Ignet

Gene Information

Gene symbol: SSTR3

Gene name: somatostatin receptor 3

HGNC ID: 11332

Related Genes

#	Gene Symbol	Number of hits
1	ADCY3	1 hits
2	ARL13B	1 hits
3	BAX	1 hits
4	BBS2	1 hits
5	INS	1 hits
6	MCHR1	1 hits
7	SST	1 hits
8	SSTR1	1 hits
9	SSTR2	1 hits
10	SSTR4	1 hits
11	SSTR5	1 hits
12	TP53	1 hits

Related Sentences

#	PMID	Sentence
1	7762657	Six SS-8 analogues that distinguish SS subtypes showed that 125I-SS-14 bound to somatostatin receptor subtype 3 (SSTR3).
2	7956902	SSTR1, SSTR2, and SSTR3 mRNA expression was reduced 80% in the pituitary of FD rats vs. fed controls, whereas pituitary levels of SSTR4 and SSTR5 mRNA were unaffected.
3	7956902	In STZ diabetes, pituitary SSTR1, SSTR2, and SSTR3 mRNA expression was reduced 50-80%, with levels of SSTR1 partially restored by insulin, whereas SSTR4 mRNA was unchanged.
4	7956902	As chronic exposure to SRIF results in desensitization of transfected SSTR2 and SSTR3, and SSTR binding is decreased in FD and STZ diabetic rats, the possibility exists that the pituitary changes result from continued exposure to SRIF.
5	7956902	SSTR1, SSTR2, and SSTR3 mRNA expression was reduced 80% in the pituitary of FD rats vs. fed controls, whereas pituitary levels of SSTR4 and SSTR5 mRNA were unaffected.
6	7956902	In STZ diabetes, pituitary SSTR1, SSTR2, and SSTR3 mRNA expression was reduced 50-80%, with levels of SSTR1 partially restored by insulin, whereas SSTR4 mRNA was unchanged.
7	7956902	As chronic exposure to SRIF results in desensitization of transfected SSTR2 and SSTR3, and SSTR binding is decreased in FD and STZ diabetic rats, the possibility exists that the pituitary changes result from continued exposure to SRIF.
8	7956902	SSTR1, SSTR2, and SSTR3 mRNA expression was reduced 80% in the pituitary of FD rats vs. fed controls, whereas pituitary levels of SSTR4 and SSTR5 mRNA were unaffected.
9	7956902	In STZ diabetes, pituitary SSTR1, SSTR2, and SSTR3 mRNA expression was reduced 50-80%, with levels of SSTR1 partially restored by insulin, whereas SSTR4 mRNA was unchanged.
10	7956902	As chronic exposure to SRIF results in desensitization of transfected SSTR2 and SSTR3, and SSTR binding is decreased in FD and STZ diabetic rats, the possibility exists that the pituitary changes result from continued exposure to SRIF.
11	8961277	Subtype-selective induction of wild-type p53 and apoptosis, but not cell cycle arrest, by human somatostatin receptor 3.
12	8961277	Whereas growth inhibition has been reported to follow stimulation of protein tyrosine phosphatase via SSTR2 or inhibition of Ca2+ channels via SSTR5 in heterologous expression systems, the subtype selectivity for signaling apoptosis has not been investigated.
13	8961277	The tumor suppressor protein p53 and the protooncogene product c-Myc regulate cell cycle progression (growth factors present) or apoptosis (growth factors absent).
14	8961277	The p53-induced G1 arrest requires induction of p21, an inhibitor of cyclin-dependent kinases, whereas apoptosis requires induction of Bax. c-Myc is capable of abrogating p53-induced G1 arrest by interfering with the inhibitory action of p21 on cyclin-dependent kinases.
15	8961277	We have, therefore, investigated the regulation of p53, p21, c-Myc, and Bax and cellular apoptosis in relation to cell cycle progression in CHO-K1 cells stably expressing individual human SSTR1-5.
16	8961277	We demonstrate that apoptosis is signaled uniquely through human SSTR3 and is associated with dephosphorylation-dependent conformational change in wild-type (wt) p53 as well as induction of Bax.
17	8961277	We show that the increase in wt p53 is not associated with the induction of p21 or c-Myc when octreotide-induced apoptosis becomes evident, suggesting that such apoptosis does not require G1 arrest and is not c-Myc dependent.
18	8961277	Subtype-selective induction of wild-type p53 and apoptosis, but not cell cycle arrest, by human somatostatin receptor 3.
19	8961277	Whereas growth inhibition has been reported to follow stimulation of protein tyrosine phosphatase via SSTR2 or inhibition of Ca2+ channels via SSTR5 in heterologous expression systems, the subtype selectivity for signaling apoptosis has not been investigated.
20	8961277	The tumor suppressor protein p53 and the protooncogene product c-Myc regulate cell cycle progression (growth factors present) or apoptosis (growth factors absent).
21	8961277	The p53-induced G1 arrest requires induction of p21, an inhibitor of cyclin-dependent kinases, whereas apoptosis requires induction of Bax. c-Myc is capable of abrogating p53-induced G1 arrest by interfering with the inhibitory action of p21 on cyclin-dependent kinases.
22	8961277	We have, therefore, investigated the regulation of p53, p21, c-Myc, and Bax and cellular apoptosis in relation to cell cycle progression in CHO-K1 cells stably expressing individual human SSTR1-5.
23	8961277	We demonstrate that apoptosis is signaled uniquely through human SSTR3 and is associated with dephosphorylation-dependent conformational change in wild-type (wt) p53 as well as induction of Bax.
24	8961277	We show that the increase in wt p53 is not associated with the induction of p21 or c-Myc when octreotide-induced apoptosis becomes evident, suggesting that such apoptosis does not require G1 arrest and is not c-Myc dependent.
25	9439624	We have reported earlier that somatostatin (SST) induced DNA fragmentation and apoptosis is signaled in a receptor subtype selective manner uniquely via human somatostatin receptor subtype 3 (hSSTR3).
26	9439624	In the present study we investigated the pH dependence and cation sensitivity of endonuclease induced in hSSTR3 expressing CHO-K1 cells by the SST agonist octreotide (OCT) and its effect on intracellular pH.
27	9439624	We have reported earlier that somatostatin (SST) induced DNA fragmentation and apoptosis is signaled in a receptor subtype selective manner uniquely via human somatostatin receptor subtype 3 (hSSTR3).
28	9439624	In the present study we investigated the pH dependence and cation sensitivity of endonuclease induced in hSSTR3 expressing CHO-K1 cells by the SST agonist octreotide (OCT) and its effect on intracellular pH.
29	9892225	The number of SSTR immunopositive cells showed a rank order of SSTR1 > SSTR5 > SSTR2 > SSTR3 > SSTR4.
30	9892225	SSTR1 was strongly colocalized with insulin in all beta-cells.
31	9892225	SSTR2 was found in 46% of beta-cells, whereas SSTR3 and SSTR4 were relatively poorly expressed.
32	9892225	SSTR2 was strongly colocalized with glucagon in 89% of alpha-cells, whereas SSTR5 and SSTR1 colocalized with glucagon in 35 and 26% of alpha-cells, respectively.
33	9892225	SSTR3 was detected in occasional alpha-cells, and SSTR4 was absent.
34	9892225	SSTR5 was preferentially expressed in 75% of SST-positive cells and was the principal delta-cell SSTR subtype, whereas SSTR1-3 were colocalized in only a few delta-cells, and SSTR4 was absent.
35	9892225	These studies reveal predominant expression of SSTR1, SSTR2, and SSTR5 in human islets.
36	9892225	Beta-cells, alpha-cells, and delta-cells each express multiple SSTR isoforms, beta-cells being rich in SSTR1 and SSTR5, alpha-cells in SSTR2, and delta-cells in SSTR5.
37	9892225	Although there is no absolute specificity of any SSTR for an islet cell type, SSTR1 is beta-cell selective, and SSTR2 is alpha-cell selective.
38	9892225	SSTR5 is well expressed in beta-cells and delta-cells and moderately well expressed in alpha-cells, and thereby it lacks the islet cell selectivity displayed by SSTR1 and SSTR2.
39	9892225	Subtype-selective SSTR expression in islet cells could be the basis for preferential insulin suppression by SSTR1-specific ligands and of glucagon inhibition by SSTR2-selective compounds.
40	9892225	The number of SSTR immunopositive cells showed a rank order of SSTR1 > SSTR5 > SSTR2 > SSTR3 > SSTR4.
41	9892225	SSTR1 was strongly colocalized with insulin in all beta-cells.
42	9892225	SSTR2 was found in 46% of beta-cells, whereas SSTR3 and SSTR4 were relatively poorly expressed.
43	9892225	SSTR2 was strongly colocalized with glucagon in 89% of alpha-cells, whereas SSTR5 and SSTR1 colocalized with glucagon in 35 and 26% of alpha-cells, respectively.
44	9892225	SSTR3 was detected in occasional alpha-cells, and SSTR4 was absent.
45	9892225	SSTR5 was preferentially expressed in 75% of SST-positive cells and was the principal delta-cell SSTR subtype, whereas SSTR1-3 were colocalized in only a few delta-cells, and SSTR4 was absent.
46	9892225	These studies reveal predominant expression of SSTR1, SSTR2, and SSTR5 in human islets.
47	9892225	Beta-cells, alpha-cells, and delta-cells each express multiple SSTR isoforms, beta-cells being rich in SSTR1 and SSTR5, alpha-cells in SSTR2, and delta-cells in SSTR5.
48	9892225	Although there is no absolute specificity of any SSTR for an islet cell type, SSTR1 is beta-cell selective, and SSTR2 is alpha-cell selective.
49	9892225	SSTR5 is well expressed in beta-cells and delta-cells and moderately well expressed in alpha-cells, and thereby it lacks the islet cell selectivity displayed by SSTR1 and SSTR2.
50	9892225	Subtype-selective SSTR expression in islet cells could be the basis for preferential insulin suppression by SSTR1-specific ligands and of glucagon inhibition by SSTR2-selective compounds.
51	9892225	The number of SSTR immunopositive cells showed a rank order of SSTR1 > SSTR5 > SSTR2 > SSTR3 > SSTR4.
52	9892225	SSTR1 was strongly colocalized with insulin in all beta-cells.
53	9892225	SSTR2 was found in 46% of beta-cells, whereas SSTR3 and SSTR4 were relatively poorly expressed.
54	9892225	SSTR2 was strongly colocalized with glucagon in 89% of alpha-cells, whereas SSTR5 and SSTR1 colocalized with glucagon in 35 and 26% of alpha-cells, respectively.
55	9892225	SSTR3 was detected in occasional alpha-cells, and SSTR4 was absent.
56	9892225	SSTR5 was preferentially expressed in 75% of SST-positive cells and was the principal delta-cell SSTR subtype, whereas SSTR1-3 were colocalized in only a few delta-cells, and SSTR4 was absent.
57	9892225	These studies reveal predominant expression of SSTR1, SSTR2, and SSTR5 in human islets.
58	9892225	Beta-cells, alpha-cells, and delta-cells each express multiple SSTR isoforms, beta-cells being rich in SSTR1 and SSTR5, alpha-cells in SSTR2, and delta-cells in SSTR5.
59	9892225	Although there is no absolute specificity of any SSTR for an islet cell type, SSTR1 is beta-cell selective, and SSTR2 is alpha-cell selective.
60	9892225	SSTR5 is well expressed in beta-cells and delta-cells and moderately well expressed in alpha-cells, and thereby it lacks the islet cell selectivity displayed by SSTR1 and SSTR2.
61	9892225	Subtype-selective SSTR expression in islet cells could be the basis for preferential insulin suppression by SSTR1-specific ligands and of glucagon inhibition by SSTR2-selective compounds.
62	12582462	Somatostatin analogues such as octreotide have shown promise as a safe and effective treatment for severe proliferative diabetic retinopathy by blocking the local and systemic production of growth hormone and insulin-like growth factor type 1 associated with angiogenesis and endothelial cell proliferation.
63	12582462	SSTR2 and SSTR3 are the most important receptor subtypes mediating growth hormone secretion and endothelial cell cycle arrest, retinal endothelial cell apoptosis and release of insulin.
64	15961235	In AD cortical brain region, somatostatin and neuropeptide-Y-positive neurons decreased (>70%), and glial fibrillary acidic protein-positive astrocytes significantly increased (>130%) in comparison to control brain.
65	15961235	SSTR2 and 4 were the predominant subtypes followed by SSTR1, 3 and 5.
66	15961235	AD cortex showed a marked reduction in neuronal expression of SSTR4 and 5 and a modest decrease in SSTR2-like immunoreactivity without any changes in SSTR1 immunoreactive neurons.
67	15961235	In AD cortex, SSTR1-, 3- and 4-like immunoreactivities were strongly expressed in glial cells but not SSTR2 and 5.
68	15961235	These findings suggest the differential loss of immunoreactivity of SSTR2, 4 and 5 but not SSTR1, and increased SSTR3 in frontal cortex of AD brain as well as subtype-selective glial expression in AD brain.
69	22581473	Alms1 is lost from this location in foz/foz mice, coinciding with a strong postnatal reduction (∼70%) in neurons displaying cilia marked with adenylyl cyclase 3 (AC3), a signaling protein implicated in obesity.
70	22581473	Notably, the reduction in AC3-bearing cilia parallels the decrease in cilia containing two appetite-regulating proteins, Mchr1 and Sstr3, as well as another established Arl13b ciliary marker, consistent with progressive loss of cilia during development.
71	22581473	Given that Mchr1 and Sstr3 localization to remaining cilia is maintained in foz/foz animals but known to be lost from BBS knockout mice, our findings suggest different molecular etiologies for the satiety defects associated with the Alström syndrome and BBS ciliopathies.
72	22581473	Alms1 is lost from this location in foz/foz mice, coinciding with a strong postnatal reduction (∼70%) in neurons displaying cilia marked with adenylyl cyclase 3 (AC3), a signaling protein implicated in obesity.
73	22581473	Notably, the reduction in AC3-bearing cilia parallels the decrease in cilia containing two appetite-regulating proteins, Mchr1 and Sstr3, as well as another established Arl13b ciliary marker, consistent with progressive loss of cilia during development.
74	22581473	Given that Mchr1 and Sstr3 localization to remaining cilia is maintained in foz/foz animals but known to be lost from BBS knockout mice, our findings suggest different molecular etiologies for the satiety defects associated with the Alström syndrome and BBS ciliopathies.