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。
GPBAR1 Rabbit pAb
GPBAR1 Rabbit pAb
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- 背景知识
Application 
| IHC-P, IHC-F, IF |
|---|---|
| Primary Accession | Q8TDU6 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 35248 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human GPCR TGR5/GPBAR1 |
| Epitope Specificity | 5-100/330 |
| 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 | Cell membrane. |
| SIMILARITY | Belongs to the G-protein coupled receptor 1 family. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | The G protein-coupled receptor TGR5 is a 330-amino acid protein that is almost universally expressed in human tissues including heart, skeletal muscle, spleen, kidney, liver, small intestine, placenta, and leukocytes, but not in brain, colon (without mucosa), thymus, or lung. TGR5 is sensitive to bile acids and responds through a significant mechanism that coordinates energy homeostasis. Bile acids activate mitogen-activated protein (MAP) kinase pathways, specifically induce TGR5 internalization, promote an increase of guanosine 5'-O-3-thio-triphosphate binding in membrane fractions, and cause rapid intracellular cAMP production. Bile acids also provoke TGR5 to suppress macrophage functions. TGR5-controlled signaling pathways may be good candidates for drug targets to treat common metabolic diseases, such as obesity, type II diabetes, hyperlipidemia, and atherosclerosis. |
| Gene ID | 151306 |
|---|---|
| Other Names | G-protein coupled bile acid receptor 1, G-protein coupled receptor GPCR19, hGPCR19, Membrane-type receptor for bile acids, M-BAR, hBG37, BG37, GPBAR1, TGR5 |
| Target/Specificity | Ubiquitously expressed. Expressed at higher level in spleen and placenta. Expressed at lower level in other tissues. In digestive tissues, it is expressed in stomach, duodenum, ileocecum, ileum, jejunum, ascending colon, transverse colon, descending colon, cecum and liver, but not in esophagus and rectum. |
| Dilution | 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 | GPBAR1 |
|---|---|
| Synonyms | TGR5 |
| Function | Receptor for bile acid. Bile acid-binding induces its internalization, activation of extracellular signal-regulated kinase and intracellular cAMP production. May be involved in the suppression of macrophage functions by bile acids. |
| Cellular Location | Cell membrane; Multi-pass membrane protein |
| Tissue Location | Ubiquitously expressed. Expressed at higher level in spleen and placenta. Expressed at lower level in other tissues. In digestive tissues, it is expressed in stomach, duodenum, ileocecum, ileum, jejunum, ascending colon, transverse colon, descending colon, cecum and liver, but not in esophagus and rectum |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
The G protein-coupled receptor TGR5 is a 330-amino acid protein that is almost universally expressed in human tissues including heart, skeletal muscle, spleen, kidney, liver, small intestine, placenta, and leukocytes, but not in brain, colon (without mucosa), thymus, or lung. TGR5 is sensitive to bile acids and responds through a significant mechanism that coordinates energy homeostasis. Bile acids activate mitogen-activated protein (MAP) kinase pathways, specifically induce TGR5 internalization, promote an increase of guanosine 5'-O-3-thio-triphosphate binding in membrane fractions, and cause rapid intracellular cAMP production. Bile acids also provoke TGR5 to suppress macrophage functions. TGR5-controlled signaling pathways may be good candidates for drug targets to treat common metabolic diseases, such as obesity, type II diabetes, hyperlipidemia, and atherosclerosis.
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