Cell Signaling Technology

Product Pathways - Apoptosis

Siva-1 Antibody #12532

No. Size Price
12532S 100 µl ( 10 western blots ) ¥3,250.00 现货查询 购买询价 防伪查询
12532 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human, Endogenous 19 Rabbit
IP 1:50

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation,

Specificity / Sensitivity

Siva-1 Antibody recognizes endogenous levels of total Siva-1 protein. This antibody does not cross-react with Siva-2. This antibody cross-reacts with a protein of unknown origin at ~70 kDa.

Siva-1 Antibody能够检测内源Siva-1总蛋白。该抗体不会与Siva-2产生交叉反应。该抗体与某未知来源~70 kDa蛋白产生交叉反应。

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro71 of human Siva-1 protein. Antibodies are purified by protein A and peptide affinity chromatography.

该多克隆抗体是由合成的人源Siva-1蛋白Pro71周围残基相应的肽段免疫动物而制备的。抗体由protein A和肽亲和层析技术纯化。

Western Blotting

Western Blotting

Immunoprecipitation of Siva-1 from MOLT-4 cell extracts using Normal Rabbit IgG #2729 (lane 2) or Siva-1 Antibody (lane 3). Lane 1 is 10% input. Western blot analysis was performed using Siva-1 Antibody.

免疫沉淀方法检测MOLT-4细胞提取物中Siva-1,使用抗体为Normal Rabbit IgG #2729 (泳道2)或Siva-1 Antibody (泳道3)。泳道1为10%对照。使用Siva-1 Antibody 进行Western blot分析。

Western Blotting

Western Blotting

Western blot analysis of extracts from MOLT-4, HBP-ALL, and CCRF-CEM cells using Siva-1 Antibody.

Western blot检测MOLT-4、HBP-ALL和CCRF-CEM 细胞系提取物,使用抗体为 Siva-1 Antibody。

Western Blotting

Western Blotting

Western blot analysis of extracts from 293T cells, mock transfected (-), transfected with a construct expressing Myc/DDK-tagged full-length human Siva-1 (hSiva-1-Myc/DDK; +), or transfected with a construct expressing Myc/DDK-tagged full-length human Siva-2 (hSiva-2-Myc/DDK; +), using Siva-1 Antibody or Myc-Tag (71D10) Rabbit mAb #2278.

Western blot方法检测293T细胞提取物:空质粒转染(-)或带Myc/DDK-标签全长人Siva-1 (hSiva-1-Myc/DDK; +)或Myc/DDK-标签全长人Siva-2 (hSiva-2-Myc/DDK; +)载体转染;使用抗体为Siva-1 Antibody或Myc-Tag (71D10) Rabbit mAb 兔单抗#2278。


First identified as a pro-apoptotic protein that binds the cytoplasmic tail of the TNF receptor superfamily member CD27 (1), Siva-1 also binds several other TNFR family members including glucocorticoid-induced tumor necrosis factor receptor (GITR) and OX40 (1-3), as well as anti-apoptotic Bcl-2 family members Bcl-xL and Bcl-2 (4,5). Siva-1 is composed of a central death domain homology region, a C-terminal box-B-like ring finger followed by a zinc finger-like domain, and a unique N-terminal amphipathic helical region (SAH) (1,4). Studies have demonstrated that Siva-1 has the ability to induce cell death via both the extrinsic and intrinsic apoptotic pathways (1-8). The SAH domain of Siva-1 is responsible for the inhibition of the pro-survival activities of Bcl-xL and Bcl-2, leading to caspase-mediated cell death (4,5,8). Siva-1 plays a role in T cell signaling and homeostasis by inhibiting NF-κB activity, also resulting in apoptotic cell death (7,9). An alternative splice variant of Siva-1, Siva-2, lacks part of the SAH and death domains and is less effective at inducing apoptosis (1,2,5,8). Studies in xenografts have shown that down-regulation of Siva-1 inhibits tumorigenesis in response to p53 activation (10). Down-regulation of Siva-1 may also play a role in tumor metastasis through its regulation of the epithelial-mesenchymal transition (EMT) and cell migration (11). Overexpression of Siva-1 is implicated in several pathological conditions including acute ischemic injury (12) and Coxsackievirus infection (13).

Siva-1首次被鉴定是作为一个促凋亡蛋白,结合肿瘤坏死因子受体超家族成员CD27胞质尾(1),Siva-1还可以结合其他一些TNFR家族成员,包括糖皮质激素诱导的肿瘤坏死因子受体(GITR)和OX40(1-3),以及抗凋亡BCL- 2家族成员Bcl-xL和Bcl-2(4,5)。Siva-1是由一个中央死亡结构域同源域、一个连接锌指样结构域的C-末端的盒B样环指和一个独特的N-末端的两亲性螺旋区(SAH)组成(1,4)。有研究表明,Siva-1具有同时通过外在和内在的凋亡途径诱导细胞死亡的能力(1-8)。Siva-1的SAH域抑制了Bcl-xL和Bcl-2的促生存活性,导致半胱天冬酶介导的细胞死亡(4,5,8)。Siva-1通过抑制NF-κB活性在T细胞信号通路和内环境稳定中发挥重要作用,也会导致凋亡性细胞死亡(7,9)。Siva-1和Siva-2的选择性剪接变异,缺乏SAH和死亡域,在诱导细胞凋亡方面是事倍功半(1,2,5,8)。异种移植的研究表明,在应答p53激活时下调Siva-1抑制肿瘤发生(10)。下调Siva-1也可能通过调控上皮-间质转化(EMT)和细胞迁移而在肿瘤转移中发挥作用(11)。Siva-1过表达与一些病理情况相关,包括急性缺血性脑损伤(12)和柯萨奇病毒感染(13)。

  1. Prasad, K.V. et al. (1997) Proc Natl Acad Sci U S A 94, 6346-51.
  2. Yoon, Y. et al. (1999) Oncogene 18, 7174-9.
  3. Spinicelli, S. et al. (2002) Cell Death Differ 9, 1382-4.
  4. Xue, L. et al. (2002) Proc Natl Acad Sci U S A 99, 6925-30.
  5. Chu, F. et al. (2004) Apoptosis 9, 83-95.
  6. Cao, C. et al. (2001) J Biol Chem 276, 11465-8.
  7. Gudi, R. et al. (2006) Oncogene 25, 3458-62.
  8. Py, B. et al. (2004) J Immunol 172, 4008-17.
  9. Hench, V.K. and Su, L. (2011) BMC Immunol 12, 54.
  10. Du, W. et al. (2009) Cell Death Differ 16, 1493-504.
  11. Li, N. et al. (2011) Proc Natl Acad Sci U S A 108, 12851-6.
  12. Padanilam, B.J. et al. (1998) Kidney Int 54, 1967-75.
  13. Henke, A. et al. (2000) J Virol 74, 4284-90.

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