万千商家帮你免费找货
0 人在求购买到急需产品
- 详细信息
- 文献和实验
- 技术资料
- 适应物种:
Human,
- 应用范围:
IHC-P,
- 抗体英文名:
Phospho-Bad (Ser134)
- 规格:
100ul
英文名称Phospho-Bad (Ser134)中文名称磷酸化相关死亡促进因子抗体别 名Bad (phospho S134); Bad (phospho Ser134); p-Bad (S134);p- Bad (Ser134); p-Bad (phospho Ser134); BBC 2; BBC2; BBC6; Bcl 2 Antagonist of Cell Death; Bcl 2 Binding Component 6; BCL X / BCL 2 Binding Protein; BCL X Binding Protein; Bcl XL/Bcl 2 Associated Death Promoter; Bcl-2-like protein 8; Bcl2 antagonist of cell death; BCL2 antagonist of cell death protein; BCL2 associated agonist of cell death; Bcl2 Associated Death Promoter; BCL2 binding component 6; BCL2 binding protein; Bcl2 Like 8 Protein; Bcl2-L-8; BCL2L8; BclXL; Proapoptotic BH3 Only Protein; BAD_HUMAN; Bcl-2-binding component 6. 产品类型磷酸化抗体 研究领域细胞生物 免疫学 神经生物学 信号转导 细胞凋亡 新陈代谢 线粒体 抗体来源Rabbit克隆类型Polyclonal交叉反应Human, 产品应用ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=3ug/Test ICC=1:100-500 IF=1:100-500 (石蜡切片需做抗原修复)
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.分 子 量18kDa细胞定位细胞浆 线粒体性 状Liquid浓 度1mg/ml免 疫 原KLH conjugated Synthesised phosphopeptide derived from human BAD around the phosphorylation site of Ser134:PK(p-S)AG 亚 型IgG纯化方法affinity purified by Protein A储 存 液0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.保存条件Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.PubMedPubMed产品介绍Bad is a member of the Bcl2 family and acts to promote apoptosis by forming heterodimers with the survival proteins Bcl2 and BclxL, thus preventing them from binding with BAX. Bad is found on the outer mitochondrial membrane and, once phosphorylated in response to growth stimuli, translocates to the cytoplasm. The phosphorylation status of Bad represents a key checkpoint for death or cell survival. JNK-induced phosphorylation of BAD serine 128 promotes the apoptotic role of Bad by opposing the inhibitory effect of growth factor on Bad-mediated apoptosis. Cdc2-induced phosphorylation of Bad serine 128 has an inhibitory effect on its interaction with 14-3-3 proteins. The latter interaction is critical for Bad phosphorylation at serine 155, a site within the BH3 domain that leads to the release of BclxL and the promotion of cell survival. Alternative splicing of this gene results in two transcript variants which encode the same isoform.
Function:
Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways.
Subunit:
Forms heterodimers with the anti-apoptotic proteins, Bcl-X(L), Bcl-2 and Bcl-W. Also binds protein S100A10. The Ser-75/Ser-99 phosphorylated form binds 14-3-3 proteins. Interacts with AKT1 and PIM3.
Subcellular Location:
Mitochondrion outer membrane. Cytoplasm. Upon phosphorylation, locates to the cytoplasm.
Tissue Specificity:
Expressed in a wide variety of tissues.
Post-translational modifications:
Phosphorylated on one or more of Ser-75, Ser-99, Ser-118 andSer-134 in response to survival stimuli, which blocks itspro-apoptotic activity. Phosphorylation on Ser-99 or Ser-75promotes heterodimerization with 14-3-3 proteins. This interactionthen facilitates the phosphorylation at Ser-118, a site within theBH3 motif, leading to the release of Bcl-X(L) and the promotion ofcell survival. Ser-99 is the major site of AKT/PKB phosphorylation, Ser-118 the major site of protein kinase A (CAPK) phosphorylation. Phosphorylation at Ser-99 by PKB/AKT1 is almost completely blockedby the apoptotic C-terminus cleavage product of PKN2 generated bycaspases-3 activity during apoptosis.
Methylation at Arg-94 and Arg-96 by PRMT1 inhibits Akt-mediated phosphorylation at Ser-99.
Similarity:
Belongs to the Bcl-2 family.
SWISS:
Q92934
Gene ID:
572
Database links:
Entrez Gene: 572 Human
Entrez Gene: 12015 Mouse
Omim: 603167 Human
SwissProt: Q92934 Human
SwissProt: Q61337 Mouse
Unigene: 370254 Human
Unigene: 4387 Mouse
Unigene: 36696 Rat
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
BAD是BCL2/BAX,BCL-XL/BAX异二聚体的负调节基因。BAD是BCL2/BCL-XL相关死亡促进因子,作为BCL2, bCL-XL异二聚体伴分子而促进细胞凋亡。
风险提示:丁香通仅作为第三方平台,为商家信息发布提供平台空间。用户咨询产品时请注意保护个人信息及财产安全,合理判断,谨慎选购商品,商家和用户对交易行为负责。对于医疗器械类产品,请先查证核实企业经营资质和医疗器械产品注册证情况。
文献和实验就在有丝分裂、细胞死亡、DNA 损伤修复、DNA 复制和重组过程中发挥着直接的作用。 组蛋白翻译后修饰多发生在组蛋白的 N-端尾部,包括甲基化、乙酰化、磷酸化、ADP-核糖基化、泛素化和小分子泛素化修饰,这些修饰有助于其他蛋白质与 DNA 的结合,从而产生协同或者拮抗作用来调控基因转录。例如,乙酰化使组蛋白尾部正电荷减少,从而削弱了与带负电荷 DNA 骨架的作用,而促进染色质呈开放状态, 甲基化激活或抑制基因功能主要依赖于修饰的位点,主要与赖氨酸残基的单甲基化、双甲基化或三甲基化有关。 组蛋白修饰最基本
-κB 下游的细胞因子和驱化因子。 进一步,研究者通过免疫印迹和免疫组化分析证实,肝细胞 Miz1 的缺失促进 IKK 介导的 MTDH 的磷酸化,从而促进了 NF-κB 的激活和 NF-κB 下游炎症相关靶基因的表达。 (3)肿瘤特有肝细胞分泌细胞因子促进肿瘤浸润巨噬细胞向促炎表型转化 对巨噬细胞亚群和肝脏特有巨噬细胞(Kupffer cell)进一步细分,并进行差异基因分析和 Qusage 分析,发现 Miz1∆hep 小鼠的肿瘤浸润巨噬细胞和 Kupffer 细胞的一些亚群 NF-κB 强烈
果糖才是肥胖的真凶?Nature 最新文章揭示高果糖饮食如何
研究背景随着现代农业和工业的发展,甜味剂的获取变得十分容易,如高果糖玉米糖浆(HFCS)。然而,这些甜味剂使得果糖的总消费量增加了两倍,并导致肥胖和相关疾病的迅速流行。全球肥胖率的提升与相关癌症的增加直接相关,例如结直肠癌(CRC),其在年轻人中的发病率和死亡率也在不断上升。一些观察结果表明,果糖摄入量与结直肠癌的发病存在因果关系。例如,果糖消耗与胃肠道癌症的发生和进展有关,并在结直肠癌小鼠模型中发现其能够驱动肿瘤生长和转移。由于肿瘤生长是由「细胞增生」驱动的,并且肿瘤细胞往往保留来自其起源
技术资料暂无技术资料 索取技术资料






