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. Mutations of ARID1A (show ARID1A Antibodies), GPRC5A and MLL2 (show MLL2 Antibodies) grant bladder cancer non-stem cells the capability of self-renewal.

2. GPRC5A is a potential oncogene (show RAB1A Antibodies) in pancreatic ductal adenocarcinoma cells that is upregulated by gemcitabine with help from HuR (show ELAVL1 Antibodies).

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

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 (show ADRA1A Antibodies), family C, group 5, member A (show CXCL14 Antibodies) protein (GPRC5A) regulates oxidative stress through vanin 1 (show VNN1 Antibodies) protein (VNN1 (show VNN1 Antibodies)).

6. Suppression of GPRC5a results in decreased cell growth, proliferation and migration in pancreatic cancer cell lines via a STAT3 (show STAT3 Antibodies) modulated pathway, independent from ERK (show EPHB2 Antibodies) activation

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

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

9. Results show how GPRC5A deficiency leads to dysregulated EGFR (show EGFR Antibodies) and STAT3 (show STAT3 Antibodies) signaling and lung tumorigenesis.

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

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

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

2. Data show that G protein-coupled receptor (show GPR34 Antibodies), family C, group 5, member A (show CXCL14 Antibodies) protein (Gprc5a) deficiency exacerbates the silica-induced tissue damages and fibrogenic response in lungs.

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

4. Gprc5a deficiency confers susceptibility to endotoxin-induced pulmonary edema and injury, mainly through NF-kappaB (show NFKB1 Antibodies) signaling in bronchioalveolar epithelium of lung.

5. Results show how GPRC5A deficiency leads to dysregulated EGFR (show EGFR Antibodies) and STAT3 (show STAT3 Antibodies) signaling and lung tumorigenesis.

6. Gprc5a deletion enhances the transformed phenotype in normal and malignant lung epithelial cells by eliciting persistent Stat3 (show STAT3 Antibodies) signaling induced by autocrine leukemia inhibitory factor (show LIF Antibodies).

7. Loss of GPRC5A is associated with lung adenocarcinomas.

8. Gprc5a loss enhances NF-kappaB (show NFKB1 Antibodies) activation in lung epithelial cells

9. 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 Antibodies)-, AP1 (show JUN Antibodies)-, and AP2 (show TFAP2A Antibodies)-binding sites, and a retinoic acid response element

10. 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.