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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 (120) and GPRC5A Kits (26) and many more products for this protein.
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Mutations of ARID1A, GPRC5A and MLL2 grant bladder cancer non-stem cells the capability of self-renewal.
GPRC5A is a potential oncogene (show RAB1A Proteins) in pancreatic ductal adenocarcinoma cells that is upregulated by gemcitabine with help from HuR (show ELAVL1 Proteins).
These results suggest RAI3 plays an important role in adipogenesis of hASCs and may have a potential use in the future application.
Study underscores genomic alterations that represent early events in the development of Kras mutant LUAD following Gprc5a loss and tobacco carcinogen exposure.
Data show that G protein-coupled receptor (show ADRA1A Proteins), family C, group 5, member A (show CXCL14 Proteins) protein (GPRC5A) regulates oxidative stress through vanin 1 (show VNN1 Proteins) protein (VNN1 (show VNN1 Proteins)).
Suppression of GPRC5a results in decreased cell growth, proliferation and migration in pancreatic cancer cell lines via a STAT3 (show STAT3 Proteins) modulated pathway, independent from ERK (show EPHB2 Proteins) activation
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.
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).
Loss of GPRC5A is associated with lung adenocarcinomas.
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