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GPRC5A encodes a member of the type 3 G protein-coupling receptor family, characterized by the signature 7-transmembrane domain motif. Additionally we are shipping GPRC5A Antibodies (111) and GPRC5A Kits (23) and many more products for this protein.
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our results implicate GPRC5A as a tumor suppressor in breast cancer cells, and GPRC5A exerts its tumor-suppressive function by inhibiting EGFR (show EGFR Proteins) and its downstream pathway
elevated levels of GPRC5A played significant roles in gastric cancer progression
Results show how GPRC5A deficiency leads to dysregulated EGFR (show EGFR Proteins) and STAT3 (show STAT3 Proteins) signaling and lung tumorigenesis.
EGFR (show EGFR Proteins) interacted with GPRC5A and phosphorylated it in two conserved double-tyrosine motifs, Y317/Y320 and Y347/ Y350, at the C-terminal tail of GPRC5A.
The interaction of miR (show MLXIP Proteins)-103a-3p with each of the two 5' UTR targets reduces the expression levels of both GPRC5A mRNA and GPRC5A protein in one normal epithelial and two pancreatic cancer cell lines.
RAI3 may contribute to the malignant progression of hepatocellular carcinoma
Data indicate that in mammary tumors, the mRNA expression of GPRC5A significantly correlated with that of BRCA1.
Decreased GPRC5A expression is associated with non-small cell lung cancers and lung inflammation.
Loss of GPRC5A is associated with lung adenocarcinomas.
RAI3 is a cell growth-promoting gene and a novel P53 (show TP53 Proteins) transcriptional target
Data show that G protein-coupled receptor (show GPR34 Proteins), family C, group 5, member A (show CXCL14 Proteins) protein (Gprc5a) deficiency exacerbates the silica-induced tissue damages and fibrogenic response in lungs.
Gprc5a deficiency leads to impaired induction of peripherally derived regulatory T-cells and increased experimental autoimmune encephalomyelitis severity.
Gprc5a deficiency confers susceptibility to endotoxin-induced pulmonary edema and injury, mainly through NF-kappaB (show NFKB1 Proteins) signaling in bronchioalveolar epithelium of lung.
Gprc5a deletion enhances the transformed phenotype in normal and malignant lung epithelial cells by eliciting persistent Stat3 (show STAT3 Proteins) signaling induced by autocrine leukemia inhibitory factor (show LIF Proteins).
Gprc5a loss enhances NF-kappaB (show NFKB1 Proteins) activation in lung epithelial cells
analysis of the Rai3 gene promoter revealed that the proximal region harbors most of the elements necessary for its regulation, including GC boxes and Sp1 (show SP1 Proteins)-, AP1 (show JUN Proteins)-, and AP2 (show TFAP2A Proteins)-binding sites, and a retinoic acid response element
Data show that targeted inactivation of Raig1 did not cause significant developmental defects, and tha epithelial cell differentiation was normal and lung structure was intact.
This gene encodes a member of the type 3 G protein-coupling receptor family, characterized by the signature 7-transmembrane domain motif. The encoded protein may be involved in interaction between retinoid acid and G protein signalling pathways. Retinoic acid plays a critical role in development, cellular growth, and differentiation. This gene may play a role in embryonic development and epithelial cell differentiation.
G-protein coupled receptor family C group 5 member A
, orphan G-protein-coupling receptor PEIG-1
, retinoic acid induced 3
, retinoic acid responsive
, retinoic acid-induced gene 1 protein
, retinoic acid-induced protein 3