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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
Show all 7 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
Show all 4 Pubmed References
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
Show all 4 Pubmed References
Polyclonal ABL1 Primary Antibody for IF, IHC (p) - ABIN4948294
Danial, Rothman: JAK-STAT signaling activated by Abl oncogenes. in Oncogene 2000
Show all 3 Pubmed References
Mouse (Murine) Polyclonal ABL1 Primary Antibody for IHC, ELISA - ABIN1584122
Chen, Ren, Liang, Zha, Liu, Chen, Singhal, Ding: c-Abl mediates angiotensin II-induced apoptosis in podocytes. in Journal of molecular histology 2013
Show all 2 Pubmed References
Human Polyclonal ABL1 Primary Antibody for 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
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
Human Monoclonal ABL1 Primary Antibody for 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
Show all 2 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 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
BCR (show BCR Antibodies)-ABL1-positive microvesicles from chronic myeloid leukemias malignantly transform human bone marrow mesenchymal stem cells.
Data indicate the Sp1 (show PSG1 Antibodies) oncogene (show RAB1A Antibodies) functions as a positive regulator for BCR/ABL expression.
dehydrocostus lactone significantly inhibits the phosphorylation expression of Bcr/Abl, STAT5 (show STAT5A Antibodies), JAK2 (show JAK2 Antibodies), and STAT3 (show STAT3 Antibodies) and downstream molecules including p-CrkL (show CRKL Antibodies), Mcl-1 (show MCL1 Antibodies), Bcl-XL (show BCL2L1 Antibodies), and Bcl-2 (show BCL2 Antibodies) proteins in K562 cells.
H19 (show NCKAP1 Antibodies) overexpression, a frequent event in chronic myeloid leukemia (show BCL11A Antibodies), was associated with higher BCR-ABL transcript and disease progression. H19 (show NCKAP1 Antibodies) DMR (show WDR20 Antibodies)/ICR hypomethylation in CML (show BCR Antibodies) may be one of the mechanisms mediating H19 (show NCKAP1 Antibodies) 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 Antibodies)-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 Antibodies)-ABL1 transcripts to these levels after stem cell transplantation.
c-Abl promotes TGF-beta (show TGFB1 Antibodies)-induced SKIP/Smad3 (show SMAD3 Antibodies) interaction.
BOC (show BOC Antibodies) interacts with ABL and activates JNK (show MAPK8 Antibodies) thereby promoting neuronal differentiation and neurite outgrowth.
These results uncover a murine hepatic steatosis regulatory axis consisting of ABL1-PPARgamma2 (show PPARG Antibodies)-MLL4 (show MLL4 Antibodies), 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 Antibodies)-TAZ (show TAZ Antibodies) master transcription factor complex that is required for osteoblastogenesis, while antagonizing PPARgamma (show PPARG Antibodies)-mediated adipogenesis.
Normal ABL1 is a tumor suppressor in BCR (show BCR Antibodies)-ABL1-induced leukemia. ABL1 inhibits expansion and proliferation of BCR (show BCR Antibodies)-ABL1-expressing leukemic stem cells. Allosteric stimulation of the normal ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase (show TYRO3 Antibodies) inhibitors.
the ABL family of tyrosine kinases rheostatically enhances IRE1alpha's enzymatic activities, thereby potentiating endoplasmic reticulum stress-induced apoptosis.
p38a (show MAPK14 Antibodies) 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 Antibodies).
Our data show that: i) HDAC2 (show HDAC2 Antibodies) levels and activity are increased in NPC (show NPC1 Antibodies) neuronal models and in Npc1 (show NPC1 Antibodies)(-/-) mice; ii) inhibition of c-Abl or c-Abl deficiency prevents the increase of HDAC2 (show HDAC2 Antibodies) protein levels and activity in NPC (show NPC1 Antibodies) neuronal models
The resistance in BCR (show BCR Antibodies)-ABL1 cells resulted either from the Y253H mutation in the BCR (show BCR Antibodies)-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 Antibodies) 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 Antibodies) signaling, we find that the Eph (show EPHA1 Antibodies) kinase-independent pathway involves the ABL-1 nonreceptor tyrosine kinase (show TYRO3 Antibodies) 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 Antibodies)-7 and the tyrosine kinase abl-1.
oxidative, osmotic, heat shock and starvation stresses induce germ cell apoptosis through a p53 (show TP53 Antibodies) and EGL-1 independent pathway; the MAPK (show MAPK1 Antibodies) kinases MEK-1 (show MAP2K1 Antibodies) and SEK-1 (show MAP2K4 Antibodies), and the p53 (show TP53 Antibodies) 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 Antibodies) 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