| 產(chǎn)品編號(hào) | bs-3249R-Gold |
| 英文名稱(chēng)1 | Rabbit Anti-phospho-LKB1(Ser428)/Gold Conjugated antibody |
| 中文名稱(chēng) | 膠體金標(biāo)記的磷酸化絲氨酸/蘇氨酸蛋白激酶抗體 |
| 別 名 | STK11(phospho S428); LKB1 (phospho S428); p-LKB1 (phospho S428); LKB1(phospho Ser428); p-LKB1(phospho Ser428); p-LKB1(S428); LKB1; PJS; Renal carcinoma antigen NY-REN-19; Serine/Threonine Kinase 11; Serine/threonine protein kinase 11; Serine/threonine protein kinase LKB1; Serine/threonine-protein kinase 11; Serine/threonine-protein kinase LKB1; Stk11; STK11_HUMAN; hLKB1; Liver kinase B1; LKB 1; NY REN 19 antigen; Peutz Jeghers syndrome; PJS; Polarization related protein LKB1; Serine/threonine protein kinase STK11; Serine/threonine-protein kinase XEEK1; STK 11. |
| 規(guī)格價(jià)格 | 100ul/2980元 購(gòu)買(mǎi) 大包裝/詢(xún)價(jià) |
| 說(shuō) 明 書(shū) | 100ul（10nm 15nm 35nm） |
| 產(chǎn)品類(lèi)型 | 磷酸化抗體 |
| 研究領(lǐng)域 | 腫瘤 免疫學(xué) 神經(jīng)生物學(xué) 信號(hào)轉(zhuǎn)導(dǎo) 細(xì)胞凋亡 轉(zhuǎn)錄調(diào)節(jié)因子 |
| 抗體來(lái)源 | Rabbit |
| 克隆類(lèi)型 | Polyclonal |
| 交叉反應(yīng) | Mouse, Rat, (predicted: Human, Dog, Cow, Horse, ) |
| 產(chǎn)品應(yīng)用 | IEM=1:20-200 ICA=1:20-200 ChIP=1:20-200
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 48kDa |
| 性 狀 | Lyophilized or Liquid |
| 濃 度 | 0.4mg/ml |
| 免 疫 原 | KLH conjugated Synthesised phosphopeptide derived from human LKB1 around the phosphorylation site of Ser428 [RL(p-S)AC] |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 儲(chǔ) 存 液 | 0.02M TBS(pH8.2) with 1% BSA, 0.03% Proclin300. |
| 保存條件 | Store at 2-8 oC for 3-6 months. Avoid repeated freeze/thaw cycles. |
| 產(chǎn)品介紹 |
background: This gene, which encodes a member of the serine/threonine kinase family, regulates cell polarity and functions as a tumor suppressor. Mutations in this gene have been associated with Peutz-Jeghers syndrome, an autosomal dominant disorder characterized by the growth of polyps in the gastrointestinal tract, pigmented macules on the skin and mouth, and other neoplasms. Alternate transcriptional splice variants of this gene have been observed but have not been thoroughly characterized. [provided by RefSeq, Jul 2008]. Function: Tumor suppressor serine/threonine-protein kinase that controls the activity of AMP-activated protein kinase (AMPK) family members, thereby playing a role in various processes such as cell metabolism, cell polarity, apoptosis and DNA damage response. Acts by phosphorylating the T-loop of AMPK family proteins, leading to promote their activity: phosphorylates PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2, MARK3, MARK4, NUAK1, NUAK2, SIK1, SIK2, SIK3 and SNRK but not MELK. Also phosphorylates non-AMPK family proteins such as STRADA and possibly p53/TP53. Acts as a key upstream regulator of AMPK by mediating phosphorylation and activation of AMPK catalytic subunits PRKAA1 and PRKAA2: it thereby regulates inhibition of signaling pathways that promote cell growth and proliferation when energy levels are low, glucose homeostasis in liver, activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage. Also acts as a regulator of cellular polarity by remodeling the actin cytoskeleton. Required for cortical neurons polarization by mediating phosphorylation and activation of BRSK1 and BRSK2, leading to axon initiation and specification. Involved in DNA damage response: interacts with p53/TP53 and recruited to the CDKN1A/WAF1 promoter to participate to transcription activation. Able to phosphorylate p53/TP53; the relevance of such result in vivo is however unclear and phosphorylation may be indirect and mediated by downstream STK11/LKB1 kinase NUAK1 Also acts as a mediator p53/TP53-dependent apoptosis via interaction with p53/TP53: translocates to mitochondrion during apoptosis and regulates p53/TP53-dependent apoptosis pathways. Subunit: Catalytic component of a trimeric complex composed of STK11/LKB1, STRAD (STRADA or STRADB) and CAB39/MO25 (CAB39/MO25alpha or CAB39L/MO25beta): the complex tethers STK11/LKB1 in the cytoplasm and stimulates its catalytic activity. Found in a ternary complex composed of SMAD4, STK11/LKB1 and STK11IP. Interacts with p53/TP53, SMAD4, STK11IP and WDR6. Subcellular Location: Nucleus. Cytoplasm. Membrane. Mitochondrion. Note=A small fraction localizes at membranes. Relocates to the cytoplasm when bound to STRAD (STRADA or STRADB) and CAB39/MO25 (CAB39/MO25alpha or CAB39L/MO25beta). Translocates to mitochondrion during apoptosis. Tissue Specificity: Ubiquitously expressed. Strongest expression in testis and fetal liver. Post-translational modifications: Phosphorylated by ATM at Thr-363 following ionizing radiations (IR). Phosphorylation at Ser-428 by RPS6KA1 and/or some PKA is required to inhibit cell growth. Phosphorylation at Ser-428 is also required during neuronal polarization to mediate phosphorylation of BRSK1 and BRSK2. DISEASE: Defects in STK11 are a cause of Peutz-Jeghers syndrome (PJS) [MIM:175200]. PJS is a rare hereditary disease in which there is predisposition to benign and malignant tumors of many organ systems. PJS is an autosomal dominant disorder characterized by melanocytic macules of the lips, multiple gastrointestinal hamartomatous polyps and an increased risk for various neoplasms, including gastrointestinal cancer. Defects in STK11 have been associated with testicular tumors (TEST) [MIM:273300]. A common solid malignancy in males. Germ cell tumors of the testis constitute 95% of all testicular neoplasms. Similarity: Belongs to the protein kinase superfamily. CAMK Ser/Thr protein kinase family. LKB1 subfamily. Contains 1 protein kinase domain. Database links: Entrez Gene: 6794 Human Entrez Gene: 20869 Mouse Omim: 602216 Human SwissProt: Q15831 Human SwissProt: Q9WTK7 Mouse Unigene: 515005 Human Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. LKB1基因是一種抑癌基因,也是一種絲氨酸/蘇氨酸蛋白激酶.LKB1的功能主要是使細(xì)胞周期阻滯在G1期、促進(jìn)細(xì)胞凋亡和調(diào)節(jié)胚胎血管形成等.LKB1基因的胚系突變是Peutz-Jeghers綜合征的主要致病因素.在散發(fā)腫瘤中也發(fā)現(xiàn)有LKB1基因突變,其中以肺腺癌和子宮頸粘液癌突變率較高。 |
