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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
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
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
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 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 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
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 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 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
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
The authors conclude that alternate splicing plays a key role in regulating cellular MTP levels by introducing distinct promoter regions and unique 5'-UTRs, which contain elements that alter translation efficiency, enabling the cell to optimize MTP activity.
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 (show BCL11A Antibodies).
JNJ-26854165, an inhibitor of MDM2 (show MDM2 Antibodies), inhibits proliferation and triggers cell death in a p53 (show TP53 Antibodies)-independent manner in various BCR/ABL-expressing cells, which include primary leukemic cells from patients with CML (show BCR Antibodies) blast crisis and cells expressing the Imatinib-resistant T315I BCR/ABL mutant.
we identified a novel c-Abl:p53:p21 (show CDKN1A Antibodies) 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 (show HSP90 Antibodies) 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 (show BCL11A Antibodies) cell adaptation to energy restriction
these data reveal clear cellular defects in induced pluripotent stem cells-derived hepatocytes and cardiomyocytes lacking MTTP (show MTTP Antibodies) activity, including a cardiomyocyte-specific regulated stress response to elevated lipids.
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
c-Abl phosphorylation of Mdm2 (show MDM2 Antibodies) has a role in regulation of p53 (show TP53 Antibodies) tumor suppression and bone marrow failure
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.
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
MTP encodes the large subunit of the heterodimeric microsomal triglyceride transfer protein. Protein disulfide isomerase (PDI) completes the heterodimeric microsomal triglyceride transfer protein, which has been shown to play a central role in lipoprotein assembly. Mutations in MTP can cause abetalipoproteinemia.
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
, microsomal triglyceride transfer protein (large polypeptide, 88kDa)
, microsomal triglyceride transfer protein large subunit
, 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