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The protein encoded by GPR82 is an orphan G protein-coupled receptor of unknown function. Additionally we are shipping GPR82 Proteins (4) and many more products for this protein.
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GPR82-deficient mice showed decreased serum triacylglyceride levels, increased insulin (show INS Antibodies) sensitivity and glucose tolerance, most pronounced under Western diet
SAF-A (show HNRNPU Antibodies), in concert with Ku, temporally regulates base damage repair in irradiated cell genome.
HNRPU (show HNRNPU Antibodies) deletion is associated with neurodevelopmental disorders.
We broaden the clinical and mutational HNRNPU (show HNRNPU Antibodies)-associated spectrum, and demonstrate that heterozygous HNRNPU (show HNRNPU Antibodies) variants cause epilepsy, severe intellectual disability with striking speech impairment and variable central nervous system, cardiac, and renal anomalies.
Results show that SAF-A (show HNRNPU Antibodies) and caRNAs form a dynamic, transcriptionally responsive chromatin mesh that organizes large-scale chromosome structures and protects the genome from instability.
results confirm and refine the complex genotype-phenotype correlations existing in the 1qter microdeletion syndrome and define more precisely the neurodevelopmental phenotypes associated with genetic alterations of AKT3 (show AKT3 Antibodies), ZBTB18 (show ZNF238 Antibodies) and HNRNPU (show HNRNPU Antibodies) in humans
mutual regulatory mechanisms exist between PP4 (show ANXA5 Antibodies) and SAF-A (show HNRNPU Antibodies). Interactions between PP4 (show ANXA5 Antibodies) and SAF-A (show HNRNPU Antibodies) played a role in prometaphase/metaphase transition.
CENP-W (show CENPW Antibodies) interacts with hnRNPU (show HNRNPU Antibodies) and may contribute to kinetochore-microtubule attachment in mitotic cells.
Nuclear TDP-43 (show TARDBP Antibodies) becomes neurotoxic by escaping from the inhibitory regulation by hnRNP-U (show HNRNPU Antibodies) or hnRNP (show HNRNPC Antibodies)-A2. hnRNP-U (show HNRNPU Antibodies) inhibits TDP-43 (show TARDBP Antibodies)-mediated alterations in splicing of POLDIP3 (show POLDIP3 Antibodies) mRNA.
These results suggest that HNRNPU, FAM36A, and NCRNA00201 are not major genes for microcephaly and corpus callosum abnormalities but are good candidates for intellectual disability (ID) and seizures.
both phosphorylation and dephosphorylation of SAF-A (show HNRNPU Antibodies) serine 59 by PLK1 (show PLK1 Antibodies) and PP2A (show PPP2R4 Antibodies), respectively, are required for accurate and timely exit from mitosis.
This gene belongs to the subfamily of ubiquitously expressed heterogeneous nuclear ribonucleoproteins (hnRNPs). The hnRNPs are RNA binding proteins and they form complexes with heterogeneous nuclear RNA (hnRNA). These proteins are associated with pre-mRNAs in the nucleus and appear to influence pre-mRNA processing and other aspects of mRNA metabolism and transport. While all of the hnRNPs are present in the nucleus, some seem to shuttle between the nucleus and the cytoplasm. The hnRNP proteins have distinct nucleic acid binding properties. The protein encoded by this gene contains a RNA binding domain and scaffold-associated region (SAR)-specific bipartite DNA-binding domain. This protein is also thought to be involved in the packaging of hnRNA into large ribonucleoprotein complexes. During apoptosis, this protein is cleaved in a caspase-dependent way. Cleavage occurs at the SALD site, resulting in a loss of DNA-binding activity and a concomitant detachment of this protein from nuclear structural sites. But this cleavage does not affect the function of the encoded protein in RNA metabolism. At least two alternatively spliced transcript variants have been identified for this gene.
G protein-coupled receptor GPR82
, probable G-protein coupled receptor 82
, heterogeneous nuclear ribonucleoprotein U
, p120 nuclear protein
, scaffold attachment factor A
, G protein-coupled receptor 82
, probable G-protein coupled receptor 82-like