anti-G Protein-Coupled Receptor, Family C, Group 5, Member A (GPRC5A) Antibodies

Human G Protein-Coupled Receptor, Family C, Group 5, Member A (GPRC5A) interaction partners

1. RAI3 overexpression is associated with poor prognosis in esophageal cancers

2. GPRC5a was upregulated in pancreatic cancer (PaCa) leading to an enhanced drug resistance in PaCa cells.

3. under-expressed GPRC5A during lung tumorigenesis enhances any transcriptional stimulation through an active translational status.

4. findings reveal an unprecedented role for GPRC5A in regulation of the ITGB1-mediated cell adhesion and it's downstream signaling, thus indicating a potential novel role for GPRC5A in human epithelial cancers.

5. miR-204 inhibits cell proliferation in gastric cancer by targeting CKS1B, CXCL1 and GPRC5A.

6. p53 overexpression and GPRC5A induction markedly inhibited tumor cell viability and induced apoptosis.

7. Mutations of ARID1A, GPRC5A and MLL2 grant bladder cancer non-stem cells the capability of self-renewal.

8. GPRC5A is a potential oncogene in pancreatic ductal adenocarcinoma cells that is upregulated by gemcitabine with help from HuR.

9. These results suggest RAI3 plays an important role in adipogenesis of hASCs and may have a potential use in the future application.

10. Study underscores genomic alterations that represent early events in the development of Kras mutant LUAD following Gprc5a loss and tobacco carcinogen exposure.

11. Data show that G protein-coupled receptor, family C, group 5, member A protein (GPRC5A) regulates oxidative stress through vanin 1 protein (VNN1).

12. Suppression of GPRC5a results in decreased cell growth, proliferation and migration in pancreatic cancer cell lines via a STAT3 modulated pathway, independent from ERK activation

13. our results implicate GPRC5A as a tumor suppressor in breast cancer cells, and GPRC5A exerts its tumor-suppressive function by inhibiting EGFR and its downstream pathway

14. elevated levels of GPRC5A played significant roles in gastric cancer progression

15. Results show how GPRC5A deficiency leads to dysregulated EGFR and STAT3 signaling and lung tumorigenesis.

16. EGFR interacted with GPRC5A and phosphorylated it in two conserved double-tyrosine motifs, Y317/Y320 and Y347/ Y350, at the C-terminal tail of GPRC5A.

17. The interaction of miR-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.

18. RAI3 may contribute to the malignant progression of hepatocellular carcinoma

19. Data indicate that in mammary tumors, the mRNA expression of GPRC5A significantly correlated with that of BRCA1.

20. Decreased GPRC5A expression is associated with non-small cell lung cancers and lung inflammation.

Mouse (Murine) G Protein-Coupled Receptor, Family C, Group 5, Member A (GPRC5A) interaction partners

1. G protein-coupled receptor family C group 5 member A (GPRC5A) deficiency contributes to dysregulated proto-oncogene protein c-mdm2 (MDM2) via activated epidermal growth factor receptor (EGFR) signaling, which promotes lung tumor development.

2. GPRC5a was upregulated in pancreatic cancer (PaCa) leading to an enhanced drug resistance in PaCa cells.

3. under-expressed GPRC5A during lung tumorigenesis enhances any transcriptional stimulation through an active translational status.

4. Study underscores genomic alterations that represent early events in the development of Kras mutant LUAD following Gprc5a loss and tobacco carcinogen exposure.

5. Data show that G protein-coupled receptor, family C, group 5, member A protein (Gprc5a) deficiency exacerbates the silica-induced tissue damages and fibrogenic response in lungs.

6. Gprc5a deficiency leads to impaired induction of peripherally derived regulatory T-cells and increased experimental autoimmune encephalomyelitis severity.

7. Gprc5a deficiency confers susceptibility to endotoxin-induced pulmonary edema and injury, mainly through NF-kappaB signaling in bronchioalveolar epithelium of lung.

8. Results show how GPRC5A deficiency leads to dysregulated EGFR and STAT3 signaling and lung tumorigenesis.

9. Gprc5a deletion enhances the transformed phenotype in normal and malignant lung epithelial cells by eliciting persistent Stat3 signaling induced by autocrine leukemia inhibitory factor.

10. Loss of GPRC5A is associated with lung adenocarcinomas.

11. Gprc5a loss enhances NF-kappaB activation in lung epithelial cells

12. 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-, AP1-, and AP2-binding sites, and a retinoic acid response element

13. 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.