FITC标记的磷酸化糖原合酶激酶3β抗体
产品名称： FITC标记的磷酸化糖原合酶激酶3β抗体
英文名称： Anti-phospho-GSK-3 Beta(Thr390) /FITC
产品编号： HZ-3148R-FITC
产品价格： null
产品产地： 中国/上海
品牌商标： HZbscience
更新时间： 2023-08-17T10:24:20
使用范围： IF=1:50-200
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Rabbit Anti-phospho-GSK-3 Beta(Thr390) /FITC Conjugated antibody
FITC标记的磷酸化糖原合酶激酶3β抗体
| 英文名称 | Anti-phospho-GSK-3 Beta(Thr390) /FITC |
| 中文名称 | FITC标记的磷酸化糖原合酶激酶3β抗体 |
| 别 名 | GSK3B(Phospho-Thr390); GSK3B(Phospho-T390); p-GSK-3 Beta(Thr390); p-GSK-3 beta(T390); Glycogen synthase kinase 3 beta; GSK 3 beta; GSK 3B; GSK3B; GSK3B protein; GSK3beta isoform; GSK3 beta; Glycogen synthase kinase-3 beta; GSK-3 beta; GSK3B_HUMAN. |
| 规格价格 | 100ul/2980元 购买 大包装/询价 |
| 说 明 书 | 100ul |
| 产品类型 | 磷酸化抗体 |
| 研究领域 | 肿瘤 细胞生物 神经生物学 信号转导 细胞凋亡 激酶和磷酸酶 新陈代谢 |
| 抗体来源 | Rabbit |
| 克隆类型 | Polyclonal |
| 交叉反应 | Human, Rat, Chicken, Dog, Pig, Rabbit, Guinea Pig, |
| 产品应用 | IF=1:50-200 not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 47kDa |
| 细胞定位 | 细胞膜 |
| 性 状 | Lyophilized or Liquid |
| 浓 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated Synthesised phosphopeptide derived from human GSK-3 Beta around the phosphorylation site of Thr390 |
| 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 | 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. |
| 产品介绍 | background: The protein encoded by this gene is a serine-threonine kinase, belonging to the glycogen synthase kinase subfamily. It is involved in energy metabolism, neuronal cell development, and body pattern formation. Polymorphisms in this gene have been implicated in modifying risk of Parkinson disease, and studies in mice show that overexpression of this gene may be relevant to the pathogenesis of Alzheimer disease. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Sep 2009] Function: Constitutively active protein kinase that acts as a negative regulator in the hormonal control of glucose homeostasis, Wnt signaling and regulation of transcription factors and microtubules, by phosphorylating and inactivating glycogen synthase (GYS1 or GYS2), EIF2B, CTNNB1/beta-catenin, APC, AXIN1, JUN, NFATC1/NFATC, MAPT/TAU and MACF1. Requires primed phosphorylation of the majority of its substrates. In skeletal muscle, contributes to insulin regulation of glycogen synthesis by phosphorylating and inhibiting GYS1 activity and hence glycogen synthesis. May also mediate the development of insulin resistance by regulating activation of transcription factors. Regulates protein synthesis by controlling the activity of initiation factor 2B (EIF2BE/EIF2B5) in the same manner as glycogen synthase. In Wnt signaling, GSK3B forms a multimeric complex with APC, AXIN1 and CTNNB1/beta-catenin and phosphorylates the N-terminus of CTNNB1 leading to its degradation mediated by ubiquitin/proteasomes. Phosphorylates JUN at sites proximal to its DNA-binding domain, thereby reducing its affinity for DNA. Phosphorylates NFATC1/NFATC on conserved serine residues promoting NFATC1/NFATC nuclear export, shutting off NFATC1/NFATC gene regulation, and thereby opposing the action of calcineurin. Phosphorylates MAPT/TAU on 'Thr-548', decreasing significantly MAPT/TAU ability to bind and stabilize microtubules. MAPT/TAU is the principal component of neurofibrillary tangles in Alzheimer disease. Plays an important role in ERBB2-dependent stabilization of microtubules at the cell cortex. Phosphorylates MACF1, inhibiting its binding to microtubules which is critical for its role in bulge stem cell migration and skin wound repair. Probably regulates NF-kappa-B (NFKB1) at the transcriptional level and is required for the NF-kappa-B-mediated anti-apoptotic response to TNF-alpha (TNF/TNFA). Negatively regulates replication in pancreatic beta-cells, resulting in apoptosis, loss of beta-cells and diabetes. Phosphorylates MUC1 in breast cancer cells, decreasing the interaction of MUC1 with CTNNB1/beta-catenin. Is necessary for the establishment of neuronal polarity and axon outgrowth. Phosphorylates MARK2, leading to inhibit its activity. Phosphorylates SIK1 at 'Thr-182', leading to sustain its activity. Subunit: Monomer. Interacts with ARRB2 and DISC1. Interacts with CABYR, MMP2, MUC1, NIN and PRUNE Interacts with AXIN1; the interaction mediates hyperphosphorylation of CTNNB1 leading to its ubiquitination and destruction. Interacts with and phosphorylates SNAI1. Interacts with DNM1L (via a C-terminal domain). Found in a complex composed of MACF1, APC, AXIN1, CTNNB1 and GSK3B. Subcellular Location: Cytoplasm. Nucleus. Cell membrane. The phosphorylated form shows localization to cytoplasm and cell membrane. The MEMO1-RHOA-DIAPH1 signaling pathway controls localization of the phosophorylated form to the cell membrane. Tissue Specificity: Expressed in testis, thymus, prostate and ovary and weakly expressed in lung, brain and kidney. Post-translational modifications: Phosphorylated by AKT1 and ILK1. Upon insulin-mediated signaling, the activated PKB/AKT1 protein kinase phosphorylates and desactivates GSK3B, resulting in the dephosphorylation and activation of GYS1. Activated by phosphorylation at Tyr-216. Similarity: Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. GSK-3 subfamily. Contains 1 protein kinase domain. Database links: Entrez Gene: 2932 Human Entrez Gene: 56637 Mouse Entrez Gene: 84027 Rat Omim: 605004 Human SwissProt: P49841 Human SwissProt: Q9WV60 Mouse SwissProt: P18266 Rat Unigene: 445733 Human Unigene: 394930 Mouse Unigene: 10426 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications |
该基因编码的蛋白是丝氨酸苏氨酸激酶，属于糖原合成酶激酶亚家族。它涉及能量代谢、神经元细胞发育和身体形态形成。该基因的多态性与帕金森病的危险性有关，而小鼠的研究表明该基因的过度表达可能与阿尔茨海默病的发病机制有关。另一种编码不同的异构体的剪接转录变体已经被发现。（RefSeq，SEP 2009提供）