產(chǎn)品編號 | bs-6165R |
英文名稱 | GTPase HRAS Rabbit pAb |
中文名稱 | 轉(zhuǎn)化蛋白p21抗體(原癌基因H-ras抗體) |
別 名 | p21ras; Transforming protein p21; GTPase HRas; GTPase KRas; HRas; HRAS1; KRas; KRAS2; RASH; RASK; RASH_HUMAN; RASK_HUMAN. |
研究領(lǐng)域 | 腫瘤 細胞生物 信號轉(zhuǎn)導(dǎo) 轉(zhuǎn)錄調(diào)節(jié)因子 G蛋白偶聯(lián)受體 |
抗體來源 | Rabbit |
克隆類型 | Polyclonal |
交叉反應(yīng) | Human (predicted: Mouse,Rat,Cow,Chicken,Horse) |
產(chǎn)品應(yīng)用 | WB=1:500-2000
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
理論分子量 | 21 kDa |
檢測分子量 | |
細胞定位 | 細胞核 細胞漿 |
性 狀 | Liquid |
濃 度 | 1mg/ml |
免 疫 原 | KLH conjugated synthetic peptide derived from human HRAS+KRAS: 51-150/189 |
亞 型 | IgG |
純化方法 | affinity purified by Protein A |
緩 沖 液 | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
保存條件 | Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles. |
注意事項 | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
PubMed | PubMed |
產(chǎn)品介紹 |
The KRAS gene encodes the human cellular homolog of a transforming gene isolated from the Kirsten rat sarcoma virus. The RAS proteins are GDP/GTP-binding proteins that act as intracellular signal transducers. The most well-studied members of the RAS (derived from 'RAt Sarcoma' virus) gene family include KRAS, HRAS, and NRAS. These genes encode immunologically related proteins with a molecular mass of 21 kD and are homologs of rodent sarcoma virus genes that have transforming abilities. While these wildtype cellular proteins in humans play a vital role in normal tissue signaling, including proliferation, differentiation, and senescence, mutated genes are potent oncogenes that play a role in many human cancers. Function: Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. Subunit: In its GTP-bound form interacts with PLCE1. Interacts with TBC1D10C. Interacts with RGL3. Interacts with HSPD1. Found in a complex with at least BRAF, HRAS1, MAP2K1, MAPK3 and RGS14. Interacts (active GTP-bound form) with RGS14 (via RBD 1 domain) (By similarity). Forms a signaling complex with RASGRP1 and DGKZ. Interacts with RASSF5. Interacts with PDE6D. Interacts with IKZF3. Interacts with GNB2L1. Interacts with PIK3CG; the interaction is required for membrane recruitment and beta-gamma G protein dimer-dependent activation of the PI3K gamma complex PIK3CG:PIK3R6 (By similarity). Subcellular Location: Isoform 2: Nucleus. Cytoplasm. Cytoplasm, perinuclear region. Note=Colocalizes with GNB2L1 to the perinuclear region. Tissue Specificity: Widely expressed. Post-translational modifications: Palmitoylated by the ZDHHC9-GOLGA7 complex. A continuous cycle of de- and re-palmitoylation regulates rapid exchange between plasma membrane and Golgi. S-nitrosylated; critical for redox regulation. Important for stimulating guanine nucleotide exchange. No structural perturbation on nitrosylation. The covalent modification of cysteine by 15-deoxy-Delta12,14-prostaglandin-J2 is autocatalytic and reversible. It may occur as an alternative to other cysteine modifications, such as S-nitrosylation and S-palmitoylation. Acetylation at Lys-104 prevents interaction with guanine nucleotide exchange factors (GEFs) (By similarity). DISEASE: Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS) [MIM:218040]. A rare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities (typically pulmonic stenosis, hypertrophic cardiomyopathy and/or atrial tachycardia), tumor predisposition, skin and musculoskeletal abnormalities. Defects in HRAS are the cause of congenital myopathy with excess of muscle spindles (CMEMS) [MIM:218040]. CMEMS is a variant of Costello syndrome. Defects in HRAS may be a cause of susceptibility to Hurthle cell thyroid carcinoma (HCTC) [MIM:607464]. Hurthle cell thyroid carcinoma accounts for approximately 3% of all thyroid cancers. Although they are classified as variants of follicular neoplasms, they are more often multifocal and somewhat more aggressive and are less likely to take up iodine than are other follicular neoplasms. Note=Mutations which change positions 12, 13 or 61 activate the potential of HRAS to transform cultured cells and are implicated in a variety of human tumors. Defects in HRAS are a cause of susceptibility to bladder cancer (BLC) [MIM:109800]. A malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and at different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences. Note=Defects in HRAS are the cause of oral squamous cell carcinoma (OSCC). Defects in HRAS are the cause of Schimmelpenning-Feuerstein-Mims syndrome (SFM) [MIM:163200]. A disease characterized by sebaceous nevi, often on the face, associated with variable ipsilateral abnormalities of the central nervous system, ocular anomalies, and skeletal defects. Many oral manifestations have been reported, not only including hypoplastic and malformed teeth, and mucosal papillomatosis, but also ankyloglossia, hemihyperplastic tongue, intraoral nevus, giant cell granuloma, ameloblastoma, bone cysts, follicular cysts, oligodontia, and odontodysplasia. Sebaceous nevi follow the lines of Blaschko and these can continue as linear intraoral lesions, as in mucosal papillomatosis. Similarity: Belongs to the small GTPase superfamily. Ras family. SWISS: P01111 Gene ID: 4893 Database links: Entrez Gene: 3265 Human Entrez Gene: 15461 Mouse Omim: 190020 Human SwissProt: P01112 Human SwissProt: Q61411 Mouse Unigene: 37003 Human Unigene: 334313 Mouse Unigene: 102180 Rat |
產(chǎn)品圖片 | |
1、抗體溶解方法 | |
2、抗體修復(fù)方式 | |
3、常用試劑的配制 | |
4、免疫組化操作步驟 | |
5、免疫組化問題解答 | |
6、Western Blotting 操作步驟 | |
7、Western Blotting 問題解答 | |
8、關(guān)于肽鏈的設(shè)計 | |
9、多肽的溶解與保存 | |
10、酶標抗體效價測定程序 | |
| 国产精品成人A片在线果冻 3d动漫精品啪啪一区二区 | 人妻少妇精品久久久久久久 | 国产一区二区视频在线 | 亚洲AV无码一区二A片清宫性史 | 黄色视频免费看午夜一级片国产 | 波多野吉衣无码内射精品视频 | 91成人无码看片在线观看 | 亚洲免费视频在线观看 | 欧性猛交ⅩXXX乱大交 | 夜精品A片一区二区无码妖精视频 | 国产一级免费观看 | 国产国语对白又又粗又大又爽 | 性感女性黄色免费观看视频网站 | 少妇无套内谢太紧了A片软件 | 日韩视频免费在线观看 | 欧美性猛交XXXX乱大交3 | 18禁在线免费观看av | 亚洲性爱视频在线观看 | 精品人伦一区二区三区蜜桃网站 | 17c精品麻豆一区二区免费 | 无码免费一区二区三区邵氏 | 国产一区二区在线免费观看 | 囯产精品久久久久久久 | 国产裸体美女免费无遮挡 | 巨爆乳肉感一区二区三区 | 人妻无码黑人又大又粗 | 91丝袜 国产在线观看 | 成在线人永久免费视频播放 | 国产无码av在线 | 成人无码精品久久久无套 | 免费A级毛片在线播放不收费换脸 | 亚洲中文字幕在线视频 | 久久久久女人精品毛片九一 | 极品美女黄片免费看看 | 成人免费无码特级毛片A片 欧美性猛交XXXXX水多 | 少妇做爰A片免费看淑女出墙 | JlZZJlZZ国产精品久久 | 久人妻精品秘书丝袜美腿 | 国内精品人妻色欲无码久久久 | 欧美日韩中文字幕 |