ABL1 Antibody, Biotin conjugated

說明書

中文名稱：

ABL1兔多克隆抗體, Biotin偶聯
貨號：

CSB-PA04355D0Rb
規格：

￥880
其他：

產品詳情
產品評價
相關產品
靶點詳情

產品詳情

產品名稱：

Rabbit anti-Homo sapiens (Human) ABL1 Polyclonal antibody
Uniprot No.：

P00519
基因名：

ABL1
別名：

Abelson murine leukemia viral oncogene homolog 1 antibody; Abelson tyrosine protein kinase 1 antibody; Abl 1 antibody; ABL antibody; ABL proto oncogene 1 non receptor tyrosine kinase antibody; ABL1 antibody; ABL1_HUMAN antibody; bcr/abl antibody; bcr/c abl oncogene protein antibody; c ABL antibody; c abl oncogene 1 non receptor tyrosine kinase antibody; c abl oncogene 1 receptor tyrosine kinase antibody; c ABL1 antibody; JTK7 antibody; p150 antibody; Proto oncogene tyrosine protein kinase ABL1 antibody; Proto-oncogene c-Abl antibody; Tyrosine-protein kinase ABL1 antibody; v abl Abelson murine leukemia viral oncogene homolog 1 antibody; v abl antibody
宿主：

Rabbit
反應種屬：

Human
免疫原：

Recombinant Human Tyrosine-protein kinase ABL1 protein (4-194AA)
免疫原種屬：

Homo sapiens (Human)
標記方式：

Biotin
克隆類型：

Polyclonal
抗體亞型：

IgG
純化方式：

>95%, Protein G purified
濃度：

It differs from different batches. Please contact us to confirm it.
保存緩沖液：

Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, PH 7.4
產品提供形式：

Liquid
應用范圍：

ELISA
Protocols：

ELISA Protocol
儲存條件：

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
貨期：

Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
用途：

For Research Use Only. Not for use in diagnostic or therapeutic procedures.

產品評價

靶點詳情

功能：

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. In response to oxidative stress, phosphorylates serine/threonine kinase PRKD2 at 'Tyr-717'. 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 the caspase CASP9 on 'Tyr-153' and regulates its processing in the apoptotic response to DNA damage. 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. Regulates T-cell differentiation in a TBX21-dependent manner. Phosphorylates TBX21 on tyrosine residues leading to an enhancement of its transcriptional activator activity.
基因功能參考文獻：
1. Findings demonstrate an important role of c-Abl kinase in Runx1-mediated megakaryocytes maturation and platelets formation and provide a potential mechanism of Abl kinase-regulated hematopoiesis. PMID: 29730354
2. Data indicate that c-Abl kinase interacts with and phosphorylates YY1 protein regulation its transcriptional activity. PMID: 29807053
3. The significant role of c-Abl kinase in barrier altering agonists-mediated cytoskeletal biomechanics has been demonstrated. PMID: 29343719
4. We did not find the AIF1L-ETV6 and ABL1-AIF1L fusions in other ETV6-ABL1-positive ALL. Nevertheless, functional studies would be needed to establish the biological role of AIF1L-ETV6 and ABL1-AIF1L and to determine whether they contribute to leukemogenesis and/or to the final leukemia phenotype. PMID: 29726059
5. Once activated, c-Abl kinase regulated the activity of Vav1, which further affected Rac1/PAK1/LIMK1/cofilin signaling pathway. PMID: 29058761
6. The combination of BCR-ABL1 transcript type and spleen size at diagnosis is significantly predictive for achieving an overall MMR and FFS. Incorporating these predictors could be important when making clinical decisions regarding changing therapy for CML patients treated initially with IM. PMID: 28540759
7. Patients with its E255K/V mutation have a poor prognosis, regardless of the stage of the disease at detection. PMID: 29464484
8. Therefore EphA4 is an emerging AbetaOs receptor and the activation of the EphA4/c-Abl axis would explain the synaptic spine alterations found in Alzheimer's disease. PMID: 29378302
9. expression of WASP inversely correlates with BCR-ABL1 levels and the progression of the disease in Chronic myeloid leukemia patients. BCR-ABL1 downregulates WASP in part by epigenetic modification of its proximal promoter. PMID: 29022901
10. The imaging method achieved ultrasensitive detection of BCR/ABL fusion gene with a low detection limit down to 23 fM. And this method exhibited wide linear ranges over seven orders of magnitude and excellent discrimination ability toward target PMID: 27577607
11. This study combines a chemical rescue approach with quantitative phosphoproteomics to identify targets of Abl and their phosphorylation sites with enhanced temporal resolution. Both known and novel putative substrates are identified, presenting opportunities for studying unanticipated functions of Abl under physiological and pathological conditions. PMID: 29341593
12. This is the first report evaluating the role of SOD2 in native and T351-mutated BCR-ABL-expressing cells and in a large cohort of chronic myeloid leukemia patients. In leukemic cells silenced for SOD2 expression a specific down-regulation of the expression of PRDX2 gene was found. PMID: 29550484
13. we identified a novel mutant p53:c-Abl cytoplasmic signaling complex that promotes MDA-MB-231 cell growth and highlights the contextual cues that confer oncogenic activity to c-Abl in breast cancer PMID: 28661474
14. c-Abl/Arg are oncogenic kinases that regulate differential gene expression PMID: 28555614
15. The compound missense mutations in BCR-ABL kinase domain responsible to elicit disease progression, drug resistance or disease relapse in chronic myeloid leukemia. PMID: 28278078
16. JNJ-26854165, an inhibitor of MDM2, inhibits proliferation and triggers cell death in a p53-independent manner in various BCR/ABL-expressing cells, which include primary leukemic cells from patients with CML blast crisis and cells expressing the Imatinib-resistant T315I BCR/ABL mutant. PMID: 27999193
17. we identified a novel c-Abl:p53:p21 signaling axis that functions as a powerful suppressor of mammary tumorigenesis and metastatic progression. PMID: 27626309
18. Double inhibition of the N- and C-terminal termini can disrupt Hsp90 chaperone function synergistically, but not antagonistically, in Bcr-Abl-positive human leukemia cells. PMID: 28036294
19. this study identifies different BCR/Abl protein suppression patterns as a converging trait of chronic myeloid leukemia cell adaptation to energy restriction PMID: 27852045
20. BGB324 does not inhibit BCR-ABL1 and consequently inhibits chronic myeloid leukemia (CML)independent of BCR-ABL1 mutational status. Our data show that Axl inhibition has therapeutic potential in BCR-ABL TKI-sensitive as well as -resistant CML and support the need for clinical trials PMID: 27856601
21. BCR-ABL1-positive microvesicles from chronic myeloid leukemias malignantly transform human bone marrow mesenchymal stem cells. PMID: 28836580
22. Data indicate the Sp1 oncogene functions as a positive regulator for BCR/ABL expression. PMID: 27144331
23. dehydrocostus lactone significantly inhibits the phosphorylation expression of Bcr/Abl, STAT5, JAK2, and STAT3 and downstream molecules including p-CrkL, Mcl-1, Bcl-XL, and Bcl-2 proteins in K562 cells. PMID: 28300289
24. H19 overexpression, a frequent event in chronic myeloid leukemia, was associated with higher BCR-ABL transcript and disease progression. H19 DMR/ICR hypomethylation in CML may be one of the mechanisms mediating H19 overexpression. PMID: 28776669
25. These findings show that drug-resistance mutations in the Abl RM exert their allosteric effect by promoting the activated state of Abl and not by decreasing the drug affinity for the kinase. PMID: 28945248
26. Germline variants in ABL1 cause a syndrome characterized by congenital heart disease, skeletal abnormalities, and failure to thrive. PMID: 28288113
27. c-Abl has a critical role in alpha-synuclein-induced neurodegeneration; selective inhibition of c-Abl may be neuroprotective PMID: 27348587
28. We demonstrate that nanopore technology is suitable for employment in the hematology laboratory for detecting BCR-ABL1 kinase domain mutation in Philadelphia-positive leukemias. PMID: 28663031
29. Frequent molecular monitoring and intervention are required for patients who do not show a reduction in BCR-ABL1 transcripts to these levels after stem cell transplantation. PMID: 27334764
30. c-Abl promotes TGF-beta-induced SKIP/Smad3 interaction. PMID: 28666867
31. Data indicate the feasibility of detecting ABL1 mutations in cerebrospinal fluid (CSF) by next-generation sequencing (NGS) in patients with central nervous system relapse in BCR-ABL1-positive acute lymphoblastic leukemia. PMID: 28451802
32. the e13a2 BCR-ABL1 fusion transcript affects the rate, the depth, and the speed of the response to treatment with imatinib firstline, and that including the transcript type in the calculation of the baseline risk scores may improve prognostic stratification and may help the choice of the best treatment policy. PMID: 28466557
33. Normal ABL1 is a tumor suppressor in BCR-ABL1-induced leukemia. Allosteric stimulation of the normal ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors. PMID: 26864341
34. the ABL family of tyrosine kinases rheostatically enhances IRE1alpha's enzymatic activities, thereby potentiating endoplasmic reticulum stress-induced apoptosis. PMID: 28380378
35. 6 overexpression may contribute to the high proliferation and low apoptosis in chronic myeloid leukemia cells and can be regulated by BCR/ABL signal transduction through downstream phosphoinositide 3-kinase/Akt and Janus kinase/signal transducer and activator of transcription pathways, suggesting cell division cycle protein 6 as a potential therapeutic target in chronic myeloid leukemia. PMID: 28639894
36. ETV6-ABL1 fusion occurs in both lymphoid and myeloid leukemias; the genomic profile and clinical behavior resemble BCR-ABL1-positive malignancies, including the unfavorable prognosis, particularly of acute leukemias. The poor outcome suggests that treatment with tyrosine kinase inhibitors should be considered for patients with this fusion. PMID: 27229714
37. the c-Abl non-receptor kinase phosphorylates DDB1 at residue Tyr-316 to recruit a small regulatory protein, DDA1, leading to increased substrate ubiquitination PMID: 28087699
38. drug sensitivity profiles of a set of compound mutations in ABL kinase were also presented in this study. Thus, our large scale computational study provides comprehensive sensitivity/resistance profiles of ABL mutations toward specific kinase inhibitors. PMID: 28475010
39. though our data support the previous findings that co-expression of BCR-ABL transcripts is due to the occurrence of exonic and intronic polymorphisms in the BCR gene, it also shows that the intronic polymorphism can arise without the linked exonic polymorphism. The occurrence of ABL kinase domain mutation is less frequent in Indian population. PMID: 27748288
40. In silico three-dimensional modeling of apoptin, molecular docking experiments between apoptin model and the known structure of Bcr-Abl, and the 3D structures of SH2 domains of CrkL and Bcr-Abl, were performed. PMID: 22253690
41. The present study screened for the presence of bcr-abl transcripts in the blood of a group of healthy individuals. PMID: 24535287
42. inhibition of c-Abl minimizes receptor recycling pathways and results in chaperone-dependent trafficking of the TfR1 to the lysosome for degradation. PMID: 27226592
43. Data indicate that the biosensor showed excellent analytical performance for the detection of the BCR/ABL oncogene in clinical samples of patients with leukemia. PMID: 27693719
44. In this review, we examine the evidence to illuminate the molecular mechanism of ABL1 in the progression of gastric cancer (GC) patients with depression and identify out new and effective methods for the initial and longterm treatment of GC. PMID: 27666407
45. Studies indicate that the prognosis of BCR-ABL-positive acute myeloid leukemia (BCR-ABL+ AML) seems to depend on the cytogenetic and/or molecular background rather than on BCR-ABL itself. PMID: 27297971
46. Results indicate that eIF4B integrates the signals from Pim and PI3K/Akt/mTOR pathways in Abl-expressing leukemic cells. PMID: 26848623
47. The notion that regular and close monitoring of MSI2 mRNA levels in chronic myeloid leukemia patients might identify patients at risk of progressing to blast crisis was not supported by this study; an increase in MSI2 transcripts does not precede an increase in BCR-ABL1 mRNA levels. PMID: 27160312
48. Collective results lead us to conclude that GADD45alpha modulates curcumin sensitivity through activation of c-Abl > JNK signaling in a mismatch repair-dependent manner PMID: 26833194
49. ABL kinases promote breast cancer osteolytic metastasis by modulating tumor-bone interactions through TAZ and STAT5 signaling. PMID: 26838548
50. mammalian c-Abl plays an important role in steroid hormone receptor-mediated transcription by regulating RBM39 PMID: 27018250
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相關疾病：

Leukemia, chronic myeloid (CML); Congenital heart defects and skeletal malformations syndrome (CHDSKM)
亞細胞定位：

Cytoplasm, cytoskeleton. Nucleus. Mitochondrion.; [Isoform IB]: Nucleus membrane; Lipid-anchor. Note=The myristoylated c-ABL protein is reported to be nuclear.
蛋白家族：

Protein kinase superfamily, Tyr protein kinase family, ABL subfamily
組織特異性：

Widely expressed.
數據庫鏈接：

HGNC: 76

OMIM: 189980

KEGG: hsa:25

STRING: 9606.ENSP00000361423

UniGene: Hs.431048

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