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phospho-c-ABL1+2 (Tyr393+439)抗体

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产品名称: phospho-c-ABL1+2 (Tyr393+439)抗体
产品型号:
产品展商: XYbscience
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简单介绍

phospho-c-ABL1+2 (Tyr393+439)抗体烧蚀原癌基因编码了一种细胞质和核蛋白酪氨酸激酶,它与细胞分化、细胞分裂、细胞粘附和压力反应有关。c-abl蛋白的活性受到其SH3域的负调控,而SH3域的删除则会变成癌基因。t(9,22)转位的结果是BCR(MIM:151410)和烧蚀的基因在许多慢性粒细胞白血病中出现。广泛表达的烧蚀性的酪氨酸激酶的dna结合活性是由cdc2介导的磷酸化来调节的,这表明了一个细胞周期的功能。phospho-c-ABL1+2 (Tyr393+439)抗体烧蚀的基因被表达为6或7-kb的信使rna转录本,或将**个外显子拼接到普通的外显子2-11中。(由RefSeq提供)。


phospho-c-ABL1+2 (Tyr393+439)抗体  的详细介绍

phospho-c-ABL1+2 (Tyr393+439)抗体特异性结合抗原:抗体本身不能直接溶解或杀伤带有特异抗原的靶细胞,通常需要补体或吞噬细胞等共同发挥效应以**病原微生物或导致病理损伤。然而,抗体可通过与病毒或**的特异性结合,直接发挥中和病毒的作用。

产品编号xy- 8440R

英文名称phospho-c-ABL1+2 (Tyr393+439)

中文名称磷酸化非受体酪氨酸激酶c-Abl抗体

别    名c Abl (phospho Y412) (isoform b); phospho-c-ABL1 (Try412) (isoform b); c-Abl 1/2(phospho Y393/439); c-ABL1/2(phospho Tyr393/439); p-c-ABL1/2(Tyr393/439); tyrosine-protein kinase ABL1 isoform b; 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; ABL1_HUMAN.  

说 明 书100ul  

产品类型磷酸化抗体

研究领域细胞生物  **学  信号转导  细胞凋亡  转录调节因子  激酶和磷酸酶  线粒体  

抗体来源Rabbit

克隆类型Polyclonal

phospho-c-ABL1+2 (Tyr393+439)抗体交叉反应 Human, Mouse, Rat, Chicken, Pig, Rabbit, Guinea Pig,

产品应用WB=1:500-2000 ELISA=1:500-1000 IHC-P=1:400-800 IHC-F=1:400-800 ICC=1:100-500 IF=1:50-200 (石蜡切片需做抗原修复)

not yet tested in other applications.

optimal dilutions/concentrations should be determined by the end user.

分 子 量124kDa

细胞定位细胞核 细胞浆 细胞膜 线粒体

性    状Lyophilized or Liquid

浓    度1mg/ml

免 疫 原KLH conjugated Synthesised phosphopeptide derived from human c-Abl isoform a around the phosphorylation site of Tyr393 or c-Abl isoform b around the phosphorylation site of Tyr412:DT(p-Y)TA

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.

phospho-c-ABL1+2 (Tyr393+439)抗体保存条件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.

PubMedPubMed

产品介绍background:

The ABL1 protooncogene encodes a cytoplasmic and nuclear protein tyrosine kinase that has been implicated in processes of cell differentiation, cell division, cell adhesion, and stress response. Activity of c-Abl protein is negatively regulated by its SH3 domain, and deletion of the SH3 domain turns ABL1 into an oncogene. The t(9;22) translocation results in the head-to-tail fusion of the BCR (MIM:151410) and ABL1 genes present in many cases of chronic myelogeneous leukemia. The DNA-binding activity of the ubiquitously expressed ABL1 tyrosine kinase is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function for ABL1. The ABL1 gene is expressed as either a 6- or 7-kb mRNA transcript, with alternatively spliced first exons spliced to the common exons 2-11. [provided by RefSeq].


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.

Polyubiquitinated. Polyubiquitination of ABL1 leads to degradation.

Isoform IB is myristoylated on Gly-2.


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.


SWISS:

P00519


Gene ID:

25

phospho-c-ABL1+2 (Tyr393+439)抗体antibody, Ab)是由效应B细胞(效应**B细胞)分泌,机体用于抵御外来物质,如病毒,**等抗原,结构呈“Y”字型的球状蛋白质,仅仅存在于脊椎动物的血液和B**细胞膜表面。凡是能够跟抗体结合的物质,均被称作抗原,因此对于抗抗体(能够结合抗体的抗体)来说,抗体本身也是一种抗原物质。

   QQ图片20171030091318

phospho-c-ABL1+2 (Tyr393+439)抗体普通抗体重链和轻链的结构

重链结构:普通的**球蛋白具有2条重链(H链),分子量约为50kD,有μ、δ、γ、ε和α五种重链亚型,对应的**球蛋白名称分别为IgMIgG、IgA、IgDIgE。

轻链结构:  普通**球蛋白具有2条轻链(L链),分子质量约25kDa,有κ链和λ链两种亚型,这两种轻链决定了Ig的亚型类别(IgG1,IgG2IgG3,IgG4)。一个天然的Ig分子两条轻链总是相同的,但在同一个体内可存在分别带有κ或λ链的抗体分子。不同种属生物体内两型轻链的比例不同,正常人血清**球蛋白κ链:λ链约为21,而在小鼠的比例为201。

2.2抗体Fab段和Fc

IgG经木瓜蛋白酶酶切后裂解为2个完全相同的Fab段和1Fc,每个Fab段都为单价,可与抗原结合但不会再发生凝集反应;经胃蛋白酶酶切后裂解为1个完整F(ab)2片段和碎片化的Fc片段,F(ab)2片段为双价,可同时结合两个抗原表位。Fab段为抗原结合片段(fragment of antigen binding,Fab),相当于抗体分子的两个臂,由一个完整的轻链和重链的VHCH1结构域组成。Fc段为可结晶段(fragment crystallizable,Fc)相当于IgCH2CH3结构域,是Ig与效应分子或者细胞相互作用的部位。Fab段包含完整的可变区,以及恒定区的CH1区域。Fc段仅指Ig恒定区CH2CH3的区域,相当于Y字结构下面那一部分。

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