SOD1 (UbetaB) Antibody (OASE00433)
- Known as:
- SOD1 (UbetaB) Antibody (OASE00433)
- Catalog number:
- oase00433
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SOD1 (UbetaB) Antibody (OASE00433)
Related genes to: SOD1 (UbetaB) Antibody (OASE00433)
- Gene:
- SOD1 NIH gene
- Name:
- superoxide dismutase 1
- Previous symbol:
- ALS, ALS1
- Synonyms:
- IPOA
- Chromosome:
- 21q22.11
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: SOD1 (UbetaB) Antibody (OASE00433)
Related articles to: SOD1 (UbetaB) Antibody (OASE00433)
- Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting motor neurons. Here, we have profiled motor neuron microRNAs (miRNAs) during motor neuron degeneration in vivo to gain a better understanding of ALS pathophysiology. We demonstrate that one miRNA, miR-146a, is downregulated in diseased motor neurons despite upregulation in bulk tissue. Genetic deletion of miR-146a significantly extended survival in SOD1 mice with heterozygous animals demonstrating the largest benefit. A corresponding reduction in spinal cord gliosis but not motor neuron loss was observed. Finally, we observed that a proportion of miR-146a knockout animals develop spontaneous paralysis, motor neuron loss and chronic neuroinflammation with advanced age. Together these findings demonstrate that a single miRNA influences multiple aspects of motor neuron disease and highlights the complex role for neuroinflammation in ALS pathogenesis. - Source: PubMed
Publication date: 2026/06/01
Galloway Dylan APatterson Hunter LHoye Mariah LShen TaoShabsovich MarkSchoch Kathleen MLy Cindy VMiller Timothy M - Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent hyperglycemia that may impair testicular function, including spermatogenesis and steroidogenesis. Creatine, an endogenously synthesized nitrogenous compound and one of the main reservoirs in the testes, is widely used, particularly among men. However, evidence regarding its effects on male reproductive health, especially under DM, remains limited. This study evaluated the impact of creatine supplementation on testicular morphology in streptozotocin-induced diabetic rats. Forty-eight adult Wistar rats were randomly assigned to four groups (n = 12 each): C, control; CT, creatine; D, diabetes; and DT, diabetes + creatine. Creatine-enriched chow was administered in two phases: a loading phase (13%; 130 g/kg) for 5 days prior to DM induction, followed by a maintenance phase (2%; 20 g/kg) for 35 days. Biochemical, histomorphometric, histopathological, and immunohistochemical analyses were performed. Compared to controls, group D showed increased seminiferous tubule and epithelial proportions, epithelial height, tubular volume (TV), and tubulosomatic index (TSI), while intertubular proportions decreased. DT normalized most morphological parameters to C group levels, and attenuated the diabetes-induced increases in TV and TSI. In the intertubular compartment, group D showed increased Leydig cell and connective tissue proportions versus C, while DT exhibited larger lymphatic spaces (vs. D) and the greatest Leydig cell nuclear diameter among all groups. Histopathological degeneration was significant in both D and DT and remained higher than in control levels. Immunohistochemistry revealed reduced SOD1 and increased NFκB-p65 expression in DT compared to D. These findings indicate that creatine supplementation is associated with morphometric and histopathological changes in the testicular parenchyma of diabetic rats, along with alterations in oxidative stress and inflammatory markers. Further studies are required to determine the functional implications for male reproductive health. - Source: PubMed
Publication date: 2026/05/29
Freitas Ludmila Thainá Chavesde Melo Júnior Hailton PereiraOliveira Emily LimaDias Fernanda Carolina Ribeirode Lima Ruthnaldo Rodrigues MeloLima João Paulo Matos SantosMedeiros Matheus Anselmoda Silva Flávio Santosde Paula Medeiros Karina Carlade Araújo Júnior Raimundo FernandesMorais Danielle BarbosaAbreu Bento João - Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease; the precise pathogenesis of sporadic ALS (sALS) has not yet been elucidated up to now. Previous studies revealed that the abnormal alterations of some non-motor neurons (non-MN) were a potential pathogenesis of sALS. Therefore, this study aims to search the potential evidences of non-MN in the pathogenesis of ALS via exploring potential relationships between 5-hydroxytryptamine (5-HT) neurons and the development of ALS. - Source: PubMed
Zhou LijunLi MenghuaDai QiLiu XiwangLi ChengJiao HuifengPan HailiXu Renshi - Diabetes mellitus is frequently associated with cognitive dysfunction, primarily attributed to impaired hippocampal neurogenesis, oxidative stress, inflammation, and pyroptosis. Caffeic acid (CA), a dietary polyphenol, has demonstrated antioxidant and neuroprotective effects. This study evaluated the protective role of CA under diabetic-like conditions using an in vitro glucolipotoxicity model in HT-22 hippocampal neurons exposed to high glucose and oleic acid (HG + OA). CA was administered at low (5 µM) and high (25 µM) concentrations prior to HG + OA treatment. CA significantly enhanced neuronal viability and restored the expression of neurogenesis markers (Nestin, DCX, NeuN) and synaptic proteins (PSD-95, Synaptophysin). Furthermore, CA elevated antioxidant enzyme levels (Nrf2, catalase, SOD-1), regulated apoptosis through increased Bcl-2 and decreased BAX expression, and attenuated inflammatory responses. Pyroptosis was also suppressed, as evidenced by reduced gasdermin D (GSDMD) expression. These findings suggest that CA confers multifactorial neuroprotection against glucolipotoxic injury, and may serve as a dietary modulator for mitigating diabetes-associated cognitive decline in vitro. - Source: PubMed
Publication date: 2026/05/28
Tsai I-NingXie Xiang-NingKo Ping-EnTsai Yung-CheChen Ching-ChunHsu Li-SungWang Chau-Jong - Amyotrophic lateral sclerosis is a progressive multifocal neurodegenerative condition involving motor neurons and other cell types. To analyze spatiotemporal cellular dynamics in amyotrophic lateral sclerosis, we performed single-nucleus ribonucleic acid sequencing and spatial transcriptomics analysis of cervical spinal cords from wild-type control mice and SOD1-G93A transgenic mice in the pre-symptomatic (d50), early symptomatic (d90), and late-stage (d130) phases of disease. Single-nucleus ribonucleic acid sequencing identified 17 cell clusters and showed that progressive neuronal loss occurred over time, paralleled by glial expansion. Spatial transcriptomics mapped these clusters anatomically onto oligodendrocytes in white matter, neurons in horns, and diffuse astrocytes/microglia. Subcluster analysis demonstrated neuronal heterogeneity, with early mitochondrial stress in ventral motor neurons evolving into synaptic dysfunction, transient maturation peaks in interneurons, and amplified age-related decline in amyotrophic lateral sclerosis. Astrocyte and oligodendrocyte subclusters, which were originally misclustered due to spot-level contamination, were reinterpreted to highlight A1-reactive states and progenitor expansions, validated by immunohistochemistry detection of serum/glucocorticoid regulated kinase 1. Temporal profiles tracked the transition from compensatory to inflammatory gliosis, while gene signatures were linked to human amyotrophic lateral sclerosis cohorts, including complement activation and mitochondrial dysfunction. This study provides a high-resolution spatiotemporal cellular map of amyotrophic lateral sclerosis pathogenesis through the integration of single-nucleus and spatial transcriptomics, uncovering early mitochondrial impairment in neurons, delineating the trajectory of neurotoxic glial states, and identifying compensatory progenitor responses, to highlight the highly intricate interaction between glial reactivity and neuronal susceptibility that drives the pathogenesis of ALS. - Source: PubMed
Publication date: 2026/05/14
Zhou QiGong TianLiu JiahaoMa JunpengZheng MinxiuZhong ZiweiDeng HaitaoLin HaiyanFeng NanLei XiaoZhang Chengsheng