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。
ASPSCR1 Rabbit pAb
ASPSCR1 Rabbit pAb
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- 实验流程
- 背景知识
Application 
| WB, IHC-P, IHC-F, IF |
|---|---|
| Primary Accession | Q9BZE9 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 60183 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human TUG/ASPC |
| Epitope Specificity | 351-420/553 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SUBCELLULAR LOCATION | Endomembrane system; Peripheral membrane protein. |
| SIMILARITY | Contains 1 UBX domain. |
| SUBUNIT | Interacts with GLUT4. |
| DISEASE | Note=A chromosomal aberration involving ASPSCR1 is found in patients with alveolar soft part sarcoma. Translocation t(X;17)(p11;q25) with TFE3 forms a ASPSCR1-TFE3 fusion protein. Note=A chromosomal aberration involving ASPSCR1 has been found in two patients with of papillary renal cell carcinoma. Translocation t(X;17)(p11.2;q25). |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | Glut4 is a twelve pass transmembrane protein (12TM) whose carboxy-terminus may dictate its cellular localization. Aberrant Glut4 expression has been suggested to contribute to such maladies as obesity and diabetes. Glut4 null mice have shown that while functional Glut4 protein is not required for maintaining normal glucose levels, it is necessary for sustained growth, normal cellular glucose, fat metabolism and prolonged longevity. TUG (ASPL in humans) regulates the trafficking of glucose via Glut4. Full-length TUG forms a complex with Glut4 and in 3T3-L1 adipocytes and this complex is present in unstimulated cells and is disassembled by insulin. TUG acts by trapping endocytosed Glut4 and tethering it intracellularly. Insulin mobilizes this pool of retained Glut4 by releasing the tether. |
| Gene ID | 79058 |
|---|---|
| Other Names | Tether containing UBX domain for GLUT4, Alveolar soft part sarcoma chromosomal region candidate gene 1 protein, Alveolar soft part sarcoma locus, Renal papillary cell carcinoma protein 17, UBX domain-containing protein 9, ASPSCR1, ASPL, RCC17, TUG, UBXD9, UBXN9 |
| Target/Specificity | Ubiquitous. Highly expressed in testis, heart, skeletal muscle and pancreas. |
| Dilution | WB=1:500-2000,IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500 |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| Name | ASPSCR1 |
|---|---|
| Synonyms | ASPL, RCC17, TUG, UBXD9, UBXN9 |
| Function | Tethering protein that sequesters GLUT4-containing vesicles in the cytoplasm in the absence of insulin. Modulates the amount of GLUT4 that is available at the cell surface (By similarity). Enhances VCP methylation catalyzed by VCPKMT. |
| Cellular Location | Endomembrane system; Peripheral membrane protein. Endoplasmic reticulum-Golgi intermediate compartment membrane; Peripheral membrane protein. Cytoplasm Nucleus |
| Tissue Location | Ubiquitous. Highly expressed in testis, heart, skeletal muscle and pancreas. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Glut4 is a twelve pass transmembrane protein (12TM) whose carboxy-terminus may dictate its cellular localization. Aberrant Glut4 expression has been suggested to contribute to such maladies as obesity and diabetes. Glut4 null mice have shown that while functional Glut4 protein is not required for maintaining normal glucose levels, it is necessary for sustained growth, normal cellular glucose, fat metabolism and prolonged longevity. TUG (ASPL in humans) regulates the trafficking of glucose via Glut4. Full-length TUG forms a complex with Glut4 and in 3T3-L1 adipocytes and this complex is present in unstimulated cells and is disassembled by insulin. TUG acts by trapping endocytosed Glut4 and tethering it intracellularly. Insulin mobilizes this pool of retained Glut4 by releasing the tether.
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