| 產(chǎn)品編號(hào) | bs-3025R-BF594 |
| 英文名稱1 | Rabbit Anti-phospho-AMPK alpha-1 (Ser496+Ser502)/BF594 Conjugated antibody |
| 中文名稱 | BF594標(biāo)記的磷酸化腺苷單磷酸活化蛋白激酶α1抗體 |
| 別 名 | AMPK alpha 2 (S496 + S502); AMPK alpha 1 (phospho S496 + S502); 5 AMP activated protein kinase alpha 1catalytic subunit; 5 AMP activated protein kinase catalytic alpha 1 chain; 5' AMP activated protein kinase catalytic subunit alpha 1; AAPK1;acetyl CoA carboxylase kinase;AI194361 antibody AI450832 ;AL024255 ;AMP -activate kinase alpha 1 subunit;AMP-activated protein kinase, catalytic, alpha -1;AMPK 1;AMPK alpha 1 chain;AMPK antibody AMPK1; AMPKa1;AMPKalpha1;C130083N04Rik;cb116 antibody EC 2.7.11.1; HMG CoA reductase kinase;hormone sensitive lipase kinase;im:7154392 antibody kinase AMPK alpha1 ;MGC33776;MGC57364 antibody PRKAA 1;PRKAA1;Protein kinase AMP activated alpha 1 catalytic subunit; SNF1-like protein AMPK;wu:fa94c10. |
| 規(guī)格價(jià)格 | 100ul/2980元 購(gòu)買(mǎi) 大包裝/詢價(jià) |
| 說(shuō) 明 書(shū) | 100ul |
| 產(chǎn)品類型 | 磷酸化抗體 |
| 研究領(lǐng)域 | 腫瘤 心血管 細(xì)胞生物 神經(jīng)生物學(xué) 信號(hào)轉(zhuǎn)導(dǎo) 細(xì)胞凋亡 激酶和磷酸酶 Alzheimer's |
| 抗體來(lái)源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應(yīng) | Mouse, Rat, |
| 產(chǎn)品應(yīng)用 | IF=1:50-200
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 64kDa |
| 性 狀 | Lyophilized or Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated Synthesised phosphopeptide derived from mouse AMPK alpha-1 around the phosphorylation site of Ser485/491 |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 儲(chǔ) 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| 保存條件 | 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. |
| 產(chǎn)品介紹 |
background: The protein encoded by this gene belongs to the ser/thr protein kinase family. It is the catalytic subunit of the 5'-prime-AMP-activated protein kinase (AMPK). AMPK is a cellular energy sensor conserved in all eukaryotic cells. The kinase activity of AMPK is activated by the stimuli that increase the cellular AMP/ATP ratio. AMPK regulates the activities of a number of key metabolic enzymes through phosphorylation. It protects cells from stresses that cause ATP depletion by switching off ATP-consuming biosynthetic pathways. Alternatively spliced transcript variants encoding distinct isoforms have been observed. [provided by RefSeq]. Function: Catalytic subunit of AMP-activated protein kinase (AMPK), an energy sensor protein kinase that plays a key role in regulating cellular energy metabolism. In response to reduction of intracellular ATP levels, AMPK activates energy-producing pathways and inhibits energy-consuming processes: inhibits protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation. AMPK acts via direct phosphorylation of metabolic enzymes, and by longer-term effects via phosphorylation of transcription regulators. Also acts as a regulator of cellular polarity by remodeling the actin cytoskeleton; probably by indirectly activating myosin. Regulates lipid synthesis by phosphorylating and inactivating lipid metabolic enzymes such as ACACA, ACACB, GYS1, HMGCR and LIPE; regulates fatty acid and cholesterol synthesis by phosphorylating acetyl-CoA carboxylase (ACACA and ACACB) and hormone-sensitive lipase (LIPE) enzymes, respectively. Regulates insulin-signaling and glycolysis by phosphorylating IRS1, PFKFB2 and PFKFB3. AMPK stimulates glucose uptake in muscle by increasing the translocation of the glucose transporter SLC2A4/GLUT4 to the plasma membrane, possibly by mediating phosphorylation of TBC1D4/AS160. Regulates transcription and chromatin structure by phosphorylating transcription regulators involved in energy metabolism such as CRTC2/TORC2, FOXO3, histone H2B, HDAC5, MEF2C, MLXIPL/ChREBP, EP300, HNF4A, p53/TP53, SREBF1, SREBF2 and PPARGC1A. Acts as a key regulator of glucose homeostasis in liver by phosphorylating CRTC2/TORC2, leading to CRTC2/TORC2 sequestration in the cytoplasm. In response to stress, phosphorylates 'Ser-36' of histone H2B (H2BS36ph), leading to promote transcription. Acts as a key regulator of cell growth and proliferation by phosphorylating TSC2, RPTOR and ATG1: in response to nutrient limitation, negatively regulates the mTORC1 complex by phosphorylating RPTOR component of the mTORC1 complex and by phosphorylating and activating TSC2. In response to nutrient limitation, promotes autophagy by phosphorylating and activating ULK1. AMPK also acts as a regulator of circadian rhythm by mediating phosphorylation of CRY1, leading to destabilize it. May regulate the Wnt signaling pathway by phosphorylating CTNNB1, leading to stabilize it. Also has tau-protein kinase activity: in response to amyloid beta A4 protein (APP) exposure, activated by CAMKK2, leading to phosphorylation of MAPT/TAU; however the relevance of such data remains unclear in vivo. Also phosphorylates CFTR, EEF2K, KLC1, NOS3 and SLC12A1. Subunit: AMPK is a heterotrimer of an alpha catalytic subunit (PRKAA1 or PRKAA2), a beta (PRKAB1 or PRKAB2) and a gamma non-catalytic subunits (PRKAG1, PRKAG2 or PRKAG3). Interacts with FNIP1 and FNIP2. Subcellular Location: Cytoplasm. Nucleus. Translocates to the nucleus during heat shock and resides in sub-nuclear structures known as SC35 speckles or nuclear splicing speckles. Tissue Specificity: Lens as well as other tissues. Post-translational modifications: Ubiquitinated. Phosphorylated at Thr-183 by STK11/LKB1 in complex with STE20-related adapter-alpha (STRADA) pseudo kinase and CAB39. Also phosphorylated at Thr-183 by CAMKK2; triggered by a rise in intracellular calcium ions, without detectable changes in the AMP/ATP ratio. CAMKK1 can also phosphorylate Thr-183, but at much lower lvel. Dephosphorylated by protein phosphatase 2A and 2C (PP2A and PP2C). Phosphorylated by ULK1 and ULK2; leading to negatively regulate AMPK activity and suggesting the existence of a regulatory feedback loop between ULK1, ULK2 and AMPK. DISEASE: Defects in CRYAB are the cause of myofibrillar alpha-B crystallin-related (MFM-CRYAB) [MIM:608810]. A neuromuscular disorder that results in weakness of the proximal and distal limb muscles, weakness of the neck, velopharynx and trunk muscles, hypetrophic cardiomyopathy, and cataract in a subset of patients. Similarity: Belongs to the protein kinase superfamily. CAMK Ser/Thr protein kinase family. SNF1 subfamily. Contains 1 protein kinase domain. Database links: Entrez Gene: 5562 Human Entrez Gene: 105787 Mouse Omim: 602739 Human SwissProt: Q13131 Human SwissProt: Q5EG47 Mouse Unigene: 43322 Human Unigene: 207004 Mouse Unigene: 87789 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. AMPKα1 (AMP-activated Protein Kinase-α1)（腺苷單磷酸活化蛋白激酶-α1）是一種參與細(xì)胞適應(yīng)能量危機(jī)的應(yīng)激反應(yīng)酶,AMPK不僅可以在細(xì)胞水平作為能量的感受器，還可以通過(guò)激素和細(xì)胞因子，如瘦素、脂聯(lián)素和ghrelin來(lái)參與調(diào)節(jié)機(jī)體的能量消耗和能量攝入. |
