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Validated All-in-One™ qPCR Primer for SSTR2(NM_001050.2) 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
Somatostatin acts at many sites to inhibit the release of many hormones and other secretory proteins. The biologic effects of somatostatin are probably mediated by a family of G protein-coupled receptors that are expressed in a tissue-specific manner. SSTR2 is a member of the superfamily of receptors having seven transmembrane segments and is expressed in highest levels in cerebrum and kidney.
Gene References into function
- SSTR transcripts are expressed and functional in retroorbital fibroblasts. SSTR1 is expressed in Grave's disease and octreotide inhibits retroorbital cell growth, explaining the SRIH therapeutic effect.
- Quantitative evaluation of somatostatin receptor subtype 2 expression in sporadic colorectal tumor and in the corresponding normal mucosa
- Somatostatin modulates G-CSF-induced but not interleukin-3-induced proliferative responses in myeloid 32D cells via activation of somatostatin receptor subtype 2.
- SSTRs 1-5 are heterogeneously expressed in gastroenteropancreatic endocrine tumors
- expression of SSTR2 transcripts up-regulated in prostatic carcinoma cells; SSTR2 agonists may have role in treatment of prostate cancer
- somatostatin receptor transcripts were found in lymphocytes both from Graves' ophthalmopathy retroorbital tissues and blood samples, with levels of expression of SST1, -2, and -4 mRNA higher than those of the SST3 and -5 transcripts
- localization and expression in human prostatic tissue and prostate cancer cell lines
- sensitizes human pancreatic cancer cells to death ligand-induced apoptosis
- Presence and intracellular localization of the spliced variant SSR2(a) and its endogenous ligand SS in the cultured human neuroblastoma (NB) cell line, SH-SY5Y.
- study demonstrates for the first time a selective and inducible expression of the recently discovered cortistatin, as well as somatostatin receptor 2, in human monocyte-derived cells
- Expression of somatostatin receptor 2 by human pancreatic cancer causes significant slowing of tumor growth by a mechanism independent of exogenous somatostatin
- Activation of SSTR 2 by SSTR 2 agonist significantly suppressed insulin secretion.
- Sst2 and sst5 were expressed in 70%, sst1 in 50%, and sst3 and sst4 subtypes only in 15-20% of insulinomas
- The receptor from somatostatinoma was completely phosphorylated. Only unphosphorylated sst2A was present in human tumors not exposed to autocrine stimulation.
- SST2R gene together with p53 and ras genes may participate in pancreatic cancerous angiogenesis.
- Expression of reintroduced human SSTR2 gene exerts its antiangiogenic effects by down-regulating expressions of factors involved in tumor angiogenesis and metastasis, suggesting SSTR2 gene transfer as new strategy of gene therapy for pancreatic cancer.
- The degree (or level) of sst2 and sst5 expression is critical for the ultimate GH response of somatotropinomas to endogenous SRIF tone and exogenous SRIF analogue therapy.
- Epithelial sst2A cells, identified as neuroendocrine, gastrin-producing cells, were found in large numbers in the antrum and the duodenum, but not in the gastric corpus.
- SSTR2 provides an anti-angiogenic effect on pancreatic cancer xenografts, susgesting gene transfer as a promising strategy of gene therapy for pancreatic cancer.
- human somatostatin receptor 2 dimers have a role in receptor trafficking
- Expression of the SSTR2 gene in pancreatic adenocarcinoma cells induces apoptosis, which may be mediated via down-regulation of Bcl-2 & up-regulation of Bax (alteration of Bcl-2/Bax ratio) & inhibits tumor angiogenesis, inhibiting of tumor growth.
- gene transfer into pancreatic neoplasm cells resulted in no apoptosis, but a significant cell proliferation inhibition
- SSTR2 and SSTR5 variants seem to have a minor role in determining the responsiveness to somatostatin analogs in acromegaly
- activation of the IKK/NFkappaB signaling cascade by SSTR2 requires a complicated network consisting of Galpha(14), protein kinase C, CamkII, ERK, and c-Src
- In the temporal lobe epilepsy, dentate gyrus, sst2 receptor mRNA expression was strongly increased in the granule cell layer, sst2 receptor-binding sites and immunoreactivity was preserved in the inner but decreased in the outer molecular layer.
- the subtype 2 receptor-mediated antiproliferative effect of SRIH on TT cell proliferation may be exerted through a decrease in cyclin D1 and cdk4 levels
- Sst2 sensitized NIH3T3 cells to TNFalpha-induced apoptosis, enhanced TNFalpha-mediated activation of NF-kappaB, resulting in JNK inhibition and subsequent executioner caspase activation and cell death.
- Physical interaction between a sst2 and p85, revealing a novel mechanism for negative regulation by ligand-activated GPCR of PI3K-dependent survival pathways, which may be an important molecular target for antineoplastic therapy.
- Cytostatic action exerted by SSTR2 analogs might account for the tumor shrinkage observed in acromegalic patients treated with long-acting somatostatin analogs.
- results show that Somatostatin receptor 2 is predominantly expressed on thyroid tissue and is a valid target for treatment of thyroid tumours
- We conclude that the somatostatin receptor plays a role in the total renal uptake of radiolabelled somatostatin analogues.
- Somatostatin caused rapid sst(2a) receptor phosphorylation and desensitization of epithelial antisecretory responses.
- 17q gain and promoter polymorphisms can play a role into the regulation of sst2 expression in neuroblastomas
- The functional interactions between human somatostatin receptor 2 (hSSTR2) and human dopamine receptor 2 (hD2R) in both co-transfected CHO-K1 or HEK-293 cells as well as in cultured neuronal cells which express both the receptors endogenously.
- Analysis of orbital tissues reveals upregulation of SSTR1 and -2 in a group of Graves' ophthalmopathy (GO) patients. Adipogenesis, a process occurring in GO orbits, provides one possible explanation for some of the observed increase.
- Sst(2) is the best target for visualization of neuroendocrine tumors(NE) tumors, whereas noradrenaline transporter is only a useful target in a subpopulation of NE tumors.
- This study was undertaken to investigate molecular mechanism of transcriptional regulation of the human sst2 gene, for which an additional exon (exon 1) in the 5'-untranslated region was recently found.
- sst2 was expressed in 67% of the patients with HCC
- Existence of a novel upstream promoter for the hSSTR2 gene that is regulated by epigenetic modifications, suggesting for complex control of the hSSTR2 transcription.
- SSTR2 is the predominant mediator of functional ocular antiangiogenic effects.
- Somatostatin regulates early trophoblast functions mainly through an interaction with SSTR2.
- Data show that human somatostatin receptors (SSTR)2 and SSTR5 heterodimerize, and that selective activation of SSTR2 and not SSTR5, or their costimulation, modulates the association.
- High somatostatin receptor 2 expression is associated with neo-angiogenesis and high grade meningiomas.
- Rabbit monoclonal antibody UMB-1 may prove of great value in the assessment of sst2A status in human neuroendocrine tumors during routine histopathological examination.
- sst2 mRNA and receptor levels were significantly higher in the meningothelial subtype than in the fibroblastic subtype of meningiomas
- Results show that glucocorticoids selectively downregulate somatostatin type 2, but not dopamine D2 and only to a minor degree sst5 receptors in human neuro-endocrine BON and TT cells.
- Immunohistochemistry stufy of SSTR2 in prostate tissue from patients with bladder outlet obstruction showed that the majority of cells showed a weak intensity.
- SSTR2 could be a promising candidate for gene therapy for SSTR2-positive and SSTR2-negative tumors
