| 產(chǎn)品編號(hào) | bs-1079R |
| 英文名稱 | SOD1 Rabbit pAb |
| 中文名稱 | 超氧化物歧化酶1（銅/鋅過(guò)氧化物歧化酶SOD）抗體 |
| 別 名 | Superoxide Dismutase 1; ALS 1; ALS; ALS1; Amyotrophic lateral sclerosis 1 adult; Amyotrophic lateral sclerosis 1; Cu/Zn SOD; Cu/Zn superoxide dismutase; Homodimer; Indophenoloxidase A; IPOA; Mn superoxide dismutase; SOD 1; SOD; SOD soluble; SOD2; SODC; Soluble indophenoloxidase A; Superoxide dismutase 1; Superoxide dismutase 1 soluble; Superoxide dismutase Cu Zn; Superoxide dismutase cystolic; SODC_HUMAN; Superoxide dismutase [Cu-Zn]; hSod1; Ipo1; SODC; Ipo-1; Sod-1; CuZnSOD; Cu/Zn-SOD; MGC107553; B430204E11Rik; superoxide-dimutase-1. |
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Specific References (4) | bs-1079R has been referenced in 4 publications.
[IF=14.404] Wu, Jianjun. et al. ROS-responsive PPGF nanofiber membrane as a drug delivery system for long-term drug release in attenuation of osteoarthritis. NPJ REGEN MED. 2022 Nov;7(1):1-15 IF ; Rat.
[IF=6.064] Mengni Bao. et al. N-Acetylcysteine, an ROS Inhibitor, Alleviates the Pathophysiology of Hyperthyroidism-Induced Cardiomyopathy via the ROS/Ca2+ Pathway. BIOMOLECULES. 2022 Sep;12(9):1195 WB ; Mouse, Rat.
[IF=4.622] Shun Zhou. et al. In vitro immunotoxicity and possible mechanisms of 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) on Ruditapes philippinarum hemocytes. FISH SHELLFISH IMMUN. 2022 Aug;127:386 WB ; Ruditapes philippinarum.
[IF=3.15] Li, Hongyan, et al. "Differential proteome and gene expression reveal response to carbon ion irradiation in pubertal mice testes." Toxicology Letters (2014). WB ; Mouse.
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| 研究領(lǐng)域 | 神經(jīng)生物學(xué) 細(xì)胞凋亡 激酶和磷酸酶 |
| 抗體來(lái)源 | Rabbit |
| 克隆類型 | Polyclonal |
| 克 隆 號(hào) | |
| 交叉反應(yīng) | Human,Mouse,Rat (predicted: Pig,Cow,Horse) |
| 產(chǎn)品應(yīng)用 | WB=1:500-2000,IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500,Flow-Cyt=1ug/test,ICC/IF=1:100
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 理論分子量 | 17 kDa |
| 檢測(cè)分子量 | |
| 細(xì)胞定位 | 細(xì)胞核 細(xì)胞漿 |
| 性 狀 | Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human SOD1: 101-154/154 |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 緩 沖 液 | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| 保存條件 | Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles. |
| 注意事項(xiàng) | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| PubMed | PubMed |
| 產(chǎn)品介紹 |
The protein encoded by this gene binds copper and zinc ions and is one of two isozymes responsible for destroying free superoxide radicals in the body. The encoded isozyme is a soluble cytoplasmic protein, acting as a homodimer to convert naturally-occuring but harmful superoxide radicals to molecular oxygen and hydrogen peroxide. The other isozyme is a mitochondrial protein. Mutations in this gene have been implicated as causes of familial amyotrophic lateral sclerosis. Rare transcript variants have been reported for this gene. [provided by RefSeq, Jul 2008] Function: Destroys radicals which are normally produced within the cells and which are toxic to biological systems. Subunit: Homodimer; non-disulfide linked. Homodimerization may take place via the ditryptophan cross-link at Trp-33. The pathogenic variants ALS1 Arg-38, Arg-47, Arg-86 and Ala-94 interact with RNF19A, whereas wild-type protein does not. The pathogenic variants ALS1 Arg-86 and Ala-94 interact with MARCH5, whereas wild-type protein does not. Subcellular Location: Cytoplasm. Note=The pathogenic variants ALS1 Arg-86 and Ala-94 gradually aggregates and accumulates in mitochondria. Post-translational modifications: Unlike wild-type protein, the pathogenic variants ALS1 Arg-38, Arg-47, Arg-86 and Ala-94 are polyubiquitinated by RNF19A leading to their proteasomal degradation. The pathogenic variants ALS1 Arg-86 and Ala-94 are ubiquitinated by MARCH5 leading to their proteasomal degradation. The ditryptophan cross-link at Trp-33 is responsible for the non-disulfide-linked homodimerization. Such modification might only occur in extreme conditions and additional experimental evidence is required. DISEASE: Defects in SOD1 are the cause of amyotrophic lateral sclerosis type 1 (ALS1) [MIM:105400]. ALS1 is a familial form of amyotrophic lateral sclerosis, a neurodegenerative disorder affecting upper and lower motor neurons and resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of cases leading to familial forms. Similarity: Belongs to the Cu-Zn superoxide dismutase family. SWISS: P00441 Gene ID: 6647 Database links: Entrez Gene: 6647 Human Entrez Gene: 20655 Mouse Omim: 147450 Human SwissProt: P00441 Human SwissProt: P08228 Mouse Unigene: 443914 Human Unigene: 276325 Mouse Unigene: 466779 Mouse Unigene: 6059 Rat 超氧化物歧化酶又稱銅/鋅過(guò)氧化物歧化酶SOD(Superoxide dismutase，簡(jiǎn)稱SOD)是參與機(jī)體抗氧化（ROS，反應(yīng)性氧離子reactive oxygen species）防御機(jī)制和抵御細(xì)胞氧化損傷最重要的酶類之一， 廣泛存在于需氧生物、耐氧生物及某些厭氧微生物中，目前已知的SOD 主要分為三類，即胞質(zhì)中Cu/Zn-SOD（即SOD1）、線粒體中的Mn-SOD（即SOD2）和ec-SOD(即SOD3)。 超氧化物歧化酶-1SOD1的水平與很多生理反應(yīng)有關(guān)，如：應(yīng)急，熱休克，紫外和X線照射等。SOD1水平降低能觸發(fā)AP2轉(zhuǎn)錄因子的激活。SOD1在臨床上對(duì)很多疾病診斷有重要意義。 |
| 產(chǎn)品圖片 |
Sample:
Lane 1: Kidney (Mouse) Lysate at 40 ug
Lane 2: Liver (Mouse) Lysate at 40 ug
Lane 3: NIH/3T3 (Mouse) Cell Lysate at 30 ug
Primary: Anti-SOD1 (bs-1079R) at 1/1000 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 17 kD
Observed band size: 19 kD
Tissue/cell: human liver cancer; 4% Paraformaldehyde-fixed and paraffin-embedded;
Antigen retrieval: citrate buffer ( 0.01M, pH 6.0 ), Boiling bathing for 15min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30min; Blocking buffer (normal goat serum,C-0005) at 37℃ for 20 min;
Incubation: Anti-SOD1 Polyclonal Antibody, Unconjugated(bs-1079R) 1:500, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(C-0010) staining
Tissue/cell: human oral squamous cell carcinoma; 4% Paraformaldehyde-fixed and paraffin-embedded;
Antigen retrieval: citrate buffer ( 0.01M, pH 6.0 ), Boiling bathing for 15min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30min; Blocking buffer (normal goat serum,C-0005) at 37℃ for 20 min;
Incubation: Anti-SOD1/SOD Polyclonal Antibody, Unconjugated(bs-1079R) 1:200, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(C-0010) staining
Hela cell; 4% Paraformaldehyde-fixed; Ice-cold methanol at -20℃ for 20 min; Blocking buffer (normal goat serum, C-0005) at 37°C for 20 min; Antibody incubation with (SOD1) polyclonal Antibody, Unconjugated (bs-1079R) 1:100, 90 minutes at 37°C; followed by a FITC conjugated Goat Anti-Rabbit IgG antibody at 37°C for 90 minutes, DAPI (blue, C02-04002) was used to stain the cell nuclei.
Blank control: HepG2.
Primary Antibody (green line): Rabbit Anti-SOD1 antibody (bs-1079R)
Dilution: 1μg /10^6 cells;
Isotype Control Antibody (orange line): Rabbit IgG .
Secondary Antibody : Goat anti-rabbit IgG-PE
Dilution: 1μg /test.
Protocol
The cells were fixed with 4% PFA (10min at room temperature)and then permeabilized with 90% ice-cold methanol for 20 min at-20℃. The cells were then incubated in 5%BSA to block non-specific protein-protein interactions for 30 min at at room temperature .Cells stained with Primary Antibody for 30 min at room temperature. The secondary antibody used for 40 min at room temperature. Acquisition of 20,000 events was performed.
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