| 產(chǎn)品編號 | bs-4085R-AP |
| 英文名稱1 | Rabbit Anti-phospho-c-Abl(Tyr272)/AP Conjugated antibody |
| 中文名稱 | 堿性磷酸酶（AP）標(biāo)記的磷酸化非受體酪氨酸激酶c-Abl抗體 |
| 別 名 | c Abl (phospho Y272); p-c Abl (phospho Y272); Abelson Murine Leukemia Viral Oncogene Homolog 1; Abelson murine leukemia viral v abl oncogene homolog 1; Abl 1; ABL; Abl protein; Abl1; Bcr/c abl oncogene protein; JTK 7; JTK7; p150 ; Proto oncogene tyrosine protein kinase ABL1; Transformation gene oncogene ABL; v abl Abelson murine leukemia viral oncogene homolog 1; v abl. |
| 規(guī)格價格 | 100ul/2980元 購買 大包裝/詢價 |
| 說 明 書 | 100ul |
| 產(chǎn)品類型 | 磷酸化抗體 |
| 研究領(lǐng)域 | 腫瘤 細(xì)胞生物 免疫學(xué) 神經(jīng)生物學(xué) 信號轉(zhuǎn)導(dǎo) 細(xì)胞凋亡 轉(zhuǎn)錄調(diào)節(jié)因子 激酶和磷酸酶 線粒體 |
| 抗體來源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應(yīng) | (predicted: Human, Mouse, Rat, Dog, Pig, Cow, Horse, Rabbit, ) |
| 產(chǎn)品應(yīng)用 | WB=1:50-200 IHC-P=1:50-200 IHC-F=1:50-200
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 126kDa |
| 性 狀 | Lyophilized or Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated Synthesised phosphopeptide derived from human c-Abl isoform b around the phosphorylation site of Tyr272 |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 儲 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 c Abl proto oncogene encodes a protein tyrosine kinase that is located in the cytoplasm and nucleus. In chronic myelogenous leukemia and in a subset of acute lymphoblastic leukemias, the c Abl proto oncogene undergoes a (9;22) chromosomal translocation producing a novel rearranged chromosome (the Philadelphia chromosome) As the result of the fusion of c Abl sequences from chromosome 9 to the Bcr gene on chromosome 22. The molecular consequence of this translocation is the generation of a chimeric Bcr/Abl mRNA encoding activated Abl protein tyrosine kinase. Function: Non-receptor tyrosine-protein kinase that plays a role in many key processes linked to cell growth and survival such as cytoskeleton remodeling in response to extracellular stimuli, cell motility and adhesion, receptor endocytosis, autophagy, DNA damage response and apoptosis. Coordinates actin remodeling through tyrosine phosphorylation of proteins controlling cytoskeleton dynamics like WASF3 (involved in branch formation); ANXA1 (involved in membrane anchoring); DBN1, DBNL, CTTN, RAPH1 and ENAH (involved in signaling); or MAPT and PXN (microtubule-binding proteins). Phosphorylation of WASF3 is critical for the stimulation of lamellipodia formation and cell migration. Involved in the regulation of cell adhesion and motility through phosphorylation of key regulators of these processes such as BCAR1, CRK, CRKL, DOK1, EFS or NEDD9. Phosphorylates multiple receptor tyrosine kinases and more particularly promotes endocytosis of EGFR, facilitates the formation of neuromuscular synapses through MUSK, inhibits PDGFRB-mediated chemotaxis and modulates the endocytosis of activated B-cell receptor complexes. Other substrates which are involved in endocytosis regulation are the caveolin (CAV1) and RIN1. Moreover, ABL1 regulates the CBL family of ubiquitin ligases that drive receptor down-regulation and actin remodeling. Phosphorylation of CBL leads to increased EGFR stability. Involved in late-stage autophagy by regulating positively the trafficking and function of lysosomal components. ABL1 targets to mitochondria in response to oxidative stress and thereby mediates mitochondrial dysfunction and cell death. ABL1 is also translocated in the nucleus where it has DNA-binding activity and is involved in DNA-damage response and apoptosis. Many substrates are known mediators of DNA repair: DDB1, DDB2, ERCC3, ERCC6, RAD9A, RAD51, RAD52 or WRN. Activates the proapoptotic pathway when the DNA damage is too severe to be repaired. Phosphorylates TP73, a primary regulator for this type of damage-induced apoptosis. Phosphorylates PSMA7 that leads to an inhibition of proteasomal activity and cell cycle transition blocks. ABL1 acts also as a regulator of multiple pathological signaling cascades during infection. Several known tyrosine-phosphorylated microbial proteins have been identified as ABL1 substrates. This is the case of A36R of Vaccinia virus, Tir (translocated intimin receptor) of pathogenic E.coli and possibly Citrobacter, CagA (cytotoxin-associated gene A) of H.pylori, or AnkA (ankyrin repeat-containing protein A) of A.phagocytophilum. Pathogens can highjack ABL1 kinase signaling to reorganize the host actin cytoskeleton for multiple purposes, like facilitating intracellular movement and host cell exit. Finally, functions as its own regulator through autocatalytic activity as well as through phosphorylation of its inhibitor, ABI1 Subunit: Interacts with SORBS1 following insulin stimulation. Found in a trimolecular complex containing CDK5 and CABLES1. Interacts with CABLES1 and PSTPIP1. Interacts with ZDHHC16, ITGB1 and HCK (By similarity). Interacts with INPPL1/SHIP2. Interacts with the 14-3-3 proteins, YWHAB, YWHAE, YWHAG, YWHAH, SFN AND YWHAZ; the interaction with 14-3-3 proteins requires phosphorylation on Thr-735 and, sequesters ABL1 into the cytoplasm. Interacts with ABI1, ABI2, BCR, CRK, FGR, FYN, HCK, LYN, PSMA7 RAD9A, RAD51, RAD52, TP73 and WASF3. A complex made of ABL1, CTTN and MYLK regulates cortical actin-based cytoskeletal rearrangement critical to sphingosine 1-phosphate (S1P)-mediated endothelial cell (EC) barrier enhancement. Subcellular Location: Cytoplasm, cytoskeleton. Nucleus. Mitochondrion. Note=Shuttles between the nucleus and cytoplasm depending on environmental signals. Sequestered into the cytoplasm through interaction with 14-3-3 proteins. Localizes to mitochondria in response to oxidative stress. Isoform IB: Nucleus membrane; Lipid-anchor. Note=The myristoylated c-ABL protein is reported to be nuclear. Tissue Specificity: Widely expressed. Post-translational modifications: Acetylated at Lys-711 by EP300 which promotes the cytoplasmic translocation. Phosphorylation at Tyr-70 by members of the SRC family of kinases disrupts SH3 domain-based autoinhibitory interactions and intermolecular associations, such as that with ABI1, and also enhances kinase activity. Phosphorylation at Tyr-226 and Tyr-393 correlate with increased activity. DNA damage-induced activation of ABL1 requires the function of ATM and Ser-446 phosphorylation. Phosphorylation at Ser-569 has been attributed to a CDC2-associated kinase and is coupled to cell division. Phosphorylation at Ser-618 and Ser-619 by PAK2 increases binding to CRK and reduces binding to ABI1. Phosphorylation on Thr-735 is required for binding 14-3-3 proteins for cytoplasmic translocation. Phosphorylated by PRKDC DISEASE: Note=A chromosomal aberration involving ABL1 is a cause of chronic myeloid leukemia. Translocation t(9;22)(q34;q11) with BCR. The translocation produces a BCR-ABL found also in acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). Similarity: Belongs to the protein kinase superfamily. Tyr protein kinase family. ABL subfamily. Contains 1 protein kinase domain. Contains 1 SH2 domain. Contains 1 SH3 domain. Database links: Entrez Gene: 25 Human Entrez Gene: 11350 Mouse Omim: 189980 Human SwissProt: P00519 Human SwissProt: P00520 Mouse Unigene: 431048 Human Unigene: 1318 Mouse Unigene: 474779 Mouse Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. 非受體酪氨酸激酶c-Abl廣泛表達(dá)于各組織細(xì)胞中,c-Abl是非受體酪氨酸激酶Src家族的一個成員。在生理狀態(tài)下,它可以定位于多個亞細(xì)胞結(jié)構(gòu)(如細(xì)胞核、細(xì)胞質(zhì)、線粒體等)中并呈現(xiàn)不同功能。經(jīng)研究認(rèn)為,細(xì)胞核內(nèi)的c-Abl在細(xì)胞凋亡調(diào)控以及DNA損傷修復(fù)過程中起重要作用,而胞質(zhì)中的c-Abl則與細(xì)胞黏附、細(xì)胞分化及氧化應(yīng)激有關(guān)聯(lián)，該蛋白主要用于細(xì)胞凋亡的研究。 |
