability. Nucleic acids research 135 22904065
2004 cC1q-R (calreticulin) and gC1q-R/p33: ubiquitously expressed multi-ligand binding cellular proteins involved in inflammation and infection. Molecular immunology 126 15159063
1996 The binding protein for globular heads of complement C1q, gC1qR. Functional expression and characterization as a novel vitronectin binding factor. The Journal of biological chemistry 121 8900153
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 113 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 87 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 79 15146564
2022 Circular RNA MTCL1 promotes advanced laryngeal squamous cell carcinoma progression by inhibiting C1QBP ubiquitin degradation and mediating beta-catenin activation. Molecular cancer 77 35366893
2011 Cell-surface receptor for complement component C1q (gC1qR) is a key regulator for lamellipodia formation and cancer metastasis. The Journal of biological chemistry 77 21536672
1999 Cytokeratin 1 and gC1qR mediate high molecular weight kininogen binding to endothelial cells. Clinical immunology (Orlando, Fla.) 72 10479529
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 69 31744753
2001 Retargeting of the mitochondrial protein p32/gC1Qr to a cytoplasmic compartment and the cell surface. Journal of cell science 69 11493647
1995 Identification of a gC1q-binding protein (gC1q-R) on the surface of human neutrophils. Subcellular localization and binding properties in comparison with the cC1q-R. The Journal of clinical investigation 69 7706463
2011 The mitochondrial protein C1qbp promotes cell proliferation, migration and resistance to cell death. Cell cycle (Georgetown, Tex.) 65 22101277
2007 The contribution of gC1qR/p33 in infection and inflammation. Immunobiology 65 17544818
2007 Plasmodium falciparum uses gC1qR/HABP1/p32 as a receptor to bind to vascular endothelium and for platelet-mediated clumping. PLoS pathogens 65 17907801
2019 C1QBP Promotes Homologous Recombination by Stabilizing MRE11 and Controlling the Assembly and Activation of MRE11/RAD50/NBS1 Complex. Molecular cell 64 31353207
2016 New p32/gC1qR Ligands for Targeted Tumor Drug Delivery. Chembiochem : a European journal of chemical biology 64 26895508
2002 Hyaluronan binding protein 1 (HABP1)/C1QBP/p32 is an endogenous substrate for MAP kinase and is translocated to the nucleus upon mitogenic stimulation. Biochemical and biophysical research communications 62 11866440
2018 Mitochondrial p32/C1qbp Is a Critical Regulator of Dendritic Cell Metabolism and Maturation. Cell reports 60 30428349
1996 Identification of functional domains on gC1Q-R, a cell surface protein that binds to the globular "heads" of C1Q, using monoclonal antibodies and synthetic peptides. Hybridoma 60 8913782
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 56 28942965
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 54 12507504
2014 cC1qR/CR and gC1qR/p33: observations in cancer. Molecular immunology 53 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 53 21205079
2011 Hyaluronan-binding protein 1 (HABP1/p32/gC1qR) induces melanoma cell migration and tumor growth by NF-kappa B dependent MMP-2 activation through integrin α(v)β(3) interaction. Cellular signalling 52 21627988
2004 Expression of gC1q-R/p33 and its major ligands in human atherosclerotic lesions. Molecular immunology 52 15234555
1999 Interaction of the alpha(1B)-adrenergic receptor with gC1q-R, a multifunctional protein. The Journal of biological chemistry 52 10409668
1997 The C1q-binding cell membrane proteins cC1q-R and gC1q-R are released from activated cells: subcellular distribution and immunochemical characterization. Clinical immunology and immunopathology 52 9191880
2012 DC-SIGN, C1q, and gC1qR form a trimolecular receptor complex on the surface of monocyte-derived immature dendritic cells. Blood 49 22700724
1998 Mam33p, an oligomeric, acidic protein in the mitochondrial matrix of Saccharomyces cerevisiae is related to the human complement receptor gC1q-R. Yeast (Chichester, England) 49 9559539
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
2001 The hemopexin-like C-terminal domain of membrane type 1 matrix metalloproteinase regulates proteolysis of a multifunctional protein, gC1qR. The Journal of biological chemistry 47 11773076
2021 Mitochondrial C1qbp promotes differentiation of effector CD8+ T cells via metabolic-epigenetic reprogramming. Science advances 46 34860557
2012 gC1qR expression in normal and pathologic human tissues: differential expression in tissues of epithelial and mesenchymal origin. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 46 22638269
1997 Evidence that the two C1q binding membrane proteins, gC1q-R and cC1q-R, associate to form a complex. Journal of immunology (Baltimore, Md. : 1950) 46 9233640
2003 HCV core/gC1qR interaction arrests T cell cycle progression through stabilization of the cell cycle inhibitor p27Kip1. Virology 45 14517080
2021 Loss of Mucosal p32/gC1qR/HABP1 Triggers Energy Deficiency and Impairs Goblet Cell Differentiation in Ulcerative Colitis. Cellular and molecular gastroenterology and hepatology 44 33515804
2001 Factor XII-dependent contact activation on endothelial cells and binding proteins gC1qR and cytokeratin 1. Thrombosis and haemostasis 44 11204562
2018 Multi-functional, multicompartmental hyaluronan-binding protein 1 (HABP1/p32/gC1qR): implication in cancer progression and metastasis. Oncotarget 39 29535843
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 39 28608366
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
2012 Overexpression of hyaluronan-binding protein 1 (HABP1/p32/gC1qR) in HepG2 cells leads to increased hyaluronan synthesis and cell proliferation by up-regulation of cyclin D1 in AKT-dependent pathway. The Journal of biological chemistry 37 22451658
2006 gC1qR/p33 blockade reduces Staphylococcus aureus colonization of target tissues in an animal model of infective endocarditis. Infection and immunity 37 16861627
2004 Differential expression of Hyaluronic Acid Binding Protein 1 (HABP1)/P32/C1QBP during progression of epidermal carcinoma. Molecular and cellular biochemistry 37 15663194
2012 Significance of hyaluronan binding protein (HABP1/P32/gC1qR) expression in advanced serous ovarian cancer patients. Experimental and molecular pathology 35 22771308
2016 Cytoadhesion to gC1qR through Plasmodium falciparum Erythrocyte Membrane Protein 1 in Severe Malaria. PLoS pathogens 34 27835682
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
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
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
2014 C1QBP negatively regulates the activation of oncoprotein YBX1 in the renal cell carcinoma as revealed by interactomics analysis. Journal of proteome research 31 25497084
2013 Soluble gC1qR is an autocrine signal that induces B1R expression on endothelial cells. Journal of immunology (Baltimore, Md. : 1950) 31 24319267
2010 A gC1qR prevents white spot syndrome virus replication in the freshwater crayfish Pacifastacus leniusculus. Journal of virology 29 20686021
2018 Porcine Circovirus Type 2 Suppresses IL-12p40 Induction via Capsid/gC1qR-Mediated MicroRNAs and Signalings. Journal of immunology (Baltimore, Md. : 1950) 28 29858268
2016 Identification of a novel mitochondrial interacting protein of C1QBP using subcellular fractionation coupled with CoIP-MS. Analytical and bioanalytical chemistry 27 26753982
2013 Elevated expression of hyaluronic acid binding protein 1 (HABP1)/P32/C1QBP is a novel indicator for lymph node and peritoneal metastasis of epithelial ovarian cancer patients. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 27 23929393
2005 Golgi localization and dynamics of hyaluronan binding protein 1 (HABP1/p32/C1QBP) during the cell cycle. Cell research 27 15780180
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
2019 Systematic Multiomics Analysis of Alterations in C1QBP mRNA Expression and Relevance for Clinical Outcomes in Cancers. Journal of clinical medicine 25 30991713
2016 HCV core protein binds to gC1qR to induce A20 expression and inhibit cytokine production through MAPKs and NF-κB signaling pathways. Oncotarget 25 27183919
2020 GC1qR Cleavage by Caspase-1 Drives Aerobic Glycolysis in Tumor Cells. Frontiers in oncology 24 33102234
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
2022 C9-ALS-Associated Proline-Arginine Dipeptide Repeat Protein Induces Activation of NLRP3 Inflammasome of HMC3 Microglia Cells by Binding of Complement Component 1 Q Subcomponent-Binding Protein (C1QBP), and Syringin Prevents This Effect. Cells 23 36231090
2017 Mitochondrial protein p32/HAPB1/gC1qR/C1qbp is required for efficient respiratory syncytial virus production. Biochemical and biophysical research communications 23 28576489
1999 The receptor for the globular "heads" of C1q, gC1q-R, binds to fibrinogen/fibrin and impairs its polymerization. Clinical immunology (Orlando, Fla.) 23 10075865
2022 Complement C1q Binding Protein (C1QBP): Physiological Functions, Mutation-Associated Mitochondrial Cardiomyopathy and Current Disease Models. Frontiers in cardiovascular medicine 21 35310974
2017 C1QBP Regulates YBX1 to Suppress the Androgen Receptor (AR)-Enhanced RCC Cell Invasion. Neoplasia (New York, N.Y.) 21 28107702
2004 Tissue factor pathway inhibitor-2 (TFPI-2) recognizes the complement and kininogen binding protein gC1qR/p33 (gC1qR): implications for vascular inflammation. Thrombosis and haemostasis 21 15467913
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
2001 Interaction between GABA(A) receptor beta subunits and the multifunctional protein gC1q-R. The Journal of biological chemistry 21 11350968
2011 The role of gC1qR in regulating survival of human papillomavirus 16 oncogene-transfected cervical cancer cells. International journal of oncology 20 21725590
2002 Reduction in the level of hyaluronan binding protein 1 (HABP1) is associated with loss of sperm motility. Journal of reproductive immunology 20 11730903
2022 An approach to p32/gC1qR/HABP1: a multifunctional protein with an essential role in cancer. Journal of cancer research and clinical oncology 19 35441886
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
2013 Autophagic vacuolation induced by excess ROS generation in HABP1/p32/gC1qR overexpressing fibroblasts and its reversal by polymeric hyaluronan. PloS one 19 24205125
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

Missed literature

Know a paper Affinage missed for C1QBP? Flag it for the maintainers and the community.

No submissions yet.