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。
JIP2 Rabbit pAb
JIP2 Rabbit pAb
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- 实验流程
- 背景知识
Application 
| WB, IHC-P, IHC-F, IF, E |
|---|---|
| Primary Accession | Q13387 |
| Predicted | Human, Mouse, Rat, Horse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 87975 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human JIP2 |
| Epitope Specificity | 31-130/824 |
| 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 | Cytoplasm. Accumulates in cell surface projections. |
| SIMILARITY | Belongs to the JIP scaffold family. Contains 1 PID domain. Contains 1 SH3 domain. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | c-Jun NH2-terminal kinases (JNKs) are distant members of the MAP kinase family (1). JNK1 is activated by dual phosphorylation at a Thr-Pro-Tyr motif in response to ultraviolet (UV) light, and it functions to phosphorylate c-Jun at amino terminal serine regulatory sites, Ser-63 and Ser-73, resulting in transcriptional activation (2-5). Two additional JNK family members have been identified as JNK2 and JNK3 (3). JIP-1 (for JNK interacting protein-1) has been identified as a cytoplasmic inhibitor of JNK that retains JNK in the cytoplasm, thereby inhibiting JNK-regulated gene expression. Evidence suggests that JNK1 and JNK2 bind to JIP-1 with greater affinity than to ATF-2 and c-Jun, which are targets of the JNK signaling pathway. JIP-1 contains an amino terminal JNK binding domain and a carboxy terminal SH3 domain. ATF-2 and c-Jun also contain the JNK binding domain and are thought to compete with JIP-1 for JNK binding (6). Multiple splice variants if JIP-1, including JIP-1b, JIP-1c (also designated islet-brain 1 or IB-1), JIP-2a, JIP-2b and JIP-3, have been identified in brain (7). |
| Gene ID | 23542 |
|---|---|
| Other Names | C-Jun-amino-terminal kinase-interacting protein 2, JIP-2, JNK-interacting protein 2, Islet-brain-2, IB-2, JNK MAP kinase scaffold protein 2, Mitogen-activated protein kinase 8-interacting protein 2, MAPK8IP2, IB2, JIP2, PRKM8IPL |
| Target/Specificity | Expressed mainly in the brain and pancreas, including insulin-secreting cells. In the nervous system, more abundantly expressed in the cerebellum, pituitary gland, occipital lobe and the amygdala. Also expressed in fetal brain. Very low levels found in uterus, ovary, prostate, colon, testis, adrenal gland, thyroid gland and salivary gland. |
| Dilution | WB=1:500-2000,IHC-P=1:100-500,IHC-F=1:100-500,ICC/IF=1:100-500,IF=1:100-500,ELISA=1:5000-10000 |
| 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 | MAPK8IP2 |
|---|---|
| Synonyms | IB2, JIP2, PRKM8IPL |
| Function | The JNK-interacting protein (JIP) group of scaffold proteins selectively mediates JNK signaling by aggregating specific components of the MAPK cascade to form a functional JNK signaling module. JIP2 inhibits IL1 beta-induced apoptosis in insulin-secreting cells. May function as a regulator of vesicle transport, through interactions with the JNK-signaling components and motor proteins (By similarity). |
| Cellular Location | Cytoplasm. Note=Accumulates in cell surface projections |
| Tissue Location | Expressed mainly in the brain and pancreas, including insulin-secreting cells. In the nervous system, more abundantly expressed in the cerebellum, pituitary gland, occipital lobe and the amygdala. Also expressed in fetal brain. Very low levels found in uterus, ovary, prostate, colon, testis, adrenal gland, thyroid gland and salivary gland |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
c-Jun NH2-terminal kinases (JNKs) are distant members of the MAP kinase family (1). JNK1 is activated by dual phosphorylation at a Thr-Pro-Tyr motif in response to ultraviolet (UV) light, and it functions to phosphorylate c-Jun at amino terminal serine regulatory sites, Ser-63 and Ser-73, resulting in transcriptional activation (2-5). Two additional JNK family members have been identified as JNK2 and JNK3 (3). JIP-1 (for JNK interacting protein-1) has been identified as a cytoplasmic inhibitor of JNK that retains JNK in the cytoplasm, thereby inhibiting JNK-regulated gene expression. Evidence suggests that JNK1 and JNK2 bind to JIP-1 with greater affinity than to ATF-2 and c-Jun, which are targets of the JNK signaling pathway. JIP-1 contains an amino terminal JNK binding domain and a carboxy terminal SH3 domain. ATF-2 and c-Jun also contain the JNK binding domain and are thought to compete with JIP-1 for JNK binding (6). Multiple splice variants if JIP-1, including JIP-1b, JIP-1c (also designated islet-brain 1 or IB-1), JIP-2a, JIP-2b and JIP-3, have been identified in brain (7).
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