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anti-Human ABL1 Antikörper:
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Human Monoclonal ABL1 Primary Antibody für 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 für 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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Human ABL1 Primary Antibody für 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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Polyclonal ABL1 Primary Antibody für IF, IHC (p) - ABIN4948294
Danial, Rothman: JAK-STAT signaling activated by Abl oncogenes. in Oncogene 2000
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Human Monoclonal ABL1 Primary Antibody für ELISA, WB - ABIN965498
Olsen, Blagoev, Gnad, Macek, Kumar, Mortensen, Mann: Global, in vivo, and site-specific phosphorylation dynamics in signaling networks. in Cell 2006
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Human Monoclonal ABL1 Primary Antibody für ELISA, WB - ABIN968942
Lu, Finnis, Xiang, Lee, Markowitz, Okhrimenko, Brodie: Tyrosine 311 is phosphorylated by c-Abl and promotes the apoptotic effect of PKCdelta in glioma cells. in Biochemical and biophysical research communications 2006
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Human Polyclonal ABL1 Primary Antibody für 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
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Human Polyclonal ABL1 Primary Antibody für 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
Human Polyclonal ABL1 Primary Antibody für WB - ABIN4285621
Yang, Roselli, Patchev, Yu, Almeida: Non-receptor-tyrosine kinases integrate fast glucocorticoid signaling in hippocampal neurons. in The Journal of biological chemistry 2013
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.
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 (zeige SOD2 Antikörper) in native and T351-mutated BCR-ABL-expressing cells and in a large cohort of chronic myeloid leukemia (zeige BCL11A Antikörper) patients. In leukemic cells silenced for SOD2 (zeige SOD2 Antikörper) expression a specific down-regulation of the expression of PRDX2 (zeige PRDX2 Antikörper) 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 (zeige BCL11A Antikörper).
JNJ-26854165, an inhibitor of MDM2 (zeige MDM2 Antikörper), inhibits proliferation and triggers cell death in a p53 (zeige TP53 Antikörper)-independent manner in various BCR/ABL-expressing cells, which include primary leukemic cells from patients with CML (zeige BCR Antikörper) blast crisis and cells expressing the Imatinib-resistant T315I BCR/ABL mutant.
c-Abl phosphorylated Drp1 (zeige CRMP1 Antikörper) at tyrosine 266, 368 and 449 in vitro and in vivo, which augmented the GTPase (zeige RACGAP1 Antikörper) activity of Drp1 (zeige CRMP1 Antikörper) and promoted Drp1 (zeige CRMP1 Antikörper)-mediated mitochondrial fragmentation.
c-Abl phosphorylation of Mdm2 (zeige MDM2 Antikörper) has a role in regulation of p53 (zeige TP53 Antikörper) tumor suppression and bone marrow failure
BOC (zeige BOC Antikörper) interacts with ABL and activates JNK (zeige MAPK8 Antikörper) thereby promoting neuronal differentiation and neurite outgrowth.
These results uncover a murine hepatic steatosis regulatory axis consisting of ABL1-PPARgamma2 (zeige PPARG Antikörper)-MLL4 (zeige MLL4 Antikörper), 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 (zeige RUNX2 Antikörper)-TAZ (zeige TAZ Antikörper) master transcription factor complex that is required for osteoblastogenesis, while antagonizing PPARgamma (zeige PPARG Antikörper)-mediated adipogenesis.
Normal ABL1 is a tumor suppressor in BCR (zeige BCR Antikörper)-ABL1-induced leukemia. ABL1 inhibits expansion and proliferation of BCR (zeige BCR Antikörper)-ABL1-expressing leukemic stem cells. Allosteric stimulation of the normal ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase (zeige TYRO3 Antikörper) inhibitors.
the ABL family of tyrosine kinases rheostatically enhances IRE1alpha's enzymatic activities, thereby potentiating endoplasmic reticulum stress-induced apoptosis.
p38a (zeige MAPK14 Antikörper) 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 (zeige MAPK14 Antikörper).
Our data show that: i) HDAC2 (zeige HDAC2 Antikörper) levels and activity are increased in NPC (zeige NPC1 Antikörper) neuronal models and in Npc1 (zeige NPC1 Antikörper)(-/-) mice; ii) inhibition of c-Abl or c-Abl deficiency prevents the increase of HDAC2 (zeige HDAC2 Antikörper) protein levels and activity in NPC (zeige NPC1 Antikörper) neuronal models
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 (zeige EPHA1 Antikörper) signaling, we find that the Eph (zeige EPHA1 Antikörper) kinase-independent pathway involves the ABL-1 nonreceptor tyrosine kinase (zeige TYRO3 Antikörper) 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 (zeige LYZ Antikörper)-7 and the tyrosine kinase abl-1.
oxidative, osmotic, heat shock and starvation stresses induce germ cell apoptosis through a p53 (zeige TP53 Antikörper) and EGL-1 independent pathway; the MAPK (zeige MAPK1 Antikörper) kinases MEK-1 (zeige MAP2K1 Antikörper) and SEK-1 (zeige MAP2K4 Antikörper), and the p53 (zeige TP53 Antikörper) 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 (zeige TYRO3 Antikörper) 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