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。
ANGPTL4 Antibody (Center)
Purified Rabbit Polyclonal Antibody (Pab)
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- 文献引用 : 2
- 实验流程
- 背景知识
Application 
| WB, IHC-P, FC, E |
|---|---|
| Primary Accession | Q9BY76 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 45214 Da |
| Antigen Region | 138-167 aa |
| Gene ID | 51129 |
|---|---|
| Other Names | Angiopoietin-related protein 4, Angiopoietin-like protein 4, Hepatic fibrinogen/angiopoietin-related protein, HFARP, ANGPTL4, ARP4, HFARP, PGAR |
| Target/Specificity | This ANGPTL4 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 138-167 amino acids from the Central region of human ANGPTL4. |
| Dilution | WB~~1:1000 IHC-P~~1:100~500 FC~~1:10~50 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | ANGPTL4 Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | ANGPTL4 |
|---|---|
| Synonyms | ARP4, HFARP, PGAR {ECO:0000303|PubMed:10 |
| Function | Mediates inactivation of the lipoprotein lipase LPL, and thereby plays a role in the regulation of triglyceride clearance from the blood serum and in lipid metabolism (PubMed:19270337, PubMed:21398697, PubMed:27929370, PubMed:29899144). May also play a role in regulating glucose homeostasis and insulin sensitivity (Probable). Inhibits proliferation, migration, and tubule formation of endothelial cells and reduces vascular leakage (PubMed:14583458, PubMed:17068295). Upon heterologous expression, inhibits the adhesion of endothelial cell to the extracellular matrix (ECM), and inhibits the reorganization of the actin cytoskeleton, formation of actin stress fibers and focal adhesions in endothelial cells that have adhered to ANGPTL4-containing ECM (in vitro) (PubMed:17068295). Depending on context, may modulate tumor-related angiogenesis (By similarity). |
| Cellular Location | Secreted. Secreted, extracellular space, extracellular matrix. Note=The unprocessed form interacts with the extracellular matrix (PubMed:17068295, PubMed:21398697). This may constitute a dynamic reservoir, a regulatory mechanism of the bioavailability of ANGPTL4 (Probable). |
| Tissue Location | Detected in blood plasma (at protein level) (PubMed:29899519). Detected in liver (PubMed:10698685). Detected in white fat tissue and placenta (PubMed:10866690). Expressed at high levels in the placenta, heart, liver, muscle, pancreas and lung but expressed poorly in the brain and kidney. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
ANGPTL4 is a member of the angiopoietin/angiopoietin-like gene family and encodes a glycosylated, secreted protein with a fibrinogen C-terminal domain. This protein is induced under hypoxic conditions in endothelial cells and is the target of peroxisome proliferation activators. The encoded protein is a serum hormone directly involved in regulating glucose homeostasis, lipid metabolism, and insulin sensitivity and also acts as an apoptosis survival factor for vascular endothelial cells. The encoded protein may play a role in several cancers and it also has been shown to prevent the metastatic process by inhibiting vascular activity as well as tumor cell motility and invasiveness. Decreased expression of this protein has been associated with type 2 diabetes.
REFERENCES
Maxwell,T.J., et.al., Int J Mol Sci 11 (1), 370-385 (2010)
Legry,V., et.al, J. Clin. Endocrinol. Metab. 94 (12), 5070-5077 (2009)
Sonnenburg,W.K., et.al, J. Lipid Res. 50 (12), 2421-2429 (2009)
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