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In cotransfected HEK (show EPHA3 ELISA Kits)-293 cells, SSTR5 and CB1R (show CNR1 ELISA Kits) existed in a constitutive heteromeric complex under basal condition, which was disrupted upon agonist treatments. Furthermore, concurrent receptor activation led to preferential formation of SSTR5 homodimer and dissociation of CB1R (show CNR1 ELISA Kits) homodimer.
Combination treatment increased both SSTR2 (show SSTR2 ELISA Kits) and SSTR5 mRNA and protein levels in DU-145 cells. The data suggest that this combination therapy may be a good candidate for patients with advanced metastatic Prostate cancer (PCa (show FLVCR1 ELISA Kits)) do not respond to androgen deprivation.
A truncated splice variant of the somatostatin receptor subtype 5, is associated to features of increased aggressiveness in pancreatic neuroendocrine tumors.
SSTR5 was the predominantly expressed receptor subtype in the cytoplasm of all GH-secreting adenomas tested, regardless of whether they came from octreotide-naive, octreotide-responsive, or octreotide-resistant patients. SSTR5 mRNA predominance was significant only in octreotide treated patients. Its expression was not correlated with baseline or post-octreotide GH or IGF-1 (show IGF1 ELISA Kits) levels or tumor volume.
Data showed that the distribution of somatostatin (show SST ELISA Kits) receptor (SSTR (show SSTR3 ELISA Kits)) subtypes among the 199 pancreatic neuroendocrine tumors (PNETs) was: SSTR2 (show SSTR2 ELISA Kits) (54.8%), SSTR1 (show SSTR1 ELISA Kits) (53.3%), SSTR4 (show SSTR4 ELISA Kits) (51.8%), SSTR5 (33.7%), and SSTR3 (show SSTR3 ELISA Kits) (28.6%).
Data indicate that somatostatin (show SST ELISA Kits) receptor scintigraphy (SRS (show SMS ELISA Kits)) and immunohistochemical results for somatostatin (show SST ELISA Kits) and dopamine receptors sstr2 (show SSTR2 ELISA Kits), sstr3 (show SSTR3 ELISA Kits), sstr5 and D2R (show DRD2 ELISA Kits) were compared in neuroendocrine neoplasms tissues.
Somatostatin (show SST ELISA Kits) receptors were expressed in a high proportion of merkel cell carcinomas, although expression was heterogeneous between tumours and was not associated with disease severity.
An immunohistochemical investigation of the expression of somatostatin (show SST ELISA Kits) receptor subtypes
SSTR2 (show SSTR2 ELISA Kits) and SSTR5 protein levels were induced as compared to any agent alone.
SSTR 5 was shown to be the main receptor subtype in the analysed differentiated or anaplastic thyroid malignancies, whereas SSTR 2 (show SSTR2 ELISA Kits) was found only in a small percentage.
The expression and localization of the three receptors (SSTR3 (show SSTR3 ELISA Kits)-SSTR5) in wild-type (WT), single-knockout (SSTR1 (show SSTR1 ELISA Kits) KO) and double-knockout SSTR1 (show SSTR1 ELISA Kits)/SSTR2 (show SSTR2 ELISA Kits) (DKO) mice, are reported.
mouse somatostatin receptor 5 is sorted by a network of PDZ-domain (show INADL ELISA Kits) containing proteins
Findings suggest that somatostatin (show SST ELISA Kits) and its receptors (SSTR2 (show SSTR2 ELISA Kits) and SSTR5) are important markers in the regulation and development of Sertoli cell.
In comparison to wt, ApoD (show APOD ELISA Kits)(-/-) mice exhibit increased SSTR5-like immunoreactivity in paraventricular nuclei and decreased receptor expression in ventromedial hypothalamus and arcuate nucleus.
Somatostatin (show SST ELISA Kits) inhibited GIP (show GIP ELISA Kits) and glucagon-like peptide-1 (GLP-1 (show GCG ELISA Kits)) secretion from primary small intestinal cultures, in part through SSTR5.
SSTR5 is a negative regulator for PDX-1 (show PDX1 ELISA Kits) expression and SSTR5 may mediate the inhibitory effects of somatostatin (show SST ELISA Kits) and its analogs on insulin (show INS ELISA Kits) expression/secretion and cell proliferation via down-regulating PDX-1 (show PDX1 ELISA Kits)
SST (show SST ELISA Kits) and SSTRs might play an important role in regulation of neurodegeneration
The existence of new truncated sst5-variants with unique ligand-selective signaling properties, which could contribute to further understanding the complex, distinct pathophysiological roles of somatostatin (show SST ELISA Kits) and cortistatin (show CORT ELISA Kits).
Extraovarian somatostatin (show SST ELISA Kits), acting through its receptors 2 and 5 present on granulosa cells, may be involved in mouse folliculogenesis by reducing recruitment of resting follicles.
The effect of sst2 (show SSTR2 ELISA Kits) receptor knockout on sst5 receptor mRNA localization and binding sites throughout the brain has been determined.
This study describes the cloning and characterization of procine sst5 and identifies two spliced variants with six and three transmembrane domains (TMD (show TTN ELISA Kits)): psst5TMD6 and psst5TMD3; psst5TMD6 and psst5TMD3 are functional (e.g., activate calcium signaling.
Data demonstrate that urotensin II (show UTS2 ELISA Kits) and urotensin II-related peptide directly activate somatostatin (show SST ELISA Kits) receptors 2 and 5 and thus mimic the effect of somatostatin (show SST ELISA Kits) on its cognate receptors.
Somatostatin and its related peptide cortistatin exert multiple biological actions on normal and tumoral tissue targets by interacting with somatostatin receptors (SSTRs). The protein encoded by this gene is one of the SSTRs, which is a multi-pass membrane protein and belongs to the G-protein coupled receptor 1 family. The activity of this receptor is mediated by G proteins which inhibit adenylyl cyclase, and different regions of this receptor molecule are required for the activation of different signaling pathways. A mutation in this gene results in somatostatin analog resistance. Alternatively spliced transcript variants have been identified in this gene.
somatostatin receptor type 5
, somatostatin receptor 5
, somatostatin receptor subtype 5
, Somatostatin receptor subtype 5