| 產(chǎn)品編號(hào) | bs-9439R-FITC |
| 英文名稱(chēng) | Rabbit Anti-FOXO1A/FITC Conjugated antibody |
| 中文名稱(chēng) | FITC標(biāo)記的叉頭蛋白O1抗體 |
| 別 名 | FKH1; FKHR; FKHR; FOXO1A; Forkhead (Drosophila) homolog 1 (rhabdomyosarcoma); Forkhead (Drosophila) homolog 1 (rhabdomyosarcoma); Forkhead box O1; Forkhead box protein O1; Forkhead box protein O1A. |
| 規(guī)格價(jià)格 | 100ul/2980元 購(gòu)買(mǎi) 大包裝/詢(xún)價(jià) |
| 說(shuō) 明 書(shū) | 100ul |
| 研究領(lǐng)域 | 細(xì)胞生物 免疫學(xué) 神經(jīng)生物學(xué) 信號(hào)轉(zhuǎn)導(dǎo) 表觀遺傳學(xué) |
| 抗體來(lái)源 | Rabbit |
| 克隆類(lèi)型 | Polyclonal |
| 交叉反應(yīng) | Human, (predicted: Mouse, Rat, Chicken, Dog, Pig, Cow, Horse, Rabbit, ) |
| 產(chǎn)品應(yīng)用 | ICC=1:50-200 IF=1:50-200
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 72kDa |
| 性 狀 | Lyophilized or Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human FKHR |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 儲(chǔ) 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| 保存條件 | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. 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. |
| 產(chǎn)品介紹 |
background: FKHR (for forkhead in rhabdomyosarcoma) and FKHRL1 are members of the forkhead family of transcription factors. Transcriptional activation of FKHR proteins is regulated by the serine/threonine kinase Akt1, which phosphorylates FKHRL1 and results in FKHRL1 associating with 14-3-3 proteins and being retained in the cytoplasm. Induction of apoptosis or withdrawal of growth factors stimulates dephosphorylation and nuclear translocation of FKHR proteins, leading to FKHR-induced gene-specific transcriptional activation. FKHR, also designated forkhead box protein O1A (FOXO1), is a ubiquitously expressed protein that shuttles between the cytoplasm and nucleus. Genetic mutations in FKHR genes, including the t(2;13) and t(1;3) translocations, are commonly found in alveolar rhabdomyosarcomas. These translocations result in the fusion of the amino terminus of Pax-3 or Pax-7, including the paired box and homeodomain DNA-binding domains, with the carboxy-terminus of FKHR, which contains a transcriptional activation domain. The Pax-3/FKHR fusion protein appears to function as an oncogenic transcription factor that enhances the activation of normal Pax-3 target genes。 Function: Transcription factor which acts as a regulator of cell responses to oxidative stress. In the presence of KIRT1, mediates down-regulation of cyclin D1 and up-regulation of CDKN1B levels which are required for cell transition from proliferative growth to quiescence. Triggers death of postmitotic neurons when phosphorylated by CDK1. Activates transcription of PMAIP1. Subunit: Interacts with LRPPRC. Interacts with SIRT1 and this interaction requires the presence of KRIT1. Interacts with NLK. Binds to CDK1 and 14-3-3 proteins. Subcellular Location: Cytoplasm. Nucleus. Note=Shuttles between cytoplasm and nucleus. Translocates to the nucleus upon oxidative stress induced phosphorylation at Ser-212 by STK4/MST1. Translocates to the nucleus upon phosphorylation of Thr-24, Ser-256 and Ser-322 by SGK1. Tissue Specificity: Ubiquitous. Post-translational modifications: Phosphorylated by AKT1; insulin-induced. Phosphorylated by NLK, which inhibits transcriptional activity and promotes nuclear export. IGF1 rapidly induces phosphorylation of Ser-256, Thr-24, and Ser-319. Phosphorylation of Ser-256 decreases DNA-binding activity and promotes the phosphorylation of Thr-24, and Ser-319, permitting phosphorylation of Ser-322 and Ser-325, probably by CK1, leading to nuclear exclusion and loss of function. Phosphorylation of Ser-329 is independent of IGF1 and leads to reduced function. Phosphorylated upon DNA damage, probably by ATM or ATR. Phosphorylation of Ser-249 by CDK1 disrupts 14-3-3 proteins binding and thereby promotes FOXO1 nuclear accumulation and subsequent transcription activation and cell death. Phosphorylated by STK4/MST1 on Ser-212 upon oxidative stress. Phosphorylated on Thr-24, Ser-256 and Ser-322 by SGK1 resulting in its translocation from the nucleus to the cytoplasm. DISEASE: Defects in FOXO1 are a cause of rhabdomyosarcoma type 2 (RMS2) [MIM:268220]. It is a form of rhabdomyosarcoma, a highly malignant tumor of striated muscle derived from primitive mesenchimal cells and exhibiting differentiation along rhabdomyoblastic lines. Rhabdomyosarcoma is one of the most frequently occurring soft tissue sarcomas and the most common in children. It occurs in four forms: alveolar, pleomorphic, embryonal and botryoidal rhabdomyosarcomas. Note=Chromosomal aberrations involving FOXO1 are found in rhabdomyosarcoma. Translocation (2;13)(q35;q14) with PAX3; translocation t(1;13)(p36;q14) with PAX7. The resulting protein is a transcriptional activator. Similarity: Contains 1 fork-head DNA-binding domain. Database links: Entrez Gene: 2308 Human Entrez Gene: 56458 Mouse Omim: 136533 Human SwissProt: Q12778 Human SwissProt: Q9R1E0 Mouse Unigene: 370666 Human Unigene: 29891 Mouse Unigene: 116108 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
