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Human ABL1 Protein expressed in Baculovirus infected Insect Cells - ABIN2004077
Wisniewski, Strife, Swendeman, Erdjument-Bromage, Geromanos, Kavanaugh, Tempst, Clarkson et al.: A novel SH2-containing phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase (SHIP2) is constitutively tyrosine phosphorylated and associated with src homologous and collagen gene (SHC) in chronic ... in Blood 1999
Show all 5 Pubmed References
This is the first report evaluating the role of SOD2 (zeige SOD2 Proteine) in native and T351-mutated BCR-ABL-expressing cells and in a large cohort of chronic myeloid leukemia (zeige BCL11A Proteine) patients. In leukemic cells silenced for SOD2 (zeige SOD2 Proteine) expression a specific down-regulation of the expression of PRDX2 (zeige PRDX2 Proteine) 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 Proteine).
JNJ-26854165, an inhibitor of MDM2 (zeige MDM2 Proteine), inhibits proliferation and triggers cell death in a p53 (zeige TP53 Proteine)-independent manner in various BCR/ABL-expressing cells, which include primary leukemic cells from patients with CML (zeige BCR Proteine) blast crisis and cells expressing the Imatinib-resistant T315I BCR/ABL mutant.
we identified a novel c-Abl:p53:p21 (zeige CDKN1A Proteine) 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 (zeige HSP90 Proteine) 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 (zeige BCL11A Proteine) cell adaptation to energy restriction
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
BCR (zeige BCR Proteine)-ABL1-positive microvesicles from chronic myeloid leukemias malignantly transform human bone marrow mesenchymal stem cells.
c-Abl phosphorylation of Mdm2 (zeige MDM2 Proteine) has a role in regulation of p53 (zeige TP53 Proteine) tumor suppression and bone marrow failure
BOC (zeige BOC Proteine) interacts with ABL and activates JNK (zeige MAPK8 Proteine) 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 (zeige RUNX2 Proteine)-TAZ (zeige TAZ Proteine) master transcription factor complex that is required for osteoblastogenesis, while antagonizing PPARgamma (zeige PPARG Proteine)-mediated adipogenesis.
Normal ABL1 is a tumor suppressor in BCR (zeige BCR Proteine)-ABL1-induced leukemia. ABL1 inhibits expansion and proliferation of BCR (zeige BCR Proteine)-ABL1-expressing leukemic stem cells. Allosteric stimulation of the normal ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase (zeige TYRO3 Proteine) inhibitors.
the ABL family of tyrosine kinases rheostatically enhances IRE1alpha's enzymatic activities, thereby potentiating endoplasmic reticulum stress-induced apoptosis.
p38a (zeige MAPK14 Proteine) 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 Proteine).
Our data show that: i) HDAC2 (zeige HDAC2 Proteine) levels and activity are increased in NPC (zeige NPC1 Proteine) neuronal models and in Npc1 (zeige NPC1 Proteine)(-/-) mice; ii) inhibition of c-Abl or c-Abl deficiency prevents the increase of HDAC2 (zeige HDAC2 Proteine) protein levels and activity in NPC (zeige NPC1 Proteine) neuronal models
The resistance in BCR (zeige BCR Proteine)-ABL1 cells resulted either from the Y253H mutation in the BCR (zeige BCR Proteine)-ABL1 gene or incubation in increasing concentrations of imatinib.
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 Proteine) signaling, we find that the Eph (zeige EPHA1 Proteine) kinase-independent pathway involves the ABL-1 nonreceptor tyrosine kinase (zeige TYRO3 Proteine) 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 Proteine)-7 and the tyrosine kinase abl-1.
oxidative, osmotic, heat shock and starvation stresses induce germ cell apoptosis through a p53 (zeige TP53 Proteine) and EGL-1 independent pathway; the MAPK (zeige MAPK1 Proteine) kinases MEK-1 (zeige MAP2K1 Proteine) and SEK-1 (zeige MAP2K4 Proteine), and the p53 (zeige TP53 Proteine) 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 Proteine) 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