Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Sélectionnez vos espèces et l'application
anti-Human C1QBP Anticorps:
anti-Mouse (Murine) C1QBP Anticorps:
anti-Rat (Rattus) C1QBP Anticorps:
Vous arrivez à notre recherche pré-filtrée.
Human Polyclonal C1QBP Primary Antibody pour ELISA, WB - ABIN544482
Kitazawa, Takenaka, Kondo, Mizoguchi, Kitazawa: Protruding disordered loop of gC1qR is specifically exposed and related to antiapoptotic property in germ cell lineage. dans Histochemistry and cell biology 2006
Show all 3 Pubmed References
Human Polyclonal C1QBP Primary Antibody pour ELISA, WB - ABIN544481
Ghebrehiwet, Tantral, Titmus, Panessa-Warren, Tortora, Wong, Warren: The exosporium of B. cereus contains a binding site for gC1qR/p33: implication in spore attachment and/or entry. dans Advances in experimental medicine and biology 2007
Show all 3 Pubmed References
Human Polyclonal C1QBP Primary Antibody pour IHC, IHC (p) - ABIN4316530
Matos, Horn, Beards, Lui, Desforges, Harris: A role for the mitochondrial-associated protein p32 in regulation of trophoblast proliferation. dans Molecular human reproduction 2014
these results demonstrate that host-derived p32 has an important immunomodulating function that helps to counterbalance an overwhelming danger-associated molecular patterns response
We propose that endogenous gC1qR/p33 physically interacts with MCP-1 causing stabilization of the MCP-1 protein and stimulation of its activity in human periodontal ligament cells, suggesting a novel gC1qR/p33-mediated pro-inflammatory mechanism of action.
C1QBP may regulate L1CAM expression in renal cell carcinoma (RCC) through the Wnt/beta-Catenin pathway, thus affecting RCC cell adhesion, migration and metastasis.
Hepatitis C virus core protein ligates gC1qR to induce A20 expression in macrophages via P38, JNK and NF-kappaB signaling pathways, which leads to a low-grade chronic inflammation during HCV infection.
The RAP80 deficiency reduces the protein level of p32 and p32 dependent mitochondrial translating proteins such as Rieske and COX1.
Mutation in C1QBP gene is associated with Severe Neonatal-, Childhood-, or Later-Onset Cardiomyopathy Associated with Combined Respiratory-Chain Deficiencies.
results implicate p32 as a key host factor for RSV virus production, and bring to light the potential importance of mitochondria in RSV infection
single nucleotide polymorphism srs2285747 of HABP1 increased breast cancer risk and elevated its protein expression in northern Chinese women
The authors identified Importin-alpha1 to bind to Coxiella burnetii AnkG and concluded that binding of AnkG to p32 and Importin-alpha1 is essential for its migration into the nucleus.
HABP1 overexpression is associated with cervical cancer.
This study supports a key role for gC1qR in malaria-associated endovascular pathogenesis
these data suggest that C1QBP could regulate YBX1 to suppress the AR-enhanced RCC cell invasion. Targeting this newly identified C1QBP/YBX1/AR/MMP9 signal pathway may provide a new potential therapy to better suppress RCC metastasis.
C1QBP interacts with DLAT and regulates the enzyme activity of pyruvate dehydrogenase.
Sp1-ZNF32-C1QBP axis protects against oxidative stress/apoptosis in hepatocellular carcinoma cells.
Findings highlight a cytoprotective role of p32 under starvation conditions by regulating ULK1 stability, and uncover a crucial role of the p32-ULK1-autophagy axis in coordinating stress response, cell survival and mitochondrial homeostasis.
p32 appeared to be a core component of herpesvirus nuclear egress complexes, like UL31 and UL34 homologs in other herpesviruses, and to play multiple roles in herpesvirus nuclear egress.
data suggest that C1QBP is a novel regulator of YBX1, and the expression of C1QBP and the nuclear expression of YBX1 could both be used as independent prognostic makers for cancer progression in the RCC patients
Data show that p32 hyaluronan binding protein (p32) is a direct transcriptional target of oncogene Myc and that high level of Myc in malignant brain cancers correlates with high expression of p32.
HABP1 protein high expression may contribute to the tumor progression and poor prognosis of TNBC, especially in predicting prognosis in TNBCs without lymph node metastasis.
our findings suggest that the C1QBP protein could be a potential proliferative marker in breast cancer
Data show that p32 (C1QBP) plays a critical role in energy homeostasis and represents a potential target for the development of anti-obesity drugs
p32 promotes lipid biosynthesis by modulating fatty acid-induced ER stress. p32 interacts with GCS1 and reduces GCS1 in a lysosome-dependent manner.
Cardiomyocyte-specific loss of mitochondrial p32/C1qbp causes cardiomyopathy and activates stress responses, leading to heart failure.
macrophage/neutrophil-specific p32 conditional knockout mice showed exacerbated inflammation and reduced survival in response to LPS. Based on these findings, p32 is an important regulator of inflammatory signaling and is a potential drug candidate for treatment of sepsis in mammals.
application of p33 significantly improved survival in mice receiving an otherwise lethal dose of histones.
Authors propose that p32 is required for functional mitoribosome formation to synthesize proteins within mitochondria.
we have identified a mitochondrial protein p32 as a novel interactor of parkin in the brain
C1qbp could directly bind to CypD. Therefore C1qbp appears to act as an endogenous inhibitor of the MPT pore, most likely through binding to CypD, and thus protects cells against oxidative stress.
Intracellular localization and further functional studies suggested that CHCHD2 and HABP1 may mutually regulate each other to balance cell migration.
Rat and mouse homologs of the HABP1 pseudogene also contain multiple mutations, leading to the insertion of premature stop codons confirming the identity of a processed pseudogene.
Study demonstrates the differential expression of HABP1 during progression of epidermal carcinoma.
p32 phosphorylation by ATM might be a new transcriptional regulatory pathway for specific DNA damage responses in heart.
The reduction in oxidant generation and drop in apoptotic cell population caused by disruption of HABP1, corroborating the fact that excess ROS generation in HABP1 overexpressing cells leading to apoptosis was due to mitochondrial HABP1 accumulation.
Differential isoform expression and interaction with the P32 regulatory protein controls the subcellular localization of the splicing factor U2AF26
Mitochondrial p32/C1QBP is a critical mediator of p14ARF-induced apoptosis.
The human complement subcomponent C1q associates with C1r and C1s in order to yield the first component of the serum complement system. The protein encoded by this gene is known to bind to the globular heads of C1q molecules and inhibit C1 activation. This protein has also been identified as the p32 subunit of pre-mRNA splicing factor SF2, as well as a hyaluronic acid-binding protein.
p32 subunit of splicing factor SF2
, 38k protein
, complement component 1, q subcomponent binding protein
, ASF/SF2-associated protein p32
, C1q globular domain-binding protein
, complement component 1 Q subcomponent-binding protein, mitochondrial
, glycoprotein gC1qBP
, hyaluronan-binding protein 1
, mitochondrial matrix protein p32
, splicing factor SF2-associated protein
, GC1q-R protein