| 產(chǎn)品編號(hào) | bs-6318R |
| 英文名稱 | Acid sphingomyelinase Rabbit pAb |
| 中文名稱 | 酸性神經(jīng)鞘磷脂酶抗體 |
| 別 名 | Acid sphingomyelinase; ASM; ASM_HUMAN; aSMase; NPD; Smpd1; Sphingomyelin phosphodiesterase 1 acid lysosomal; Sphingomyelin phosphodiesterase. |
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Specific References (4) | bs-6318R has been referenced in 4 publications.
[IF=6.126] Pe?ate T et al. Lipid-Iron Nanoparticle with a Cell Stress Release Mechanism Combined with a Local Alternating Magnetic Field Enables Site-Activated Drug ReleaseCancers (Basel).2020 Dec 14;12(12):3767. IHC ; Mouse.
[IF=6.081] Tuula Penate Medina. et al. Utilizing Sphingomyelinase Sensitizing Liposomes in Imaging Intestinal Inflammation in Dextran Sulfate Sodium-Induced Murine Colitis. Biomedicines. 2022 Feb;10(2):413 IHC ; Human.
[IF=6.02] Bodas M et al. Autophagy augmentation alleviates cigarette smoke-induced CFTR-dysfunction, ceramide-accumulation and COPD-emphysema pathogenesis.(2018) Free Radic Biol Med.131:81-97. FCM ; Human.
[IF=2.87] Anastasia M. Ravodina. et al. Facile Cholesterol Loading with a New Probe ezFlux Allows for Streamlined Cholesterol Efflux Assays. Acs Omega. 2020;5(36):23289–23298 WB ; Mouse.
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| 研究領(lǐng)域 | 細(xì)胞生物 神經(jīng)生物學(xué) 信號(hào)轉(zhuǎn)導(dǎo) 細(xì)胞凋亡 |
| 抗體來(lái)源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應(yīng) | Human,Mouse,Rat (predicted: Rabbit,Pig,Cow,Dog) |
| 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=2ug/Test
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 理論分子量 | 64 kDa |
| 檢測(cè)分子量 | |
| 細(xì)胞定位 | 細(xì)胞漿 |
| 性 狀 | Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human Acid sphingomyelinase: 201-300/629 |
| 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 |
Converts sphingomyelin to ceramide. Also has phospholipase C activities toward 1,2-diacylglycerolphosphocholine and 1,2-diacylglycerolphosphoglycerol. Isoform 2 and isoform 3 have lost catalytic activity. Involvement in disease: Defects in SMPD1 are the cause of Niemann-Pick disease type A (NPDA) ; also known as Niemann-Pick disease classical infantile form. It is an early-onset lysosomal storage disorder caused by failure to hydrolyze sphingomyelin to ceramide. It results in the accumulation of sphingomyelin and other metabolically related lipids in reticuloendothelial and other cell types throughout the body, leading to cell death. Niemann-Pick disease type A is a primarily neurodegenerative disorder characterized by onset within the first year of life, mental retardation, digestive disorders, failure to thrive, major hepatosplenomegaly, and severe neurologic symptoms. The severe neurological disorders and pulmonary infections lead to an early death, often around the age of four. Clinical features are variable. A phenotypic continuum exists between type A (basic neurovisceral) and type B (purely visceral) forms of Niemann-Pick disease, and the intermediate types encompass a cluster of variants combining clinical features of both types A and B. Function: Converts sphingomyelin to ceramide. Also has phospholipase C activities toward 1,2-diacylglycerolphosphocholine and 1,2-diacylglycerolphosphoglycerol. Isoform 2 and isoform 3 have lost catalytic activity. Subunit: Monomer. Subcellular Location: Lysosome. DISEASE: Defects in SMPD1 are the cause of Niemann-Pick disease type A (NPDA) [MIM:257200]; also known as Niemann-Pick disease classical infantile form. It is an early-onset lysosomal storage disorder caused by failure to hydrolyze sphingomyelin to ceramide. It results in the accumulation of sphingomyelin and other metabolically related lipids in reticuloendothelial and other cell types throughout the body, leading to cell death. Niemann-Pick disease type A is a primarily neurodegenerative disorder characterized by onset within the first year of life, mental retardation, digestive disorders, failure to thrive, major hepatosplenomegaly, and severe neurologic symptoms. The severe neurological disorders and pulmonary infections lead to an early death, often around the age of four. Clinical features are variable. A phenotypic continuum exists between type A (basic neurovisceral) and type B (purely visceral) forms of Niemann-Pick disease, and the intermediate types encompass a cluster of variants combining clinical features of both types A and B. Defects in SMPD1 are the cause of Niemann-Pick disease type B (NPDB) [MIM:607616]; also known as Niemann-Pick disease visceral form. It is a late-onset lysosomal storage disorder caused by failure to hydrolyze sphingomyelin to ceramide. It results in the accumulation of sphingomyelin and other metabolically related lipids in reticuloendothelial and other cell types throughout the body, leading to cell death. Clinical signs involve only visceral organs. The most constant sign is hepatosplenomegaly which can be associated with pulmonary symptoms. Patients remain free of neurologic manifestations. However, a phenotypic continuum exists between type A (basic neurovisceral) and type B (purely visceral) forms of Niemann-Pick disease, and the intermediate types encompass a cluster of variants combining clinical features of both types A and B. In Niemann-Pick disease type B, onset of the first symptoms occurs in early childhood and patients can survive into adulthood. Similarity: Belongs to the acid sphingomyelinase family. Contains 1 saposin B-type domain. SWISS: P17405 Gene ID: 6609 Database links: Entrez Gene: 100720041 Guinea pig Entrez Gene: 6609 Human Entrez Gene: 20597 Mouse Entrez Gene: 100353898 Rabbit Omim: 607608 Human SwissProt: P17405 Human SwissProt: Q04519 Mouse Unigene: 498173 Human Unigene: 4628 Mouse Unigene: 485064 Mouse Unigene: 18277 Rat ASM酸性神經(jīng)鞘磷脂酶是ASMase神經(jīng)鞘磷脂酶最重要的一個(gè)亞型,是細(xì)胞膜的重要組成成分。ASM在細(xì)胞凋亡、調(diào)節(jié)腫瘤細(xì)胞生長(zhǎng)、參與Fas信號(hào)系統(tǒng)傳遞等方面均可發(fā)揮重要作用。 |
| 產(chǎn)品圖片 |
Sample:
HepG2(human) cell Lysate at 30 ug
MCF-7(human) cell Lysate at 30 ug
A431(human) cell Lysate at 30 ug
Hale(human) cell Lysate at 30 ug
Primary: Anti- Acid sphingomyelinase (bs-6318R) at 1/300 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 64kD
Observed band size: 69 kD
Paraformaldehyde-fixed, paraffin embedded (Rat brain); Antigen retrieval by boiling in sodium citrate buffer (pH6.0) for 15min; Block endogenous peroxidase by 3% hydrogen peroxide for 20 minutes; Blocking buffer (normal goat serum) at 37°C for 30min; Antibody incubation with (Acid sphingomyelinase) Polyclonal Antibody, Unconjugated (bs-6318R) at 1:400 overnight at 4°C, followed by operating according to SP Kit(Rabbit) (sp-0023) instructionsand DAB staining.
Blank control:A431.
Primary Antibody (green line): Rabbit Anti-Acid sphingomyelinase antibody (bs-6318R)
Dilution: 2μg /10^6 cells;
Isotype Control Antibody (orange line): Rabbit IgG .
Secondary Antibody : Goat anti-rabbit IgG-AF488
Dilution: 1μg /test.
Protocol
The cells were fixed with 4% PFA (10min at room temperature)and then permeabilized with 0.1% PBST for 20 min at room temperature.The cells were then incubated in 5%BSA to block non-specific protein-protein interactions for 30 min 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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