SEPN1 Blocking Peptide
- Known as:
- SEPN1 Blocking Peptide
- Catalog number:
- 33r-1411
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- SEPN1 Blocking Peptide
Related genes to: SEPN1 Blocking Peptide
- Gene:
- SELENON NIH gene
- Name:
- selenoprotein N
- Previous symbol:
- RSMD1, MDRS1, SEPN1
- Synonyms:
- SELN, RSS
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-11
- Date modifiied:
- 2019-04-23
Related products to: SEPN1 Blocking Peptide
Related articles to: SEPN1 Blocking Peptide
- This review systematically maps the causal and mechanistic connections between selenium status and sarcopenia, a debilitating condition characterized by age-related loss of muscle mass, strength, and function. Current evidence reveals a strong and consistent association across studies. Epidemiological data demonstrate that lower levels of various selenium biomarkers, including serum/plasma selenium, whole blood selenium, the selenium transport protein SELENOP, and dietary selenium intake, are significantly associated with poorer muscle outcomes, such as decreased grip strength, reduced muscle mass, and a higher prevalence of sarcopenia, following a dose-response pattern. A clinical study further confirms significantly lower serum selenium levels and glutathione peroxidase activity in patients with sarcopenia, linking elevated muscle oxidative stress to depleted selenium status. In animal models, sarcopenia is associated with reduced muscle selenium content, whereas selenium supplementation effectively prevents this decline and attenuates muscle atrophy and weakness. The underlying protective mechanisms are primarily mediated through specific selenoproteins. GPX4 preserves mitochondrial function and muscle mass by detoxifying lipid peroxides, suppressing inflammation, and preventing ferroptosis. SELENOP, secreted by macrophages, resolves inflammation and supports muscle stem cell-mediated regeneration. SELENOW, highly expressed in skeletal muscle, maintains protein homeostasis by regulating the RAC1-mTOR pathway to counteract atrophy. Additionally, SELENOT and SELENON are critical for maintaining intracellular calcium homeostasis, which is essential for normal muscle contraction. In conclusion, selenium deficiency constitutes a significant risk factor for sarcopenia. Ensuring adequate selenium intake supports a network of selenoproteins that combat oxidative stress, regulate inflammation, promote muscle regeneration, and maintain protein and calcium homeostasis, underscoring its importance in nutritional strategies for preserving muscle health in aging populations. - Source: PubMed
Publication date: 2026/09/18
Ni QingqingWang HuadongZhang JinsongWang Huali - Selenium is an essential trace element incorporated into selenoproteins, which regulate redox balance, thyroid hormone metabolism, protein folding, and stress signaling. The relationship between selenium and metabolic health is complex, with growing evidence of a U-shaped association. This review synthesizes current evidence on selenium and selenoproteins in age-related metabolic diseases, with a focus on MASLD, obesity, and cardiovascular disease. Mechanistic data from experimental models are integrated with human observational and intervention studies to evaluate how selenium status, chemical form, dose, and timing influence metabolic outcomes. Evidence indicates a narrow biological window for selenium. Selenium deficiency impairs glucose metabolism and antioxidant defenses and promotes liver injury. However, excessive selenium exposure in selenium-replete individuals may exacerbate insulin resistance, adiposity, and cardiometabolic risk. Several selenoproteins, including GPX1, SELENOP, SELENOM, SELENON, SELENOS, SELENOK, DIO2, and SELENOH, are implicated in various metabolic pathways, acting as protective mediators or disease-associated regulators. Their roles depend on tissue type, expression level, and disease stage. Current evidence does not support widespread selenium supplementation but prioritizes dietary sources, restricts supplementation to cases of confirmed or probable deficiency, and emphasizes the U-shaped risk profile associated with selenium exposure. - Source: PubMed
Publication date: 2026/08/25
Apalowo Oladayo EAdewole Taiwo SYusuf Ismaila FSchilling M Wes - Congenital myopathies (CMs) are a heterogeneous group of rare or ultra-rare inherited muscular disorders in which cognitive, neuropsychological and psychosocial outcomes remain poorly characterized. - Source: PubMed
Publication date: 2026/08/06
Rinella SergioAnastasio GennaroSapuppo AnnamariaBianco Manuela LoLeonardi RobertaPavone PieroRuggieri MartinoPolizzi Agata - BackgroundLAMA2-related muscular dystrophy (LAMA2-MD) and SELENON-related myopathy (SELENON-RM) are rare congenital muscle diseases characterized by slowly progressive proximal muscle weakness, spinal rigidity and respiratory insufficiency. The LAST STRONG study is a natural history study to identify suitable outcome measures and reach trial readiness for LAMA2-MD and SELENON-RM.MethodsPatients had four visits over 1.5-years. Assessments included neurological examination, hand-held dynamometry (HHD), functional assessments (Motor Function Measurements(MFM)-20/32, graded and timed function tests), accelerometry, and questionnaires on quality of life, activities and participation, pain, and fatigue.ResultsA total of 27 LAMA2-MD (21 years, range 3-50; 9 males) and 11 SELENON-RM (20 years, range 3-42; 8 males) patients were included. In LAMA2-MD, mean HHD scores for neck extensors, biceps brachii, quadriceps, foot plantar flexors and handgrip strength increased (all p < 0.02). In SELENON-RM, biceps brachii and foot plantar flexors increased (p < 0.01). In LAMA2-MD, functional assessments did not change significantly. In SELENON-RM, MFM-20/32 total score and domain 1 decreased (p < 0.05), 6-Minute Walk Test (6MWT) decreased (p < 0.01) and 10-Meter Walk Test (10MWT) increased (p < 0.01). Accelerometry showed a significant change in moderate activity in LAMA2-MD (p <0.01), no changes were observed in SELENON-RM.DiscussionOver 1.5 years, LAMA2-MD remained mostly stable, while SELENON-RM showed minimal functional decline on select outcome measures. Both cohorts showed HHD increases, likely reflecting age-related development. Most measures did not capture disease progression, however MFM-20/32, 6MWT and 10MWT showed small significant changes in SELENON-RM, suggesting potential trial endpoints. - Source: PubMed
Publication date: 2026/08/01
de Laat Elisabeth C MGroothuis Jan TBouman KarlijnHouwen-van Opstal Saskia L SErasmus Corrie EVoermans Nicol C - Variants in the SELENON gene cause a myopathy with axial weakness, scoliosis, and respiratory failure. This study aimed to characterize the temporal and spatial distribution of fat replacement across the whole body in patients with SELENON-related myopathy. - Source: PubMed
Publication date: 2026/04/13
Shimazaki RuiNoguchi SatoruYoshioka WakakoTakizawa HotakeOya YasushiTakahashi YujiSato NorikoKimura YukioHayashi ShinichiroNishino Ichizo