| 產(chǎn)品編號(hào) | bs-16354R-BF488 |
| 英文名稱 | Rabbit Anti-GTF2IRD1/BF488 Conjugated antibody |
| 中文名稱 | BF488標(biāo)記的通用轉(zhuǎn)錄因子III/WBSCR11抗體 |
| 別 名 | CREAM1; General transcription factor II I repeat domain containing protein 1; General transcription factor II-I repeat domain-containing protein 1; General transcription factor III; GT2D1_HUMAN; GTF2I repeat domain containing protein 1; GTF2I repeat domain-containing protein 1; GTF2IRD1; GTF3; Muscle TFII I repeat domain-containing protein 1; Muscle TFII-I repeat domain-containing protein 1; MUSTRD1; MusTRD1/BEN; RBAP2; Slow muscle fiber enhancer binding protein; Slow-muscle-fiber enhancer-binding protein; USE B1 binding protein; USE B1-binding protein; WBSCR11; WBSCR12; Williams Beuren syndrome chromosome region 11 protein; Williams-Beuren syndrome chromosomal region 11 protein; Williams-Beuren syndrome chromosomal region 12 protein. |
| 規(guī)格價(jià)格 | 100ul/2980元 購買 大包裝/詢價(jià) |
| 說 明 書 | 100ul |
| 研究領(lǐng)域 | 細(xì)胞生物 轉(zhuǎn)錄調(diào)節(jié)因子 表觀遺傳學(xué) |
| 抗體來源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應(yīng) | (predicted: Human, Mouse, Rat, Dog, Pig, Cow, Horse, Sheep, ) |
| 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 | 106kDa |
| 性 狀 | Lyophilized or Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human GTF2IRD1 |
| 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: The protein encoded by this gene contains five GTF2I-like repeats and each repeat possesses a potential helix-loop-helix (HLH) motif. It may have the ability to interact with other HLH-proteins and function as a transcription factor or as a positive transcriptional regulator under the control of Retinoblastoma protein. This gene plays a role in craniofacial and cognitive development and mutations have been associated with Williams-Beuren syndrome, a multisystem developmental disorder caused by deletion of multiple genes at 7q11.23. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Nov 2010] Function: May be a transcription regulator involved in cell-cycle progression and skeletal muscle differentiation. May repress GTF2I transcriptional functions, by preventing its nuclear residency, or by inhibiting its transcriptional activation. May contribute to slow-twitch fiber type specificity during myogenesis and in regenerating muscles. Binds troponin I slow-muscle fiber enhancer (USE B1). Binds specifically and with high affinity to the EFG sequences derived from the early enhancer of HOXC8. Subcellular Location: Nucleus. Tissue Specificity: Highly expressed in adult skeletal muscle, heart, fibroblast, bone and fetal tissues. Expressed at lower levels in all other tissues tested. DISEASE: Note=GTF2IRD1 is located in the Williams-Beuren syndrome (WBS) critical region. WBS results from a hemizygous deletion of several genes on chromosome 7q11.23, thought to arise as a consequence of unequal crossing over between highly homologous low-copy repeat sequences flanking the deleted region. Haploinsufficiency of GTF2IRD1 may be the cause of certain cardiovascular and musculo-skeletal abnormalities observed in the disease. Similarity: Belongs to the TFII-I family. Contains 5 GTF2I-like repeats. Database links: Entrez Gene: 9569 Human Entrez Gene: 57080 Mouse Omim: 604318 Human SwissProt: Q9UHL9 Human SwissProt: Q9JI57 Mouse Unigene: 647056 Human Unigene: 332735 Mouse Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
