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Validated All-in-One™ qPCR Primer for GRPR(NM_005314.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
Gastrin-releasing peptide (GRP) regulates numerous functions of the gastrointestinal and central nervous systems, including release of gastrointestinal hormones, smooth muscle cell contraction, and epithelial cell proliferation and is a potent mitogen for neoplastic tissues. The effects of GRP are mediated through the gastrin-releasing peptide receptor. This receptor is a glycosylated, 7-transmembrane G-protein coupled receptor that activates the phospholipase C signaling pathway. The receptor is aberrantly expressed in numerous cancers such as those of the lung, colon, and prostate. An individual with autism and multiple exostoses was found to have a balanced translocation between chromosome 8 and a chromosome X breakpoint located within the gastrin-releasing peptide receptor gene. [provided by RefSeq].
Gene References into function
- GRP/GRP-R play a transient and non-critical role in intestinal development
- hGRP-R activation stimulated sustained cyclic AMP response element binding protein (CREB) phosphorylation and transactivation in duodenal cancer cells through a protein kinase C and partially p38 mitogen-activated protein kinase-dependent pathway.
- Bombesin-dependent activation (through GRP receptor) of the transcription factor Elk-1 and significant increase of cell proliferation in prostate cancer cell lines
- mRNA transcripts are expressed in tumor cells of patients with small cell lung cancer
- accumulation of mutations within the GRPR gene allows for the dedifferentiation of tumor cells within any particular colon cancer; poorly-differentiated tumor cells within any individual cancer may arise clonally from better-differentiated precursors
- Increased gastrin-releasing peptide (GRP) receptor expression in small cell lung cancer cells confers sensitivity to [Arg6,D-Trp7,9,NmePhe8]-substance P (6-11)-induced growth inhibition
- The expression of GRP-R in uterine tissue during specific phases of the cycle suggests a timely precise physiological action of GRP in these targets; in certain uterine neoplasms, the GRP-R overexpression may contribute to tumor development
- Gastrin-releasing peptide receptor mediates activation of the epidermal growth factor receptor in lung cancer cells
- GRP appears to rescue NSCLC cells exposed to gefitinib through release of amphiregulin and activation of the Akt pathway, suggesting GRPR and/or EGFR autocrine pathways in NSCLC cells may modulate therapeutic response to EGFR inhibitors.
- The large amounts of GRP-receptors in ovarian tumor vessels suggest a role in tumoral vasculature and possibly angiogenesis.
- There is a potential role of C6S and L181F mutations on GRPR function, and possibly in the pathogenesis of the autistic disorders.
- genes encoding corticotropin releasing hormone receptor 1, tachykinin receptor 1, gastrin releasing peptide, and gastrin releasing peptide receptor were selected as candidates for PD based on their biology
- CREB is a critical regulator of human GRP-R expression in gastrointestinal cancer and might be activated through different upstream intracellular pathways
- Widespread GRPR expression in human cervical cancer.
- These findings demonstrate that GRP and GRP-R have important oncogenic properties beyond their established mitogenic functions.
