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。
NPM1 Antibody
Purified Mouse Monoclonal Antibody (Mab)
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Application 
| WB |
|---|---|
| Primary Accession | P06748 |
| Reactivity | Human, Mouse |
| Host | Mouse |
| Clonality | Monoclonal |
| Isotype | IgG1 |
| Calculated MW | 38 KDa |
| Gene ID | 4869 |
|---|---|
| Other Names | B23;MGC104254;NMP1;NO38;NPM 1;NPM;NPM_HUMAN;NPM1;Nucleolar Phosphoprotein B23;Nucleolar protein NO38;Nucleophosmin (nucleolar phosphoprotein B23 numatrin);Nucleophosmin; Nucleophosmin/B23.2;Nucleophosmin/nucleoplasmin family member 1;Nucleoplasmin Family Member 1;Numatrin;OTTHUMP00000161024;OTTHUMP00000161025;OTTHUMP00000223397; OTTHUMP00000223398;TRK fused gene. |
| Dilution | WB~~1:1000 |
| Format | Purified mouse monoclonal in buffer containing 0.1M Tris-Glycine (pH 7.4, 150 mM NaCl) with 0.02% sodium azide, 50%,glycerol |
| Storage | Store at -20 °C.Stable for 12 months from date of receipt |
| Name | NPM1 |
|---|---|
| Synonyms | NPM |
| Function | Involved in diverse cellular processes such as ribosome biogenesis, centrosome duplication, protein chaperoning, histone assembly, cell proliferation, and regulation of tumor suppressors p53/TP53 and ARF. Binds ribosome presumably to drive ribosome nuclear export. Associated with nucleolar ribonucleoprotein structures and bind single-stranded nucleic acids. Acts as a chaperonin for the core histones H3, H2B and H4. Stimulates APEX1 endonuclease activity on apurinic/apyrimidinic (AP) double- stranded DNA but inhibits APEX1 endonuclease activity on AP single-stranded RNA. May exert a control of APEX1 endonuclease activity within nucleoli devoted to repair AP on rDNA and the removal of oxidized rRNA molecules. In concert with BRCA2, regulates centrosome duplication. Regulates centriole duplication: phosphorylation by PLK2 is able to trigger centriole replication. Negatively regulates the activation of EIF2AK2/PKR and suppresses apoptosis through inhibition of EIF2AK2/PKR autophosphorylation. Antagonizes the inhibitory effect of ATF5 on cell proliferation and relieves ATF5-induced G2/M blockade (PubMed:22528486). In complex with MYC enhances the transcription of MYC target genes (PubMed:25956029). |
| Cellular Location | Nucleus, nucleolus Nucleus, nucleoplasm. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Note=Generally nucleolar, but is translocated to the nucleoplasm in case of serum starvation or treatment with anticancer drugs. Has been found in the cytoplasm in patients with primary acute myelogenous leukemia (AML), but not with secondary AML. Can shuttle between cytoplasm and nucleus Co- localizes with the methylated form of RPS10 in the granular component (GC) region of the nucleolus. Colocalized with nucleolin and APEX1 in nucleoli. Isoform 1 of NEK2 is required for its localization to the centrosome during mitosis |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Involved in diverse cellular processes such as ribosome biogenesis, centrosome duplication, protein chaperoning, histone assembly, cell proliferation, and regulation of tumor suppressors p53/TP53 and ARF. Binds ribosome presumably to drive ribosome nuclear export. Associated with nucleolar ribonucleoprotein structures and bind single-stranded nucleic acids. Acts as a chaperonin for the core histones H3, H2B and H4. Stimulates APEX1 endonuclease activity on apurinic/apyrimidinic (AP) double- stranded DNA but inhibits APEX1 endonuclease activity on AP single-stranded RNA. May exert a control of APEX1 endonuclease activity within nucleoli devoted to repair AP on rDNA and the removal of oxidized rRNA molecules. In concert with BRCA2, regulates centrosome duplication. Regulates centriole duplication: phosphorylation by PLK2 is able to trigger centriole replication. Negatively regulates the activation of EIF2AK2/PKR and suppresses apoptosis through inhibition of EIF2AK2/PKR autophosphorylation.
REFERENCES
Chan W.-Y.,et al.Biochemistry 28:1033-1039(1989).
Li X.,et al.Biochem. Biophys. Res. Commun. 163:72-78(1989).
Zhang X.T.,et al.Biochem. Biophys. Res. Commun. 164:176-184(1989).
Chan P.-K.,et al.Nucleic Acids Res. 25:1225-1232(1997).
Okuwaki M.,et al.Submitted (APR-2000) to the EMBL/GenBank/DDBJ databases.
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