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H19 (show NCKAP1 ELISA Kits) overexpression, a frequent event in chronic myeloid leukemia (show BCL11A ELISA Kits), was associated with higher BCR-ABL transcript and disease progression. H19 (show NCKAP1 ELISA Kits) DMR (show WDR20 ELISA Kits)/ICR hypomethylation in CML (show BCR ELISA Kits) may be one of the mechanisms mediating H19 (show NCKAP1 ELISA Kits) overexpression.
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.
Germline variants in ABL1 cause a syndrome characterized by congenital heart disease, skeletal abnormalities, and failure to thrive.
c-Abl has a critical role in alpha-synuclein-induced neurodegeneration; selective inhibition of c-Abl may be neuroprotective
We demonstrate that nanopore technology is suitable for employment in the hematology laboratory for detecting BCR (show BCR ELISA Kits)-ABL1 kinase domain mutation in Philadelphia-positive leukemias.
Frequent molecular monitoring and intervention are required for patients who do not show a reduction in BCR (show BCR ELISA Kits)-ABL1 transcripts to these levels after stem cell transplantation.
c-Abl promotes TGF-beta (show TGFB1 ELISA Kits)-induced SKIP/Smad3 (show SMAD3 ELISA Kits) interaction.
Data indicate the feasibility of detecting ABL1 mutations in cerebrospinal fluid (CSF (show CSF2 ELISA Kits)) by next-generation sequencing (NGS) in patients with central nervous system relapse in BCR (show BCR ELISA Kits)-ABL1-positive acute lymphoblastic leukemia.
the e13a2 BCR (show BCR ELISA Kits)-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.
Normal ABL1 is a tumor suppressor in BCR (show BCR ELISA Kits)-ABL1-induced leukemia. Allosteric stimulation of the normal ABL1 kinase (show BCR ELISA Kits) activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors.
BOC (show BOC ELISA Kits) interacts with ABL and activates JNK (show MAPK8 ELISA Kits) thereby promoting neuronal differentiation and neurite outgrowth.
These results uncover a murine hepatic steatosis regulatory axis consisting of ABL1-PPARgamma2 (show PPARG ELISA Kits)-MLL4 (show MLL4 ELISA Kits), 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 (show RUNX2 ELISA Kits)-TAZ (show TAZ ELISA Kits) master transcription factor complex that is required for osteoblastogenesis, while antagonizing PPARgamma (show PPARG ELISA Kits)-mediated adipogenesis.
Normal ABL1 is a tumor suppressor in BCR (show BCR ELISA Kits)-ABL1-induced leukemia. ABL1 inhibits expansion and proliferation of BCR (show BCR ELISA Kits)-ABL1-expressing leukemic stem cells. Allosteric stimulation of the normal ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase (show TYRO3 ELISA Kits) inhibitors.
the ABL family of tyrosine kinases rheostatically enhances IRE1alpha's enzymatic activities, thereby potentiating endoplasmic reticulum stress-induced apoptosis.
p38a (show MAPK14 ELISA Kits) 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 (show MAPK14 ELISA Kits).
Our data show that: i) HDAC2 (show HDAC2 ELISA Kits) levels and activity are increased in NPC (show NPC1 ELISA Kits) neuronal models and in Npc1 (show NPC1 ELISA Kits)(-/-) mice; ii) inhibition of c-Abl or c-Abl deficiency prevents the increase of HDAC2 (show HDAC2 ELISA Kits) protein levels and activity in NPC (show NPC1 ELISA Kits) neuronal models
The resistance in BCR (show BCR ELISA Kits)-ABL1 cells resulted either from the Y253H mutation in the BCR (show BCR ELISA Kits)-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 (show DGCR8 ELISA Kits) stimulates the processing of selective primary miRNAs.
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 (show EPHA1 ELISA Kits) signaling, we find that the Eph (show EPHA1 ELISA Kits) kinase-independent pathway involves the ABL-1 nonreceptor tyrosine kinase (show TYRO3 ELISA Kits) 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 (show LYZ ELISA Kits)-7 and the tyrosine kinase abl-1.
oxidative, osmotic, heat shock and starvation stresses induce germ cell apoptosis through a p53 (show TP53 ELISA Kits) and EGL-1 independent pathway; the MAPK (show MAPK1 ELISA Kits) kinases MEK-1 (show MAP2K1 ELISA Kits) and SEK-1 (show MAP2K4 ELISA Kits), and the p53 (show TP53 ELISA Kits) 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 (show TYRO3 ELISA Kits) 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