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anti-Human SSTR5 Antibodies:
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Human Monoclonal SSTR5 Primary Antibody for IHC (p) - ABIN2476552
Schmid, Lambertini, van Vugt, Barzaghi-Rinaudo, Schäfer, Hillenbrand, Sailer, Kaufmann, Nuciforo: Monoclonal antibodies against the human somatostatin receptor subtypes 1-5: development and immunohistochemical application in neuroendocrine tumors. in Neuroendocrinology 2012
Human Polyclonal SSTR5 Primary Antibody for FACS, ICC - ABIN261628
Chung, Han, Heo, Lee, Kim: Overexpression of WNK1 in POMC-expressing neurons reduces weigh gain via WNK4-mediated degradation of Kir6.2. in Molecular and cellular biochemistry 2018
IHC of SSTR subtypes in the different cohorts showed SSTR2 staining intensity scores higher than SSTR5 in TSHoma, acromegaly and prolactinoma, whereas the expression of SSTR5 was stronger than SSTR2 in corticotropinoma and NFPA.
Somatostatin receptor 5 variant (sst5TMD4) was expressed in a subset of breast cancers, where it correlated with angiogenic markers, lymphatic metastasis, and reduced disease-free survival.
sst5TMD4 is overexpressed in PCa, especially in those patients with a worse prognosis, and plays an important pathophysiologic role in PCa, which suggesting its potential as a biomarker and/or therapeutic target
In cotransfected HEK-293 cells, SSTR5 and CB1R 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 homodimer.
Combination treatment increased both SSTR2 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) 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 levels or tumor volume.
Data showed that the distribution of somatostatin receptor (SSTR) subtypes among the 199 pancreatic neuroendocrine tumors (PNETs) was: SSTR2 (54.8%), SSTR1 (53.3%), SSTR4 (51.8%), SSTR5 (33.7%), and SSTR3 (28.6%).
This is the first evidence indicating that sst5TMD4 is expressed in human medullary thyroid carcinoma cells, where it associates with more aggressive behavior, suggesting that sst5TMD4 might play a functionally relevant role.
Data indicate that somatostatin receptor scintigraphy (SRS) and immunohistochemical results for somatostatin and dopamine receptors sstr2, sstr3, sstr5 and D2R were compared in neuroendocrine neoplasms tissues.
Somatostatin 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 receptor subtypes
SSTR2 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 was found only in a small percentage.
A truncated sst5-variant (sst5TMD4) can influence the secretory response of somatotropinomas to somatostatin analogues-therapy.
SSTR5 protein is overexpressed in poorly differentiated thyroid cancer and may be involved in the lack of response to somatostatin analogue treatment.
Tumor cells in the tissue samples of the patients diagnosed with advanced-stage hepatocellular carcinoma expressed a high proportion of SSTR1 and SSTR5.
High SSTR5 expression is associated with gallbladder cancer.
Whereas sst2 receptors might play a primary role in the differentiation and regulation of TSH, LH, and FSH cells, sst5 receptors appear to be mainly involved in GH regulation from birth onward
We studied the expression of SSTR(2A) and SSTR(5) with new procedures in 108 pituitary tumors
The expression and localization of the three receptors (SSTR3-SSTR5) in wild-type (WT), single-knockout (SSTR1 KO) and double-knockout SSTR1/SSTR2 (DKO) mice, are reported.
mouse somatostatin receptor 5 is sorted by a network of PDZ-domain containing proteins
Findings suggest that somatostatin and its receptors (SSTR2 and SSTR5) are important markers in the regulation and development of Sertoli cell.
In comparison to wt, ApoD(-/-) mice exhibit increased SSTR5-like immunoreactivity in paraventricular nuclei and decreased receptor expression in ventromedial hypothalamus and arcuate nucleus.
Somatostatin inhibited GIP and glucagon-like peptide-1 (GLP-1) secretion from primary small intestinal cultures, in part through SSTR5.
SSTR5 is a negative regulator for PDX-1 expression and SSTR5 may mediate the inhibitory effects of somatostatin and its analogs on insulin expression/secretion and cell proliferation via down-regulating PDX-1
SST 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 and cortistatin.
Extraovarian somatostatin, 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 receptor knockout on sst5 receptor mRNA localization and binding sites throughout the brain has been determined.
the mouse gene promoter has been characterized, and functional activity and nuclear factor interactions were mapped to two specific promoter regions
Brain somatostatin receptors 1,2,4 and 5 are up-regulated in somatostatin-deficient mice, and SSTR3 is down-regulated.
Expression of SSTR3, SSTR4, and SSTR5 in mouse proximal tubules complements the expression of SSTR1 and SSTR2 in collecting ducts as seen in other species
results of these studies suggest sst(5) mediates SRIF inhibition of pancreatic insulin secretion and contributes to the regulation of glucose homeostasis and insulin sensitivity
A role for SSTR-5 in regulating insulin secretion.
in AtT-20 cells, SST5 regulates the dominant SST2 action, attenuating SST2 effects on intracellular calcium oscillation and internalization
SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas
results suggest that somatostatin receptor 5(SSTR5) plays a pivotal role in insulin secretion and glucose regulation in mice and that its regulatory effects are age-related
the presence of sst(5) in the same cells modulates trafficking and cell surface regulation of sst(2A) and cellular desensitization to the effects of SRIF
we identified 2 sets of SSTR5 regulated pancreatic genes in SSTR5 deficient mice that belong to the pathways regulating cell proliferation, apoptosis neogenesis, angiogenesis, and tumorigenesis.
This study describes the cloning and characterization of procine sst5 and identifies two spliced variants with six and three transmembrane domains (TMD): psst5TMD6 and psst5TMD3; psst5TMD6 and psst5TMD3 are functional (e.g., activate calcium signaling.
Data demonstrate that urotensin II and urotensin II-related peptide directly activate somatostatin receptors 2 and 5 and thus mimic the effect of somatostatin 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