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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
Data indicate the Sp1 (show PSG1 Proteins) oncogene (show RAB1A Proteins) functions as a positive regulator for BCR/ABL expression.
dehydrocostus lactone significantly inhibits the phosphorylation expression of Bcr/Abl, STAT5 (show STAT5A Proteins), JAK2 (show JAK2 Proteins), and STAT3 (show STAT3 Proteins) and downstream molecules including p-CrkL (show CRKL Proteins), Mcl-1 (show MCL1 Proteins), Bcl-XL (show BCL2L1 Proteins), and Bcl-2 (show BCL2 Proteins) proteins in K562 cells.
H19 (show NCKAP1 Proteins) overexpression, a frequent event in chronic myeloid leukemia (show BCL11A Proteins), was associated with higher BCR-ABL transcript and disease progression. H19 (show NCKAP1 Proteins) DMR (show WDR20 Proteins)/ICR hypomethylation in CML (show BCR Proteins) may be one of the mechanisms mediating H19 (show NCKAP1 Proteins) 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 Proteins)-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 Proteins)-ABL1 transcripts to these levels after stem cell transplantation.
c-Abl promotes TGF-beta (show TGFB1 Proteins)-induced SKIP/Smad3 (show SMAD3 Proteins) interaction.
Data indicate the feasibility of detecting ABL1 mutations in cerebrospinal fluid (CSF (show CSF2 Proteins)) by next-generation sequencing (NGS) in patients with central nervous system relapse in BCR (show BCR Proteins)-ABL1-positive acute lymphoblastic leukemia.
BOC (show BOC Proteins) interacts with ABL and activates JNK (show MAPK8 Proteins) 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 (show RUNX2 Proteins)-TAZ (show TAZ Proteins) master transcription factor complex that is required for osteoblastogenesis, while antagonizing PPARgamma (show PPARG Proteins)-mediated adipogenesis.
Normal ABL1 is a tumor suppressor in BCR (show BCR Proteins)-ABL1-induced leukemia. ABL1 inhibits expansion and proliferation of BCR (show BCR Proteins)-ABL1-expressing leukemic stem cells. Allosteric stimulation of the normal ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase (show TYRO3 Proteins) inhibitors.
the ABL family of tyrosine kinases rheostatically enhances IRE1alpha's enzymatic activities, thereby potentiating endoplasmic reticulum stress-induced apoptosis.
p38a (show MAPK14 Proteins) 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 Proteins).
Our data show that: i) HDAC2 (show HDAC2 Proteins) levels and activity are increased in NPC (show NPC1 Proteins) neuronal models and in Npc1 (show NPC1 Proteins)(-/-) mice; ii) inhibition of c-Abl or c-Abl deficiency prevents the increase of HDAC2 (show HDAC2 Proteins) protein levels and activity in NPC (show NPC1 Proteins) neuronal models
The resistance in BCR (show BCR Proteins)-ABL1 cells resulted either from the Y253H mutation in the BCR (show BCR Proteins)-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 Proteins) 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 Proteins) signaling, we find that the Eph (show EPHA1 Proteins) kinase-independent pathway involves the ABL-1 nonreceptor tyrosine kinase (show TYRO3 Proteins) 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 Proteins)-7 and the tyrosine kinase abl-1.
oxidative, osmotic, heat shock and starvation stresses induce germ cell apoptosis through a p53 (show TP53 Proteins) and EGL-1 independent pathway; the MAPK (show MAPK1 Proteins) kinases MEK-1 (show MAP2K1 Proteins) and SEK-1 (show MAP2K4 Proteins), and the p53 (show TP53 Proteins) 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 Proteins) 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