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。
NDC1 Rabbit pAb
NDC1 Rabbit pAb
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Application 
| IHC-P, IHC-F, IF, E |
|---|---|
| Primary Accession | Q9BTX1 |
| Predicted | Human, Mouse, Rat, Dog, Pig, Horse, Cat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 76305 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human NDC1 |
| Epitope Specificity | 551-650/674 |
| 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 | Nucleus; nuclear pore complex; multipass membrane protein |
| SIMILARITY | Belongs to the NDC1 family. |
| SUBUNIT | Interacts with the NUP35/NUP53 By similarity. Interacts with AAAS, anchoring it to the nuclear envelope. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | NDC1 is a 674 amino acid multi-pass membrane protein, central core structure of the nuclear pore complex (NPC) and member of the NDC1 family that is crucial for selective nuclear protein import. Existing as four alternatively spliced isoforms that are encoded by a gene located on human chromosome 1, NDC1 interacts with Nup35 and anchors Aladin to the nuclear envelope of the NPC, a region of macromolecular transport between the nucleus and cytoplasm. In the absence of NDC1, Aladin becomes mislocalized and may lead to the development of an autosomal recessive disorder termed achalasia-addisonianism-alacrima (triple A) syndrome. Triple A syndrome is characterized by achalasia, alacrima and adrenocortico-tropin-resistant adrenal insufficiency. Robust expression in neural systems associated with cognitive, motor and sensory functions is consistent with the myriad of symptoms experienced by patients with triple A syndrome. |
| Gene ID | 55706 |
|---|---|
| Other Names | Nucleoporin NDC1, hNDC1, Transmembrane protein 48, NDC1, TMEM48 |
| Dilution | 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 | NDC1 |
|---|---|
| Synonyms | TMEM48 |
| Function | Component of the nuclear pore complex (NPC), which plays a key role in de novo assembly and insertion of NPC in the nuclear envelope. Required for NPC and nuclear envelope assembly, possibly by forming a link between the nuclear envelope membrane and soluble nucleoporins, thereby anchoring the NPC in the membrane. |
| Cellular Location | Nucleus, nuclear pore complex. Nucleus membrane; Multi-pass membrane protein. Note=Central core structure of the nuclear pore complex |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
NDC1 is a 674 amino acid multi-pass membrane protein, central core structure of the nuclear pore complex (NPC) and member of the NDC1 family that is crucial for selective nuclear protein import. Existing as four alternatively spliced isoforms that are encoded by a gene located on human chromosome 1, NDC1 interacts with Nup35 and anchors Aladin to the nuclear envelope of the NPC, a region of macromolecular transport between the nucleus and cytoplasm. In the absence of NDC1, Aladin becomes mislocalized and may lead to the development of an autosomal recessive disorder termed achalasia-addisonianism-alacrima (triple A) syndrome. Triple A syndrome is characterized by achalasia, alacrima and adrenocortico-tropin-resistant adrenal insufficiency. Robust expression in neural systems associated with cognitive, motor and sensory functions is consistent with the myriad of symptoms experienced by patients with triple A syndrome.
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