SOD1, 1_154aa, Human, Recombinant, E.coli
- Known as:
- SOD1, 1_154aa, Human, Recombinant, E.coli
- Catalog number:
- SOD0801
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- SOD1 1_154aa Human Recombinant .coli
Related genes to: SOD1, 1_154aa, Human, Recombinant, E.coli
- Gene:
- FCN2 NIH gene
- Name:
- ficolin 2
- Previous symbol:
- -
- Synonyms:
- P35, FCNL, EBP-37, ficolin-2
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-11
- Date modifiied:
- 2016-10-05
- 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, 1_154aa, Human, Recombinant, E.coli
Related articles to: SOD1, 1_154aa, Human, Recombinant, E.coli
- Peripheral factors that systemically regulate amyotrophic lateral sclerosis (ALS) have remained elusive-until now. Here, by integrating population-scale epidemiology with mechanistic dissection, we identify platelet factor 4 (PF4) as the central driver of a circulating neuroprotective axis that restores proteostasis and rescues ALS. In a prospective cohort of >500 000 UK Biobank participants, platelet indices were strongly associated with ALS risk, and serum PF4 levels were significantly reduced in ALS patients. Systemic administration of recombinant PF4 in hSOD1 mice produced dramatic therapeutic effects: extended survival, preserved motor function, attenuated neuroinflammation, and reduced neuromuscular junction denervation. Remarkably, this efficacy appears pathology-selective-robust in SOD1-driven models but shows no observable effect in TDP-43 or C9orf72 ALS models. Mechanistically, PF4 achieves what few molecules can: it engages the cell surface receptor LRP1 to activate the TBK1-OPTN signaling axis, restoring impaired autophagic flux through a PINK1/Parkin-independent pathway requiring ATG7, establishing a previously unrecognized peripheral platelet-autophagy-neuron axis that facilitates the co-clearance of pathological SOD1 aggregates and damaged mitochondria. This study unveils PF4 as a first-in-class circulating autophagy regulator with therapeutic potential in ALS. Beyond identifying a candidate biomarker and drug lead, it reveals that systemic factors can directly engage central proteostatic machinery-opening a new frontier for ALS therapy. - Source: PubMed
Publication date: 2026/07/23
Xie QingjianZhu YanboJiang WenhuaXie HaoboLi YaojiaHu MengjieLi KezhengYu HuanPan YixuanJiang ChaoyiSong XueqinFan DongshengDeng Binbin - : To describe clinical and biomarker experience using an SOD1 antisense oligonucleotide (ASO) in a patient with non- amyotrophic lateral sclerosis (ALS). : Case report. : In a 72-year-old male with non-SOD1 ALS, rapid decline on the ALS functional rating scale revised (ALSFRS-R) and a rise in serum neurofilament light chain (NfL) concentration were observed following 3 loading doses of an SOD1 ASO before the patient succumbed to disease. The time from symptom onset to death was 9 months. : While treatment was initiated relatively late (∼7 months) after symptom onset and follow-up duration was short, the observed increase (as opposed to a reduction) in serum NfL and accompanying rapid functional decline, suggest the lack of a therapeutic effect in someone with fast progressing non- ALS. - Source: PubMed
Publication date: 2026/07/22
Carberry NathanWuu JoanneBenatar Michael - Acanthocystis turfacea chlorella virus 1 (ATCV-1) is a giant virus that is part of the human oral microvirome. Previously we showed that ATCV-1 infects mouse macrophages, stimulates production of inflammatory cytokines, and accelerates motor neuron disease in the Amyotrophic Lateral Sclerosis (ALS) model SOD1-G93A transgenic mice. This, coupled with significantly elevated levels of serum IgG1 antibody to ATCV-1 in ALS patients compared with healthy controls, suggests involvement of ATCV-1 in ALS. Herein, using serum and CSF from a different ALS cohort we again show elevated antibodies to ATCV-1 in ALS patients compared with healthy controls. To assess ATCV-1 in human macrophages, we challenged immature (IMM), M0, M1, and M2 human THP-1 macrophage cells containing an Interferon Stimulated Response Element (ISRE) promoter-reporter with ATCV-1 or its Major Capsid protein (MCP) glycans. ATCV-1 infected M1 THP-1 to a greater degree than IMM, M0, or M2 THP-1. The initial high ISRE-promoter activity of M1 THP-1 was suppressed by the MCP-Glycans of ATCV-1. M0, but not IMM or M2 THP-1 produced IL-6 in response to ATCV-1 or its MCP-glycan, while high levels of IL-6 from unchallenged M1 THP-1 increased further by ATCV-1 or its MCP glycan. In contrast, ATCV-1 or its MCP-Glycan significantly reduced the high levels of IL-10 produced by M2 THP-1. Thus, antibody to ATCV-1 in ALS patients and the susceptibility of human M1 macrophages to ATCV-1 infection with boosted inflammatory cytokine and diminished anti-inflammatory cytokine production suggest that ATCV-1 may contribute to ALS motor neuron disease. - Source: PubMed
Publication date: 2026/07/21
Petro Thomas MPattee Gary LEsmael AhmedAgarkova Irina VDunigan David DChiodo FabrizioDe Castro CristinaVan Etten James L - Atherosclerosis-induced oxidative stress drives skeletal muscle myopathy in peripheral artery disease, yet the combined effects of hypoxia and hypoxia sprint interval training (SIT) remain unclear. The present study was designed to evaluate how a six-week regimen of hypoxia exposure and SIT influences redox balance and myokine production in the skeletal muscle of high-fat diet (HFD) (21% fat, 1.5% (w/w) cholesterol; 43% (w/w) sucrose-free carbohydrate, 4.554 kcal/g)-fed atherosclerotic ApoE mice. Forty male ApoE mice fed a HFD were randomly assigned to four groups: Control-Normoxia, Control-Hypoxia, SIT-Normoxia, and SIT-Hypoxia. The hypoxia protocol involved exposures to 11.2% oxygen three times (40 min each) per week. Key assessment parameters included plasma lipid profiles, skeletal muscle reactive oxygen species (ROS), protein carbonyls, key components of the Nrf2 antioxidant pathway, glutathione metabolism, and myokine-related markers. Compared with the control group, both hypoxia and SIT-Normoxia significantly reduced levels of ROS, protein carbonyls, and Vegfa165 mRNA expression in the skeletal muscle. Hypoxia alone enhanced the levels of GSH-synthesizing enzymes and promoted myokine production. SIT-Normoxia improved plasma lipid profiles, activated the Nrf2 pathway, enhanced the GSH system, and upregulated myokines. SIT under hypoxia further reduced ROS and Vegfa165 while increasing plasma HDL-C and levels of SOD1 protein in the skeletal muscle, but failed to synergistically activate the Nrf2 pathway or enhance GSH production. Paradoxically, both intervention combinations suppressed the mRNA expression of myokine precursor Fndc5, BAIBA-synthesizing enzyme Hadh and Hadha. Overall, six weeks of isolated hypoxia exposure or SIT training independently reduced oxidative stress and promoted beneficial myokine responses in the skeletal muscle of ApoE mice fed a HFD. The wild-type (WT) mice fed a low-fat diet (LFD) was included to validate successful induction of hyperlipidemia, vascular remodeling, and skeletal muscle oxidative stress in ApoE mice after six weeks of HFD feeding. - Source: PubMed
Publication date: 2026/07/21
Wang YangwenjieLavier JessicaWang LinjiaHua WeichengWei HaoZhao ChanglePellegrin MaximeMillet Grégoire PZhang Ying - Amyotrophic lateral sclerosis (ALS) is a progressive and fatal neurodegenerative disorder driven by neuroinflammation involving activated microglia and astrocytes, which accelerates the loss of motor neurons. While Secretory leukocyte protease inhibitor (SLPI) is known for its immunomodulatory properties, its specific role in ALS pathogenesis has not been fully established. This study aimed to characterize the expression patterns and functional significance of SLPI in ALS models. - Source: PubMed
Publication date: 2026/07/17
Li Ming-AnSong Yi-ZhiLi TingWu JianTao YueHu RuiQiao Chen-MengCui ChunZhao Wei-JiangShen Yan-Qin