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Hepatitis C virus core protein ligates gC1qR to induce A20 (show TNFAIP3 ELISA Kits) expression in macrophages via P38 (show CRK ELISA Kits), JNK (show MAPK8 ELISA Kits) and NF-kappaB (show NFKB1 ELISA Kits) signaling pathways, which leads to a low-grade chronic inflammation during HCV infection.
The RAP80 (show UIMC1 ELISA Kits) deficiency reduces the protein level of p32 and p32 dependent mitochondrial translating proteins such as Rieske and COX1 (show COX1 ELISA Kits).
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 (show YBX1 ELISA Kits) to suppress the AR-enhanced RCC (show XRCC1 ELISA Kits) cell invasion. Targeting this newly identified C1QBP/YBX1 (show YBX1 ELISA Kits)/AR/MMP9 (show MMP9 ELISA Kits) signal pathway may provide a new potential therapy to better suppress RCC (show XRCC1 ELISA Kits) metastasis.
C1QBP interacts with DLAT (show DLAT ELISA Kits) and regulates the enzyme activity of pyruvate dehydrogenase (show PDP ELISA Kits).
application of p33 (show LTB ELISA Kits) 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 (show COX6B2 ELISA Kits) p32 as a novel interactor of parkin (show PARK2 ELISA Kits) 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 (show ATM ELISA Kits) 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 (show ROS1 ELISA Kits) generation in HABP1 overexpressing cells leading to apoptosis was due to mitochondrial HABP1 accumulation.
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