Cell Signaling Technology

Product Pathways - Chromatin Regulation / Epigenetics

SirT2 (D4S6J) Rabbit mAb #12672


No. Size Price
12672S 100 µl ( 10 western blots ) ¥3,250.00 现货查询 购买询价 防伪查询
12672 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse,Rat,Monkey, Endogenous 39, 43 Rabbit IgG

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting,

Specificity / Sensitivity

SirT2 (D4S6J) Rabbit mAb recognizes endogenous levels of total SirT2 protein. This antibody does not cross-react with other sirtuin proteins.

SirT2(D4S6J)Rabbit mAb 兔单抗能够检测内源性的SirT2总蛋白水平。该抗体不会与其他sirtuin蛋白发生交叉反应。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a recombinant protein specific to human SirT2 protein.


Western blot analysis of extracts from various cell lines using SirT2 (D4S6J) Rabbit mAb.Western blot方法检测多种细胞系的提取物,使用的抗体为SirT2 (D4S6J) Rabbit mAb。

Western Blotting

Western Blotting

Western blot analysis of extracts from SirT2 wild-type (WT) and knockout (KO) mouse brain using SirT2 (D4S6J) Rabbit mAb (upper) or GAPDH (D16H11) XP® Rabbit mAb #5174 (lower). SirT2 WT and KO mouse brain extracts were kindly provided by Dr. Gizem Donmez, Tufts University School of Medicine.Western blot方法检测多种细胞系的提取物,使用的抗体为SirT2 (D4S6J) Rabbit mAb。


The Silent Information Regulator (SIR2) family of genes is a highly conserved group of genes that encode nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylases, also known as Class III histone deacetylases. The first discovered and best characterized of these genes is Saccharomyces cerevisiae SIR2, which is involved in silencing of mating type loci, telomere maintenance, DNA damage response, and cell aging (1). SirT2, a mammalian homolog of Sir2, deacetylates α-tubulin at Lys40 and histone H4 at Lys16 and has been implicated in cytoskeletal regulation and progression through mitosis (2,3). SirT2 protein is mainly cytoplasmic and is associated with microtubules and HDAC6, another tubulin deacetylase (2). Deacetylation of α-tubulin decreases its stability and may be required for proper regulation of cell shape, intracellular transport, cell motility, and cell division (2,4). The abundance and phosphorylation state of SirT2 increase at the G2/M transition of the cell cycle, and SirT2 relocalizes to chromatin during mitosis when histone H4 Lys16 acetylation levels decrease (3,5). Overexpression of SirT2 prolongs mitosis, while overexpression of the CDC14B phosphatase results in both decreased phosphorylation and abundance of SirT2, allowing for proper mitotic exit (5). Thus, the deacetylation of both histone H4 and α-tubulin by SirT2 may be critical for proper chromatin and cytoskeletal dynamics required for completion of mitosis.

沉默信息调节因子(SIR2)基因家族是一类高度保守的基因,能够编码烟酰胺腺嘌呤二核苷酸(NAD)依赖性的去乙酰化酶,亦称III类组蛋白去乙酰化酶。在这些基因中,酿酒酵母Sir2是最早被发现,并且了解得最清楚的。Sir2 参与了交配型基因座的沉默,端粒维持,DNA损伤应答和细胞衰老(1)。SirT2,是哺乳动物中Sir2的同源基因,能够将 α-微管蛋白 Lys40位点和组蛋白H4 Lys16位点去乙酰化,在细胞骨架调控和有丝分裂进程中都会涉及(2,3)。SirT2蛋白质主要存在于细胞质中,和微管、HDAC6以及其他微管蛋白去乙酰化酶关联在一起(2)。α-微管蛋白去乙酰化后会降低其自身的稳定性,可能这正是细胞形态、胞内运输、细胞运动和细胞分裂的正确调控所需要的。在细胞周期 G2/M 转换时,SirT2的丰度和磷酸化状态都会提高,而且在有丝分裂期间当组蛋白 H4 Lys16位点的乙酰化水平降低时SirT2会重新定位到染色体上(3,5)。SirT2 过表达后会延长有丝分裂,而CDC14B磷酸酶的过表达会导致SirT2的丰度和磷酸化水平降低,从而允许正确退出有丝分裂(5)。因此,SirT2对组蛋白H4和α-微管蛋白的去乙酰化作用对于完整有丝分裂所需的正确染色体和细胞骨架动力学是至关重要的。

  1. Guarente, L. (1999) Nat. Genet. 23, 281-285.
  2. North, B.J. et al. (2003) Mol. Cell 11, 437-444.
  3. Vaquero, A. et al. (2006) Genes Dev. 20, 1256-1261.
  4. Nogales, E. (2000) Annu. Rev. Biochem. 69, 277-302.
  5. Dryden, S.C. et al. (2003) Mol. Cell Biol. 23, 3173-3185.

Application References

Have you published research involving the use of our products? If so we'd love to hear about it. Please let us know!


Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.

Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.

用户评论 --- 共 0


我要参与评论 :