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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.
Data suggest that amphipathic beta-strands in 200 N-terminal residues of beta1 domain of APOB (show APOB ELISA Kits) are required for secretion of lipid-rich or lipid-poor particles; residues 300-700 or 1050-1500 of beta1 domain appear to be required for secretion of lipid-rich particles; MTTP (show MTTP ELISA Kits) is required for secretion of intact APOB (show APOB ELISA Kits) but not of truncated APOB (show APOB ELISA Kits). (APOB (show APOB ELISA Kits) = apolipoprotein B (show APOB ELISA Kits); MTTP (show MTTP ELISA Kits) = microsomal triglyceride transfer protein (show MTTP ELISA Kits))
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.
the ABL family of tyrosine kinases rheostatically enhances IRE1alpha's enzymatic activities, thereby potentiating endoplasmic reticulum stress-induced apoptosis.
6 overexpression may contribute to the high proliferation and low apoptosis in chronic myeloid leukemia (show BCL11A ELISA Kits) cells and can be regulated by BCR/ABL signal transduction through downstream phosphoinositide 3-kinase/Akt (show AKT1 ELISA Kits) and Janus kinase/signal transducer and activator of transcription (show STAT1 ELISA Kits) pathways, suggesting cell division cycle protein 6 as a potential therapeutic target in chronic myeloid leukemia (show BCL11A ELISA Kits).
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.
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.
These findings connect the EphB signaling pathway to the regulation of intestinal adenoma initiation via Abl kinase.
overexpression of Id2 in primary alveolar epithelial cells promotes proliferation by inhibiting a retinoblastoma protein/c-Abl interaction leading to greater c-Abl activity.
MIG-13 (show DHPS ELISA Kits)-WAVE pathway provides the major force for directional cell motility, whereas MIG-13 (show DHPS ELISA Kits)-WASP (show WASL ELISA Kits) 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
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.
c-abl oncogene 1, receptor tyrosine kinase
, v-abl Abelson murine leukemia viral oncogene homolog 1
, Abelson murine leukemia viral (v-abl) oncogene homolog 1
, v-abl Abelson murine leukemia viral oncogene homolog 2 (arg, Abelson-related gene)
, tyrosine kinase ABL
, Abelson murine leukemia viral (v-abl) oncogene homolog 2
, Abelson tyrosine-protein kinase 2
, arg, Abelson-related
, tyrosine-protein kinase ABL2
, v-abl Abelson murine leukemia viral oncogene homolog 2
, arg tyrosine kinase
, tyrosine-protein kinase ABL2-like
, Abelson tyrosine-protein kinase 1
, bcr/c-abl oncogene protein
, proto-oncogene c-Abl
, proto-oncogene tyrosine-protein kinase ABL1
, tyrosine-protein kinase ABL1
, Abelson murine leukemia oncogene
, abelson murine leukemia viral oncogene homolog 1
, v-abl Abelson murine leukemia oncogene 1
, v-abl Abelson murine leukemia viral oncogene 1
, microsomal triglyceride transfer protein (large polypeptide, 88kDa)
, microsomal triglyceride transfer protein large subunit