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- 详细信息
- 文献和实验
- 技术资料
- 免疫原:
sirtuin (silent mating type information regulation 2 homolog) 7 (S. cerevisiae)
- 亚型:
IgG
- 形态:
liquid
- 保存条件:
负20摄氏度
- 克隆性:
Polyclonal antibody
- 标记物:
Non-conjugated
- 适应物种:
Human,Mouse ,Rat
- 保质期:
6个月
- 抗原来源:
Rabbit
- 目录编号:
P67936
- 级别:
纯化级别
- 库存:
50
- 供应商:
LSM bio
- 宿主:
E. coli - derived recombinant protein
- 应用范围:
ELISA,WB,IP
- 浓度:
≥95% as determined by SDS-PAGE
- 靶点:
sirtuin (silent mating type information regulation 2 homolog) 7 (S. cerevisiae)
- 抗体英文名:
anti-SIRT7 antibody,SIRT7 antibody
- 抗体名:
anti-SIRT7 抗体,SIRT7 抗体
- 规格:
100μg
SIRT7抗体| SIRT7 antibody
货号 PAab07885
蛋白别名 SIR2 like protein 7 antibody, SIR2L7 antibody, SIRT7
蛋白介绍
NAD-dependent protein deacetylase that specifically mediates deacetylation of histone H3 at 'Lys-18' (H3K18Ac). In contrast to other histone deacetylases, displays selectivity for a single histone mark, H3K18Ac, directly linked to control of gene expression. H3K18Ac is mainly present around the transcription start site of genes and has been linked to activation of nuclear hormone receptors. SIRT7 thereby acts as a transcription repressor. Moreover, H3K18 hypoacetylation has been reported as a marker of malignancy in various cancers and seems to maintain the transformed phenotype of cancer cells. These data suggest that SIRT7 may play a key role in oncogenic transformation by suppresses expression of tumor suppressor genes by locus-specific deacetylation of H3K18Ac at promoter regions. Also required to restore the transcription of ribosomal RNA (rRNA) at the exit from mitosis: promotes the association of RNA polymerase I with the rDNA promoter region and coding region. Stimulates transcription activity of the RNA polymerase I complex. May also deacetylate p53/TP53 and promotes cell survival, however such data need additional confirmation.
产品描述
anti-SIRT7 antibody is a Rabbit Polyclonal antibody againstSIRT7..
建议稀释比例
WB : 1:200-1:2000 IP : 1:200-1:1000
IHC
Western blot
mouse liver tissue were subjected to SDS PAGE followed by western blot with PAab07885(SIRT7 antibody) at dilution of 1:300(本抗体仅供体外科研用途,不可用于临床诊断!) "">
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文献和实验粒细胞的扩增,可引发小叶乳腺癌 GEM 模型的自发性转移形成,导致 GEM 移植模型的自发转移疾病。GEM 模型在揭示相关基因参与抑制肿瘤转移机制方面也发挥了重要作用。最近,刘宝华课题组应用 Tet-ON 可诱导 Sirt7 表达的 GEM 模型,揭示了 Sirt7 抑制原发胰腺癌转移作用机制,该研究结果证实,由 Dox 诱导表达的 Sirt7 具有明显抑制 MMTV-PyMT 小鼠乳腺肿瘤肺转移的作用,且其作用机制是通过调节 TGF-β信号通路实现的。因此,GEM 模型在揭示肿瘤转移复杂性,挑战当下普遍
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