FITC标记的磷酸化非受体*激酶c-Abl抗体-,FITC标记的磷酸化非受体*激酶c-Abl抗体上海泛柯实业有限公司手机版

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英文名称	Anti-phospho-c-Abl (Tyr70)/FITC
中文名称	FITC标记的磷酸化非受体*激酶c-Abl抗体
别名	c-Abl(phospho Y70); c-Abl(phospho Tyr70); p-c-Abl(Tyr70); 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	肿瘤细胞生物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
交叉反应	Human, Mouse, Rat, Dog, Pig, Cow, Horse, Rabbit,
产品应用	ICC=1:50-200 IF=1:50-200 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 Tyr70
亚型	IgG
纯化方法	affinity purified by Protein A
储存液	Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.01M PBS, pH 7.4
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.
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.

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