Ask about this productRelated genes to: SSTR1 antibody
- Gene:
- SSTR1 NIH gene
- Name:
- somatostatin receptor 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 14q13
- Locus Type:
- gene with protein product
- Date approved:
- 1992-08-25
- Date modifiied:
- 2015-08-26
Related products to: SSTR1 antibody
Related articles to: SSTR1 antibody
- Pheochromocytomas and Paragangliomas (PPGL) are rare neuroendocrine tumors with favorable prognosis, although a significant subset (20-25%) progress to metastasis, worsening patient prognosis. For metastatic cases, pharmacological interventions become essential, yet most tumors show poor response to treatment. While clinical trials are ongoing, there is no established treatment for metastatic PPGL. Like other neuroendocrine tumors, PPGL exhibit high membrane expression of somatostatin receptors, and despite Peptide Receptor Radionuclide Therapy, PRRT, strategies have successfully been implemented, trials with cold somatostatin analogs were abandoned prematurely due to inconsistent results. To investigate this issue and identify potential therapeutic tools, we widely profiled somatostatin receptors expression in PPGL and conducted a comprehensive functional screening on wild-type and SDHB knockdown PPGL cell lines of native and synthetic somatostatin analogs. Results revealed that pheochromocytomas and paragangliomas similarly display a predominant SSTR2 and SSTR1 expression regardless of molecular cluster. Treatment with somatostatin, cortistatin, octreotide or pasireotide did not exert clear antitumoral effects on model cell lines. Notably, the selective SST agonist BIM-23120 significantly reduced cell proliferation and induced apoptosis in an SST-dependent manner, but only in SDHB knocked-down PPGL cells. Indeed, only SDHB KD cells showed stronger membrane-enriched SST and clear receptor internalization upon BIM-23120 treatment. Molecular analysis revealed a generalized dephosphorylation affecting key proliferation, growth and cell survival pathways in response to BIM-23120 (unlike when treating with octreotide). Altogether, our results provide novel information on the status of the somatostatin system in PPGL and identify new potential therapeutic tools selectively targeting somatostatin receptors on this refractory tumor. - Source: PubMed
Publication date: 2026/04/03
García-Vioque VíctorPedraza-Arevalo SergioMoreno-Montilla María TrinidadRivero-Cortés EstherBlázquez-Encinas RicardoMangili FedericaArroba EsterHerrera-Martínez Aura DCuller Michael DGálvez-Moreno María ÁngelesBarlier AnneBotella Luisa MaríaRobledo MercedesCastaño Justo PIbáñez-Costa Alejandro - Alzheimer's disease (AD) is a progressive neurodegenerative disorder with limited treatment options. Currently approved agents, such as acetylcholinesterase inhibitors and NMDA receptor antagonists, provide only modest symptomatic benefit without modifying disease progression. Increasing evidence highlights the somatostatin (SST) system and its analogues (SSAs) as potential multitarget therapies. Somatostatin receptors (SSTR1-5) are widely expressed in cognition-related brain regions and participate in amyloid-β metabolism, tau phosphorylation, neuroinflammation, and synaptic plasticity. Preclinical studies suggest that SSAs enhance amyloid clearance via neprilysin activation, attenuate tau pathology through PI3K/Akt signaling, regulate APOE4 expression, and modulate microglial function, thereby protecting synaptic integrity. Compared with current monotherapies, SSAs may provide broader therapeutic benefits, particularly if applied in prodromal or early stages of AD. Advances in delivery strategies, including peptide modification, nanocarrier-based transport, and physically assisted blood-brain barrier (BBB) penetration, further improve translational potential. However, challenges such as poor BBB permeability, incomplete mechanistic understanding, and limited clinical data remain. Integration of systems biology, biomarker-driven precision medicine, and novel delivery technologies may facilitate the development of SSA-based interventions as complementary strategies for AD management. - Source: PubMed
Publication date: 2026/03/19
Liu KaiZhang Xi-YuWang Yan-TingWang RunJin Run-HaoBing Yan-Hua - Small intestinal neuroendocrine tumors (SI-NET) frequently present as multifocal lesions, but the molecular mechanisms underlying their development and heterogeneity remain unclear. This study aimed to characterize the phenotypes of tumor cell populations across anatomic sites in patients with multifocal SI-NET and identify local microenvironmental factors influencing tumor development. - Source: PubMed
Yogo AkitadaAkanuma NaokiKim Grace EMäkinen NettaThirlwell ChrissieNakakura Eric K - Somatostatin is a peptide hormone exerting actions through 5 different somatostatin receptors (SSTR1-5). Somatostatin-positive cells have previously been found in intestinal mucosa and may be implicated in the pathophysiology of type 2 diabetes. Here, we characterized the distribution of somatostatin-positive cells and the mRNA expression profiles of somatostatin and SSTR1-5 along the intestinal tract of healthy individuals and patients with type 2 diabetes. - Source: PubMed
Nielsen Sophie WGilliam-Vigh HannahJorsal TinaWahlgren Camilla DVestergaard Mark BForman Julie LPedersen JensPoulsen Steen SVilsbøll TinaGasbjerg Lærke SKnop Filip K - Somatostatin (SST), a neuropeptide primarily synthesized by GABAergic interneurons, modulates neuronal excitability and synaptic transmission through its interaction with somatostatin receptors (SSTRs). Dysregulation of SST signaling has been implicated in neurodevelopmental disorders, including tuberous sclerosis complex (TSC). However, its precise role in these pathologies remains incompletely understood. We investigated SST and SSTR expression across diverse brain cell types in control and TSC cortical samples using single-cell RNA sequencing (scRNA-seq). We conducted functional assessments of SST signaling using electrophysiological recordings in Xenopus laevis oocytes microtransplanted with human brain membranes. We pharmacologically modulated SST receptor activity to elucidate receptor-specific effects on GABAergic transmission. scRNA-seq analysis revealed that SST expression is predominantly confined to GABAergic interneurons, while SSTR1 and SSTR2 exhibit strong expression in both glutamatergic and GABAergic neuronal populations. In TSC samples, SSTR5 was upregulated in GABAergic neurons, SSTR2 in glutamatergic neurons, while SSTR3 was downregulated in both glutamatergic neurons and microglia. Functional experiments demonstrated that SST enhances GABAergic currents in control tissues through a receptor-mediated mechanism involving protein kinase C activation. In contrast, SST application in TSC samples resulted in a significant suppression of GABAergic currents. Pharmacological inhibition of SSTR3 further exacerbated this effect, suggesting a compensatory role for this receptor subtype. Our findings reveal a disruption of SST signaling in TSC, contributing to altered coordination of excitatory-inhibitory activity and epileptogenesis. Targeting SST signaling may represent a therapeutic strategy for restoring inhibitory network function in TSC and related disorders. - Source: PubMed
Publication date: 2025/12/04
Scheper MirteGaeta AlessandroRuffolo GabrieleLissner Lilian JLe Bihan MarieAnink Jasper JJansen Floor Evan Hecke WimMühlebner AngelikaSchubert DirkMills James DPalma EleonoraAronica Eleonora