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anti-Human ABL1 Antibodies:
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Human Monoclonal ABL1 Primary Antibody for IF, IP - ABIN967410
Guo, Lian, Xian, Lee, Deisseroth, Stass, Champlin, Talpaz, Wang, Arlinghaus: BCR-ABL protein expression in peripheral blood cells of chronic myelogenous leukemia patients undergoing therapy. in Blood 1994
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Human Polyclonal ABL1 Primary Antibody for IHC (p), ELISA - ABIN537547
Aichberger, Mayerhofer, Krauth, Skvara, Florian, Sonneck, Akgul, Derdak, Pickl, Wacheck, Selzer, Monia, Moriggl, Valent, Sillaber: Identification of mcl-1 as a BCR/ABL-dependent target in chronic myeloid leukemia (CML): evidence for cooperative antileukemic effects of imatinib and mcl-1 antisense oligonucleotides. in Blood 2005
Show all 4 Pubmed References
Human Polyclonal ABL1 Primary Antibody for IHC - ABIN965709
Kawai, Nie, Yuan: Inactivation of NF-kappaB-dependent cell survival, a novel mechanism for the proapoptotic function of c-Abl. in Molecular and cellular biology 2002
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Polyclonal ABL1 Primary Antibody for IF, IHC (p) - ABIN4948294
Danial, Rothman: JAK-STAT signaling activated by Abl oncogenes. in Oncogene 2000
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Human Polyclonal ABL1 Primary Antibody for DB, IHC (p) - ABIN537546
Kim, Cho, Yoon, Park, Kim, Lee, Chun, Kim, Lee et al.: Interpretation of submicroscopic deletions of the BCR or ABL gene should not depend on extra signal-FISH: problems in interpretation of submicroscopic deletion of the BCR or ABL gene with extra ... in Genes, chromosomes & cancer 2005
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Human ABL1 Primary Antibody for IHC - ABIN965708
Sionov, Coen, Goldberg, Berger, Bercovich, Ben-Neriah, Ciechanover, Haupt: c-Abl regulates p53 levels under normal and stress conditions by preventing its nuclear export and ubiquitination. in Molecular and cellular biology 2001
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Human Polyclonal ABL1 Primary Antibody for ELISA, WB - ABIN548465
Van Etten: Cycling, stressed-out and nervous: cellular functions of c-Abl. in Trends in cell biology 1999
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Human Polyclonal ABL1 Primary Antibody for DB, IHC (p) - ABIN389501
Barnes, McIntosh, Whetton, Daley, Bentley, Baldwin: Chronic myeloid leukaemia: an investigation into the role of Bcr-Abl-induced abnormalities in glucose transport regulation. in Oncogene 2005
Show all 6 Pubmed References
Human Monoclonal ABL1 Primary Antibody for ELISA, WB - ABIN965498
Olsen, Blagoev, Gnad, Macek, Kumar, Mortensen, Mann: Global, in vivo, and site-specific phosphorylation dynamics in signaling networks. in Cell 2006
Show all 2 Pubmed References
Human Polyclonal ABL1 Primary Antibody for ICC, IF - ABIN4285624
Sun, Chen, Zhang, Xie, Hou, Hui, Xu, Du, Zhou, Su, Gao: Reduced miR-3127-5p expression promotes NSCLC proliferation/invasion and contributes to dasatinib sensitivity via the c-Abl/Ras/ERK pathway. in Scientific reports 2014
We report the clinical evolution of a Philadelphia-positive ALL patient co-expressing the e1a2 and e14a2 BCR-ABL transcript at diagnosis
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.
Data indicate that c-Abl kinase interacts with and phosphorylates YY1 protein regulation its transcriptional activity.
The significant role of c-Abl kinase in barrier altering agonists-mediated cytoskeletal biomechanics has been demonstrated.
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.
Once activated, c-Abl kinase regulated the activity of Vav1, which further affected Rac1/PAK1/LIMK1/cofilin signaling pathway.
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.
Patients with its E255K/V mutation have a poor prognosis, regardless of the stage of the disease at detection.
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.
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.
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
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.
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.
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
c-Abl/Arg are oncogenic kinases that regulate differential gene expression
The compound missense mutations in BCR-ABL kinase domain responsible to elicit disease progression, drug resistance or disease relapse in chronic myeloid leukemia.
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.
we identified a novel c-Abl:p53:p21 signaling axis that functions as a powerful suppressor of mammary tumorigenesis and metastatic progression.
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.
this study identifies different BCR/Abl protein suppression patterns as a converging trait of chronic myeloid leukemia cell adaptation to energy restriction
WAVE2/c-Abl survival signal required at the hematopoietic stem cell (HSC) fetal liver to marrow transition that confers fitness to the HSC for marrow hematopoiesis
Results indicate that c-Abl may play roles in preimplantation embryo development, especially in TE formation and differentiation.
c-Abl phosphorylated Drp1 at tyrosine 266, 368 and 449 in vitro and in vivo, which augmented the GTPase activity of Drp1 and promoted Drp1-mediated mitochondrial fragmentation.
c-Abl phosphorylation of Mdm2 has a role in regulation of p53 tumor suppression and bone marrow failure
BOC interacts with ABL and activates JNK thereby promoting neuronal differentiation and neurite outgrowth.
These results uncover a murine hepatic steatosis regulatory axis consisting of ABL1-PPARgamma2-MLL4, which may serve as a target of anti-steatosis drug development.
this study shows that signaling downstream of murine inhibitory receptors does not involve c-Abl and that c-Abl plays no major role in NK cell education in the mouse
ABL potentiated the assembly and activation of the RUNX2-TAZ master transcription factor complex that is required for osteoblastogenesis, while antagonizing PPARgamma-mediated adipogenesis.
Normal ABL1 is a tumor suppressor in BCR-ABL1-induced leukemia. ABL1 inhibits expansion and proliferation of BCR-ABL1-expressing leukemic stem cells. Allosteric stimulation of the normal ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors.
the ABL family of tyrosine kinases rheostatically enhances IRE1alpha's enzymatic activities, thereby potentiating endoplasmic reticulum stress-induced apoptosis.
p38a as a major substrate of c-Abl both in vitro and in vivo and c-Abl-mediated phosphorylation is critical for the dimerization of p38a.
Our data show that: i) HDAC2 levels and activity are increased in NPC neuronal models and in Npc1(-/-) mice; ii) inhibition of c-Abl or c-Abl deficiency prevents the increase of HDAC2 protein levels and activity in NPC neuronal models
The resistance in BCR-ABL1 cells resulted either from the Y253H mutation in the BCR-ABL1 gene or incubation in increasing concentrations of imatinib.
These results reveal a new pathway in the DNA damage response wherein ABL-dependent tyrosine phosphorylation of DGCR8 stimulates the processing of selective primary miRNAs.
These findings connect the EphB signaling pathway to the regulation of intestinal adenoma initiation via Abl kinase.
overexpression of Id2 in primary alveolar epithelial cells promotes proliferation by inhibiting a retinoblastoma protein/c-Abl interaction leading to greater c-Abl activity.
The study demonstrates a previously unrecognized mechanism that controls insulin expression through c-Abl-regulated NKx2.2 and GLUT2.
Oocyte-specific inactivation of Omcg1 leads to DNA damage and c-Abl/TAp63-dependent oocyte death associated with dramatic remodeling of ovarian somatic cells.
LPS-induced paxillin phosphorylation at Y31 and Y118 was mediated by c-Abl tyrosine kinase
c-Abl modulates tumor cell sensitivity to antibody-dependent cellular cytotoxicity.
MIG-13-WAVE pathway provides the major force for directional cell motility, whereas MIG-13-WASP partially compensates for its loss, underscoring their coordinated activities in facilitating robust cell migration.
By screening candidate genes involved in Eph signaling, we find that the Eph kinase-independent pathway involves the ABL-1 nonreceptor tyrosine kinase and possibly the phosphatidylinositol 3-kinase pathway
The trade-off in immunological susceptibility in C. elegans is further mediated by the reciprocal activity of lys-7 and the tyrosine kinase abl-1.
oxidative, osmotic, heat shock and starvation stresses induce germ cell apoptosis through a p53 and EGL-1 independent pathway; the MAPK kinases MEK-1 and SEK-1, and the p53 antagonist protein ABL-1, are essential for stress-induced germ cell apoptosis
findings demonstrate that ABL-1, the C. elegans homolog of the mammalian c-Abl nonreceptor tyrosine kinase ABL1, is required for Shigella flexneri pathogenesis in nematodes
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.
Abelson tyrosine-protein kinase 1
, bcr/c-abl oncogene protein
, c-abl oncogene 1, receptor tyrosine kinase
, proto-oncogene c-Abl
, proto-oncogene tyrosine-protein kinase ABL1
, tyrosine-protein kinase ABL1
, v-abl Abelson murine leukemia viral oncogene homolog 1
, Abelson murine leukemia oncogene
, abelson murine leukemia viral oncogene homolog 1
, v-abl Abelson murine leukemia oncogene 1
, Abelson murine leukemia viral (v-abl) oncogene homolog 1
, v-abl Abelson murine leukemia viral oncogene 1