癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
ACOX1 Rabbit mAb
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- 实验流程
- 背景知识
Application 
| WB, FC, IP |
|---|---|
| Primary Accession | Q9R0H0 |
| Reactivity | Rat, Human, Mouse |
| Host | Rabbit |
| Clonality | Monoclonal Antibody |
| Isotype | IgG |
| Conjugate | Unconjugated |
| Purification | Affinity Purified |
| Calculated MW | 74649 Da |
| Gene ID | 11430 |
|---|---|
| Other Names | Acox1 |
| Dilution | WB~~1:5000-1:50000 FC~~1 IP~~1:20-1:50 |
| Format | 1xPBS(pH 7.4), 150mM NaCl, 50% Glycerol, 0.02% Sodium azide and 0.05% BSA |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Name | Acox1 {ECO:0000312|MGI:MGI:1330812} |
|---|---|
| Synonyms | Acox, Paox |
| Function | Involved in the initial and rate-limiting step of peroxisomal beta-oxidation of straight-chain saturated and unsaturated very-long- chain fatty acids. Catalyzes the desaturation of fatty acyl-CoAs that have a saturated bond between C2 and C3 (2,3-saturated acyl-CoA) to 2- trans-enoyl-CoAs ((2E)-enoyl-CoAs), and donates electrons directly to molecular oxygen (O(2)), thereby producing hydrogen peroxide (H(2)O(2)). |
| Cellular Location | Peroxisome {ECO:0000250|UniProtKB:P07872}. |
| Tissue Location | Highest levels of isoform 1 are found in liver and kidney while highest levels of isoform 2 are found in white adipose tissue. Isoform 1 is expressed at higher levels than isoform 2 in liver and kidney while isoform 2 is expressed at higher levels in brain, heart, lung, muscle, white adipose tissue and testis |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Defects in ACOX1 are the cause of adrenoleukodystrophy pseudoneonatal (Pseudo-NALD); also known as peroxisomal acyl-CoA oxidase deficiency. Pseudo-NALD is a peroxisomal single-enzyme disorder. Clinical features include mental retardation, leukodystrophy, seizures, mild hepatomegaly, hearing deficit. Pseudo-NALD is characterized by increased plasma levels of very-long chain fatty cids, due to decreased or absent peroxisome acyl-CoA oxidase activity. Peroxisomes are intact and functioning.
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