anti-Gastrin-Releasing Peptide Receptor (GRPR) Antibodies

Mouse (Murine) Gastrin-Releasing Peptide Receptor (GRPR) interaction partners

1. these results suggest that the regulation of GRP-R activity or expression has an influence on adipogenesis through regulating adipogenic related genes.

2. These data suggest that GRPR expression in fibroblast-like synoviocytes (FLS)and that exogenous GRP are able to activate FLS invasion. This effect occurs at least in part through the AKT activation. Therefore, understanding of the GRP/GRPR pathway could be relevant in the development of FLS-targeted therapy for Rheumatoid arthritis .

3. ablating GRP receptor-expressing neurons eliminated basal and hypoxia-induced sighing, but left breathing otherwise intact initially

4. Together, we define the respective function of NMBR and GRPR in itch transmission, and reveal an unexpected relationship not only between the two receptors but also between the two populations of interneurons in itch signaling.

5. BNP-NPRA signaling is involved in both itch and pain and does not function upstream of the GRP-GRPR dedicated neuronal pathway.

6. The present results suggest that BB2 receptor-expressing spinal neurons transmit herpes-associated itch by BB2 receptor-independent signaling.

7. spinal GRPr and NMBr independently drive itch neurotransmission in mice.

8. GRPR and stathmin control in opposite directions both cued fear extinction and neural activities of the amygdala and prefrontal cortex

9. Gastrin-releasing peptide receptor mediates chemotaxis in neutrophils, and may be an alternative chemotactic receptor playing a role in the pathogenesis of inflammatory disorders.

10. The data suggest that opioid-induced itch is an active process concomitant with but independent of opioid analgesia, occurring via the unidirectional cross-activation of GRPR signaling by MOR1D heterodimerization

11. We propose that deletion of GRPR leads to the induction of depression-like behavior which is paralleled by dysregulation of amygdala gene expression, potentially resulting from deficient light-induced corticosterone release in GRPR-knockout mice

12. GRP-R-deficient mice showed no significant different in risk assessment behavior of conventional anxiwety parameters, so GRP-R may not impact this anxiety or emotional behavior.

13. GRP/GRP-R play a transient and non-critical role in intestinal development

14. GRPR has a role in regulation of fear and memory for fear in the mouse amygdala

15. GRPR gene expression was detected predominantly in utero in lung development

16. MCH was significantly enhanced in BRS-3-deficient mice but not in GRP-R-deficient mice

17. GRP-R immunoreactivity was observed in the lateral (LA), central, and basolateral amygdaloid (BLA) nuclei and NTS, which are important regions for memory performance.

18. Changes in GRPr are light driven and not endogenously organized. Diurnal variation in GRPr activity probably underlies intra-SCN signaling important for entrainment and phase shifting.

19. GRPR may represent the first molecule that is dedicated to mediating the itch sensation in the dorsal horn of the spinal cord

20. New evidence for the occurrence of marked effects of bombesin/gastrin-releasing peptide concerning both the articular chondrocytes and the inflammatory process is obtained in this study

Human Gastrin-Releasing Peptide Receptor (GRPR) interaction partners

1. GRP/GRP-R signaling activation contributes to castration-resistant prostate cancer progression

2. Expression of Gastrin-Releasing Peptide Receptor in Breast Cancer and Its Association with Pathologic, Biologic, and Clinical Parameters

3. Our results suggest that, similar to what happens in neutrophils, gastrin-releasing peptide is a migratory, rather than a proliferative, stimulus, for non-small cell lung carcinoma cells, indicating a putative role for gastrin-releasing peptide and gastrin-releasing peptide receptor in metastasis

4. GRP-R regulates glucose metabolism in neuroblastoma by modulating HIF-1alpha, PDK4 and PDP2.

5. BBS caused a significant increase in Shh gene transcription and protein secretion that was dependent on BBS-induced GPCR/Galphaq-//Rho mediated activation of nuclear factor kappaB (NFkappaB), which can stimulate a NF-kappaB response element in the Shh gene promoter

6. No association of 16 GRP and 7 GRPR variants were found with agoraphobia with/without panic disorder.

7. GRPR is highly expressed in epidermoid carcinoma of the anal canal, suggesting this receptor might have a role in anal carcinogenesis.

8. a key mechanism for GRPR-regulated colon cancer cell migration through the Galpha13-PRG-RhoA-ROCK pathway.

9. GRPR expression was more pronounced in an advanced-stage lung cancer

10. integrin ss1 subunit critically regulates GRP-R-mediated neuroblastoma cell migration and invasion

11. Elevated buccal GRPR espression was significantly associated with squamous cell carcinoma of the head and neck.

12. These findings highlight the role of GRPR signaling in sepsis outcome.

13. Protein kinase C is critically responsible for rapid VEGF secretion by gastrin-releasing peptide receptor signaling in neuroblastoma cells

14. Tonic stretch of human myometrium increases contractility and stimulates the expression of a known smooth muscle stimulatory agonist, GRP. GRP receptor antagonists attenuate the effect of stretch.

15. High GRPR is associated with prostate carcinoma.

16. Bronchial gastrin-releasing peptide receptor expression was significantly associated with lung cancer in a multivariable logistic regression model adjusted for age, sex, smoking status and pulmonary function. Lung cancer risk was not modified by sex.

17. Concomitant vascular GRP-receptor and VEGF-receptor expression in human tumors provides molecular basis for dual targeting of tumoral vasculature.

18. GRP promotes the growth of HepG2 cells through interaction with GRPR co-expressed in tumor cells, and subsequently activates MAPK/ERK1/2 via EGFR-independent mechanisms.

19. This study is the first to confirm the presence of gastrin-releasing peptide receptor in human glioma specimens and normal human neurons.

20. The results suggest that brain-derived neurotrophic factor/TrkB and cAMP phosphodiesterase-4, but not the gastrin-releasing peptide receptor, regulate the viability of medulloblastoma cells.